new feature: see page 14 for asbmb journal …...biochemical advances that are of great relevance to...

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Constituent Society of FASEB

A M E R I C A N S O C I E T Y F O R B I O C H E M I S T R Y A N D M O L E C U L A R B I O L O G Y

J U N E 2006J U N E 2006 w w w . a s b m b . o r g

Constituent Society of FASEB


NEW FEATURE:See page 14 for ASBMB

journal highlights

f e a t u r e s7 JBC Institutes Submission Fee

8 Cell Division Rewind Button Found

9 Viral Protein Helps Infected T-cells Stickto Uninfected Cells

10 Inhibition of Iron-Metabolizing EnzymeReduces Tumor Growth

11 New Hybrid Virus Provides TargetedMolecular Imaging of Cancer

13 New Patient Oriented Research in JLR

d e p a r t m e n t s2 Letters

3 From the Desk of the President

4 News From the Hill

6 Washington Update

10 Spotlight on ASBMB Members

14 ASBMB Bio Bits

16 Biotech Business

17 For Your Lab

19 Career Opportunities

20 Calendar


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O N T H E C O V E R :

12 How ProteinFolding ControlsCellular Routing

JUNE 2006Volume 5, Issue 3

BRONZE AWARD WINNER 2003

AWARDS OF EXCELLENCE:MOST IMPROVED MAGAZINE

COLUMNS & EDITORIALS

DESIGN & LAYOUT

14 NEW FEATURE: ASBMB Bio Bits, Science from ASBMB Journals

13

http://www.asbmb.org

Exploring the BiochemicalBasis of Evolut ion?

L E T T E R S

ASBMBToday JUNE 20062

A S B M B C o u n c i l

OfficersJudith S. Bond PresidentHeidi E. Hamm President-electPeggy J. Farnham SecretaryKenneth E. Neet TreasurerMerle Olson Treasurer-elect

Council MembersWilliam R. Brinkley CouncilorJoan W. Conaway CouncilorRobert A. Copeland CouncilorLila M. Gierasch CouncilorFrederick P. Guengerich CouncilorWilliam J. Lennarz CouncilorPeter J. Parker Councilor William S. Sly CouncilorWilliam L. Smith CouncilorSuzanne Pfeffer CouncilorLinda Pike Councilor

Ex-Officio MembersDennis VoelkerChair, Meetings CommitteeGeorge M. CarmanLaurie S. KaguniCo-chairs, 2006 Program CommitteeJ. Ellis BellChair, Education and ProfessionalDevelopment CommitteeJuliette BellChair, Minority Affairs CommitteeWilliam R. BrinkleyChair, Public Affairs Advisory CommitteeAnthony E. PeggChair, Publications CommitteeHerbert TaborEditor, JBCRalph A. BradshawEditor, MCPEdward A. DennisEditor, JLR

ASBMB Todayis a monthly publication

of The American Society for Biochemistry and Molecular Biology

Editorial Advisory BoardIrwin FridovichRichard W. HansonBettie Sue MastersJ. Evan SadlerRobert D. Wells

CommentsPlease direct any comments or questionsconcerning ASBMB Today to:John D. ThompsonEditor, ASBMB Today9650 Rockville PikeBethesda, MD 20814-3996Phone: 301-634-7145; Fax: 301-634-7126E-mail: [email protected]

For information on advertising contact FASEB AdNet at 800-433-2732

ext. 7157 or 301-634-7157, or email [email protected].

T e l l U s W h a t Y o u

T h i n k

We appreciate receiving lettersthat are suitable for publicationregarding issues of importance orcommenting on articles appear-ing in ASBMB Today. Lettersshould be sent to the editor, JohnThompson, at the address foundat left. Letters must be signedand must contain the writer’saddress and telephone number.The editor reserves the right toedit all letters.

Reference OmittedA reference was omitted from a para-

graph in Professor Kendric C. Smith’sletter, “Ethics in Science: what has hap-pened to it?” in the May issue ofASBMB Today. The paragraph and thereference in question follow:

“Recombinational DNA repairaccounts for 50% of survival after UVirradiation, and excision repair accountsfor 50%, i.e., not the 100% that someauthors would have you believe (for areview on recombinational DNA repair,and the citation of some of these badpapers, see reference).

“Smith, K.C., Recombinational DNARepair: the ignored repair systems.BioEssays 26:1322-1326 (2004).”

To the Editor:In his last book, America’s leading

evolutionist, the recently deceasedStephen Jay Gould, lamented his “rela-tive ignorance” of “the nature ofgenomes” and the “realm of the small-est.”1 Indeed, it is possible that few evo-lutionists are fully aware of recentbiochemical advances that are of greatrelevance to evolutionary theory.2 Thus,at face value, we should have welcomedProfessor Michael Behe’s book, “Dar-win’s Black Box: The Biochemical Chal-lenge to Evolution” as one of the fewwritten on this subject by a professionalbiochemist.3 Unfortunately, as ProfessorSjoerd Bonting points out in the Aprilissue of ASBMB Today, Behe’s argumentsare severely flawed. However, Bontingdoes not point out that Behe alsoignores many of the issues that evolu-tionists have long considered funda-

mental—issues to which biochemistryand molecular biology have made majorcontributions. These include the ques-tions: what are species, how do theyusually originate, and does this origina-tion occur genetically or non-geneti-cally? Indeed, had Behe fully consideredthese issues his title might more appro-priately have been “Darwin’s Black Box:The Biochemical Basis of Evolution.”

Donald R. Forsdyke,Department of Biochemistry,Queen’s University, Kingston,

Ontario, Canada K7L3N6

(1) Gould, S. J. (2002) The Structure of Evolu-tionary Theory. Harvard University Press.

(2) Forsdyke, D. R. (2006) Evolutionary Bioin-formatics. Springer, New York.

(3) Behe, M. J. (1996) Darwin’s Black Box:The Biochemical Challenge to Evolution.The Free Press, New York.

tific leadership. We go into the nextcentury with Heidi Hamm as Presidentand a devoted Council.

Our Journals are of the highest qualitywith outstanding editorial boards andHerb Tabor, Editor, and Bob Simoni,Deputy Editor, of JBC, Ed Dennis, Editor,and Joe Witzum, Deputy Editor, of JLR,and Ralph Bradshaw and Al Burling-ham, Co-Editors, of MCP at the helm.

We have a host of committees, com-posed of volunteers and staff that workbehind the scenes to fulfill our missions.The Program and Meetings Committees

have worked toorganize highquality annualand small meet-ings. The Educa-t i o n a l a n dPro f e s s iona lDevelopmentand MinorityAffairs Commit-t e e s s u p p o r t

activities for the next generation of sci-entists and for diversity. The PublicAffairs Advisory Committee deals withissues in the public arena that affect thelives of our members. The PublicationsCommittee handles the policies andoverarching issues of our Society’s jour-nals. The Awards and Nominating Com-mittees select individuals for recognitionand leadership positions in the Society.One of the Committees that has beenworking to sustain the Society and Jour-nals in these changing times is theFinance Committee. Ken Neet has donean excellent job of chairing this commit-tee for the last six years, and this year heturns over the reigns to Merle Olson.

It is true that we have many challengesto face, for example, procuring fundingfor research, educating the public andour political leaders about the impor-tance of science and science education,and understanding and curing diseases. Iam optimistic that with the brains,energy and vision of biochemists andmolecular biologists we will find solu-tions, continue to be creative, makeadvances, and contribute to the qualityof life through our science. So, thanks toall for a very memorable two years, andbest wishes for the future.

Judith S BondPresident, ASBMB

une 2006 is busting out allover, and is the last month ofmy ASBMB Presidency. The

two years have flown by and are chockfull of great memories. It was a very greatpleasure to be serving in the role of Presi-dent in these transitional years betweenthe first and second century of the Soci-ety and the JBC. It has reaffirmed for mewhat a great tradition/discipline webelong to, as members of the Society andas practitioners/devoted members of thediscipline, and how fundamentallyimportant our science is to advances inmedicine, agriculture, the environment,safety, and the quality of life worldwide.

It is difficult to envision how scientificpublications and communications/infor-mation exchange will evolve in the nextcentury. The information and computersciences are changing so rapidly, that tokeep up with the technology is challeng-ing, no less predicting years ahead. Itseems certain that paper communicationsare dwindling, and that globalization ofall aspects of our discipline is growing.

It is clear that our Society and ourJournals are in good hands. We have astrong and committed staff and scien-

J

JUNE 2006 ASBMBToday 3

From the Desk of the Pres ident :

Dr. Judith Bond

Thanks for the Memories!

ASBMB Finance Committee. From left to right are Judith Bond, Director ofPublications Anthony Pegg, Larry Solomonson, Treasurer-Elect Merle Olson,ASBMB Comptroller Steve Miller, JBC Editor Herbert Tabor, TreasurerKenneth Neet, Ken Mann, Gerry Hart, President-Elect Heidi Hamm, andASBMB Executive Officer Barbara Gordon.

ASBMB Council. From left to right in back are William R. Brinkley, Linda J. Pike, Juliette Bell,Suzanne R. Pfeffer, J. Ellis Bell, Kuan-Teh Jeang, Dennis R. Voelker, William Sly, Edward A. Dennis,William L. Smith, Joan Conaway, F. Peter Guengerich, and Anthony E. Pegg. In front, from left, areRobert Copeland, Kenneth Neet, Judith Bond, Heidi Hamm, Merle S. Olson, and Herbert Tabor.

N E W S F R O M T H E H I L L


by Peter Farnham , CAE , ASBMB Pub l i c A f fa i rs O f ficer

all those that funded at least $100million year in extramural research.

Both Cornyn and Lieberman madepublic statements about the bill. “Ourlegislation,” Cornyn said, “is a simple,common sense approach that willadvance the public’s access to theresearch it funds.” Cornyn said the billhelps three groups as well as the gen-eral public. First, patients can find arti-cles discussing the latest informationon treatment and prognosis for theirdiseases. Second, students will haveaccess to research articles to completeassignments and further their studies.Finally, researchers’ findings will bedisseminated more quickly andbroadly, thus sparking further discov-ery and innovation.

“We wrote this legislation to givetaxpayers access to scientific discover-ies and advancements that they arepaying for,” said Lieberman. “The goalis to share information, avoid duplica-tion of effort and help spur new ideaswhich down the road can mean newtreatments and cures for researchers,medical professionals and patients inConnecticut.”

Mila Becker, Director of GovernmentRelations at the American Society forHematology, said that “The bill is vastin terms of who it would affect,” butshe and other observers are not surewhat immediate impact it is going tohave, as the Senate has many other,more pressing issues on its plate at thistime. But Becker noted that the billhaving been introduced “proves thewhole movement toward public accessis alive and well.”

Martin Frank is the coordinator ofDC Principles for Free Access to Sci-

ence, a coalition of about 50 scientificpublishers (including ASBMB) thatadvocates on public access issues.Frank spoke with ASBMB Today aboutthe many problems associated withthe bill. “The bill does not take intoaccount the potential impacts uponsociety publishers that have served aslong-standing filters and evaluators ofscientific research, including the abil-ity to provide adequate and unbiasedpeer review.”

A reduced ability for some publishersto innovate may be a further result ofthe bill, Frank said. “Many of the non-profit publishers in biomedicalresearch were in the forefront inputting publications on-line. Some ofthe publishers of research in fieldsother than biomedical are not asadvanced as the biomedical publishers,and will thus have less money tospend on innovation.”

Frank also raised cost issues.“Mandatory submission of manu-scripts and publications within sixmonths will negatively impact quar-terly and ‘niche’ journals because ofdifficulties associated with recovery ofsubscriptions costs. The bill also hasthe potential for shifting costs fromreader to the author, with an associ-ated diminution of funds the authorhas available for research.”

Finally, as many as 11 federal agen-cies will be required to arrange for theirfunded research to be deposited insome type of repository, either set upby the agencies themselves or inanother suitable one. The additionalinfrastructure needed will eat up pre-cious resources that could be betterused to support actual research.

Senate bill requiring most sci-entists to submit their feder-ally funded papers to agency

databases within six months of publi-cation was introduced May 2. Thesponsors of the legislation, the FederalResearch Public Access Act of 2006, areSenators John Cornyn (R-TX) and JoeLieberman (D-CT).

The bill greatly expands the publicaccess concept in government. Cur-rently, only the National Institutes ofHealth (NIH) has an active policyregarding public access to federally-funded research (although languageto this effect has been on the booksat almost all federal agencies formany years). The NIH’s current pol-icy is that scientists are encouraged(not required) to submit an elec-tronic copy of any final manuscriptthat has been accepted by a peer-reviewed journal and funded inwhole or in part by NIH, to the NIHresearch database, PubMed Central,and make it publicly accessible assoon as possible, but no later thanwithin 12 months following publica-tion. The Cornyn/Lieberman bill,S.2695, makes a number of impor-tant changes in this policy.

First, the bill would make the sub-mission policy mandatory. A scientistwould be required to submit an elec-tronic copy of his or her final manu-script to a digital library, either to onemaintained by the funding agency orto another repository that permitsfree public access. Further, the workmust become publicly available aftersix months, rather than twelve.Finally, the bill would expand thenumber of federal agencies affected to

Open Access Bil l Introduced in Senate—A

N E W S F R O M T H E H I L L


The bill has been referred to theHomeland Security and GovernmentAffairs Committee. Senator Liebermanis the ranking minority member there.

Watch Events in theHouse

In spite of the attention that theCornyn-Lieberman bill has garnered inthe press, most observers do not expectit to make much progress towardbecoming law any time soon. However,an equally if not more important movemay be afoot in the House. Rep. ErnestIstook (R-OK), following his pattern onthis issue in recent years, has reportedlyprepared language to include in thereport that will accompany the 2007Labor/HHS appropriations bill when itis reported out of subcommittee.

We have also learned that the chair-man of that subcommittee, Rep. RalphRegula (R-OH), has developed an inter-est in mandating public access withina shorter amount of time than the cur-rent 12-month policy at NIH. Weunderstand that Regula is also verybothered by the low compliance rate(about 4 %) at NIH.

Another player in the debate is, ofcourse, NIH Director Elias Zerhouni.He has expressed public sympathywith scientific publishers and hasstated his support for a 12-monthlimit (the original public access policypromulgated by NIH called for a six-month limit, subsequently expandedto 12 in the final version). We alsounderstand that there is more sympa-thy in the Senate for the 12-monthlimit than in the House, in spite of theCornyn-Lieberman legislation havingbeen introduced.

But Watch House Appropriat ions

Although the House has still notapproved a 2007 budget resolution,there will be a minimum of $5 bil-lion more for health and educationprograms than there would havebeen under the President’s Februaryproposal, thanks to the efforts of adetermined group of moderateRepublicans led by Rep. Mike Castle(R-DE) and Nancy Johnson (R-CT)—and also due to the public and vocalsupport of hundreds of affectedgroups, including ASBMB.

As we reported in last month’sissue, GOP moderates have contin-ued to refuse to support any budgetresolution that does not include atleast $7.1 billion in additionalhealth and education spending overthe President’s proposal. Since then,ASBMB and almost 800 other orga-nizations have signed a letter to theHouse leadership urging support forCastle’s position. As the letter notes,“While our organizations representa wide array of domestic priorities,we are united in our effort toadvance the bipartisan goal ofadding $7 billion in discretionaryfunding for health, education, laborenforcement, job training and socialservices programs as the budgetprocess moves forward. On behalfof our millions of constituents, westrongly urge you to provide at least$7 billion in additional federal sup-port…This is essential to sustain the

well-being and prosperity of ournation.” ASBMB also supported abroader FASEB effort to contact soci-ety members in key congressionaldistricts to urge support for the Cas-tle position.

The letter and constituent con-tacts, along with the pressure twodozen dissident Republicans canbring to bear on a new leadershipteam in a closely divided House,apparently worked. The leadershipmet with Castle in early May andoffered to move $5.1 billion out ofdefense and homeland securityspending and into social spending,of which more than $4 billionwould be included in theLabor/HHS appropriations bill(which funds the National Insti-tutes of Health).

Castle issued a statement callingthe leadership’s offer a “significantstep forward,” and a “refreshingapproach.” However, he remainscommitted to a $7.1 billion increasefor health, education and commu-nity programs, which he noted“would take us to FY06 levels whilealso accounting for 2 % inflation. Itis my hope we can continue tonegotiate the difference that remainsso we can adequately fund theseimportant programs.”

ASBMB members in Delaware areurged to contact Rep. Castle andthank him for his efforts.

GOP Moderates, with Community Support,Force Changes in Budget Resolut ion

F A S E B W A S H I N G T O N U P D A T E F A S E B W A S H I N G T O N U P D A T E


What remains perhaps a greater dan-ger to the research community is thatthe Senate stem cell bill would be sent tothe floor as a package of bills. Amongthese would be a bill opposing somaticcell nuclear transfer (SCNT) for the pur-poses of reproductive cloning and mayberesearch, as well, and a bill recently intro-duced by Senator Sam Brownback (R-KS),the Human Chimera Prohibition Act of2006 (S.1373). This bill would criminal-ize a number of experiments involvinghuman-animal chimeras, including theproduction of hybrid embryos throughhetergenuous gamete fertilization andproduction of “a non-human life formengineered such that it contains ahuman brain or a brain derived whollyor predominantly from human neuraltissues.” Although many in the scientificcommunity would undoubtedly agreethere exist ethical boundaries in chimericscience that should not be crossed, someprovisions of the bill could prohibit exist-ing lines of inquiry. These include theintroduction of a human nucleus into anon-human oocyte and the productionof human gametes by a non-humanspecies. The latter has been proposed as apotential method for solving the SCNTrelated problem of having enoughhuman eggs to make SCNT a feasibletechnology.

Unfortunately, while FASEB and therest of the research and stem cell advo-cacy community have done an excellentjob of educating Congress and the pub-lic about the importance of embryonicstem cells, education about chimerasremains an uphill battle. The co-min-gling of human and animal cells inspiresa frightening vision straight out of sci-ence fiction in many non-scientists, andexplaining the details of the science is

proving difficult. President Bush himself,in his State of the Union address, calledfor passage of “legislation to prohibit themost egregious abuses of medicalresearch…creating human-animalhybrids.” If the Brownback bill comes tothe floor, accompanying the stem cellbill, both of them may pass, but onlythe chimera prohibition will survive thePresidential veto. This situation leavesstem cell advocates in an untenable situ-ation: push for the Senate stem cell billin this Congress, knowing it may resultin unintended negative consequences;or let it go for now, and begin fromsquare one in passing the House bill inthe next Congress following the elec-tion. A year ago we were celebrating ahard won victory with passage of theCastle-DeGette bill; this year’s anniver-sary will be far more bittersweet.

May 24, 2006 marked the one yearanniversary of the landmark passage ofthe Stem Cell Research EnhancementAct (H.R. 810) by the U.S. House ofRepresentatives. Many stem cell advo-cates are using this date to buildmomentum for passing the Senate ver-sion of the House bill, or the Castle-DeGette bill, as it is often referred to, inrecognition of its chief sponsors, Rep-resentatives Mike Castle (R-DE) andDiana DeGette (D-CO). The Senate ver-sion (S.471) was introduced by Sena-tors Arlen Specter (R-PA) and TomHarkin (D-IA), and as of this writinghas 40 additional bipartisan sponsors.The legislation would expand federalfunding eligibility to existing stem celllines, created from discarded in vitrofertilized embryos, regardless of whenthey were derived. It seems likely thatif this bill were introduced in the Sen-ate, it would pass. However, there are anumber of extenuating circumstancesthat may make bringing the Senate billto the floor a detrimental scenario forthe research community.

The first, and sadly perhaps best, sce-nario is that the bill passes and is vetoedimmediately by President George W.Bush. The President has threatened toveto any stem cell legislation thatexpanded his existing federal policy,and it is almost certain he would carrythrough on that threat. It remains to beseen if the House and Senate wouldhave enough votes to override a veto,but with very few days in the legislativecalendar in this election year, and anumber of pressing issues facing theCongress, including appropriations,immigration, and the continuing war inIraq, it is improbable that stem cells willremain a top priority.

Stem Cell Researchers’ Dilemma:Seek Vote Now or Wait for New Congress

Deceased MembersASBMB would like to recognize

the following members who passedaway earlier this year:

David W. AllmannLaurence CezanneNicholas R. CozzarelliBernard J. FinkleLawrence GrossmanBeverly M. GuirardRobert J. KadnerAndre S. MeyerCecile M. PickartMartin A. RizackHugh RobertsonJohn R. SokatchKay TanakaAlvin TaurogHarold WerbinWilliam L. Williams


stability, as well as discussions with theJBC Associate Editors, the ASBMB Pub-lications Committee, and the ASBMBCouncil, we feel the decision to insti-

tute the $60 submission fee is war-ranted. The fee is miniscule comparedto the cost of doing the research, andall are aware these days that there areconsiderable costs for handling manu-scripts, even those that do not meetthe JBC Guidelines.

The ASBMB staff will continue toexamine the pricing, subscriptions,marketing and advertising of our jour-nals. There may well be ways toincrease revenues and all avenues todo this will be explored. We will fur-ther investigate the cost structure forour journals and possibilities for goingforward, and bring new options to thetable for the long-range fiscal health ofour journals and Society.

Judith Bond, ASBMB PresidentKenneth E. Neet, ASBMB Treasurer

Nancy J. Rodnan, Director of Publications

fter considerable thought, theleadership of the ASBMB hasdecided to introduce a sub-

mission fee for the Journal of BiologicalChemistry. The $60 fee will be insti-tuted in September 2006. The intent isto offset the cost of processing submit-ted manuscripts. The fee will becharged at the time the manuscript issubmitted to the Journal and must bepaid before the manuscript is reviewed.

The decision to institute the submis-sion fee was in part due to the chang-ing financial profile of our scientificpublications. In addition, there hasbeen a recent decrease in the percent-age of manuscripts accepted (downfrom about 45% to near 30%) and anincrease in production costs. On thebasis of financial projections and theoptions we have available for financial

AJ BC Inst i tutes Submission Fee

cientists have found a way toreverse the process of celldivision, previously thought

to be unstoppable. The discovery couldhave important implications for thetreatment of cancer, birth defects andnumerous other diseases and disorders.The findings appear in the April 13issue of the journal Nature.

“No one has gotten the cell cycle togo backwards before now,” said princi-ple author Gary J. Gorbsky, a scientistwith the Oklahoma Medical ResearchFoundation (OMRF). “This shows thatcertain events in the cell cycle thathave long been assumed irreversiblemay, in fact, be reversible.”

Gorbsky and his OMRF colleagueswere able to block the degradation of aprotein called cyclin B which normallyplays a key role in instigating cell divi-sion. This caused the cell cycle to gobackwards, sending duplicate chromo-somes back to the center of the origi-nal cell, which had been thoughtimpossible, rather than continuing thedivision process. This appeared to be


SCell Division Rewind Button Found


because cyclin B was still present in thecell when, under natural circum-stances, it should not be.

But the researchers had to act at aparticular point, or the interventionfailed to reverse cell division. This sug-gests many other factors involved inregulating cell division.

“Our studies indicate that the fac-tors pointing cells toward division canbe turned and even reversed,” Gorb-sky said. “If we wait too long, how-ever, it doesn't work; so we know thatthere are multiple regulators in thecell division cycle. Now we will beginto study the triggers that set theseevents in motion.”

The findings may prove importantto controlling the development andmetastasis of certain cancers. It alsoholds promise for the prevention andtreatment of birth defects and a widevariety of other conditions.

“Dr. Gorbsky's results provide ele-gant proof that the cell cycle must beprecisely controlled,” said Dr. RodgerMcEver, OMRF vice president

of research. “Nowhe and his lab can work towarddeveloping innova-tive methods toprobe and betterunderstand thecomplex process ofcell division.”

ASBMB member Gary J. Gorbskyholds the W.H. and Betty PhelpsChair in Developmental Biology andheads the Molecular, Cell and Devel-opmental Biology (MCDB ) ResearchProgram at OMRF. He is also AdjunctProfessor in the Department of CellBiology and a member of the CancerInstitute at the University of Okla-homa Health Science Center. Heobtained his B.S. from the College ofWilliam and Mary in 1976, and bothhis M.S. and Ph.D. from PrincetonUniversity in 1978 and 1982, respec-tively. Gorbsky carried out his PhDstudies with Dr. Malcolm Steinbergand his postdoctoral research wasdone with Dr. Gary Borisy and Dr.Hans Ris at the University of Wiscon-sin. He became Assistant then Associ-ate Professor in the Department ofCell Biology at the University of Vir-ginia, and then went on to becomeProfessor of Cell Biology at the Uni-versity of Oklahoma Health SciencesCenter. In 2003 he joined the OMRFas Program Head of MCDB.

Xenopus S3 tissueculture cells labeled for

microtubules (green)and for DNA

(magenta). The cell inthe upper middle area

is in mitosis. Theculture was treated 10

min earlier withflavopiridol, which is

causing the cell to beginto exit mitosis.

Photograph courtesy of Joseph Mills.

Dr. Gary J. Gorbsky


cent of those infected develop adult Tcell leukemia or lymphoma (ATLL), anaggressive disease characterized by along latent period and the proliferationof T cells. The infected cells are spreadfrom person to person during sexualactivity and by blood and breast milk.

In the body, the HTLV-1 mainly targetsimmune-system cells known as CD4 Tlymphocytes. These immune cells coor-dinate immune responses in partthrough physical contact with otherimmune cells. The cells adhere to oneanother using a protein known as LFA-1,which is found on the cells' surface.

In this study, Lairmore and his col-laborators examined the influence ofthe p12 protein on LFA-1 adhesion.The researchers compared cellsinfected with HTLV-1 that lacked thep12 protein to cells that were infectedby normal HTLV-1.

They found that the p12 protein notonly activated the T cells, but caused

the cells infected with normal HTLV-1to have far greater adherence than cellsinfected with viruses that lacked p12 ina standardized adherence test.

In addition, they showed that thegreater adherence did not occurbecause the infected cells made moreof the LFA-1 protein, but ratherbecause already existing LFA-1 proteinmolecules gathered into large clusterson the cell surface.

(LFA-1 proteins float in the cellmembrane like buoys in semisolidgelatin. They can move across the sur-face of the cell and form clusters whendirected to do so by signals fromwithin the cell.)

“Our study is the first to show thatHTLV-1 p12 not only enhances theactivity of infected T cells, but that itpromotes the spread of the virusfrom cell to cell by causing LFA-1receptors to cluster on the cell sur-face,” Lairmore says.

ew research shows that a pro-tein made by a cancer viruscauses infected immune cells

to cling to other immune cells,enabling the virus to spread.

The virus, the human T lym-photropic virus type 1 (HTLV-1), istransmitted mainly when infected cellsknown as T lymphocytes, or T cells,touch uninfected T cells.

The finding helps explain how thiscell-to-cell transmission happens. Itsuggests that an HTLV-1 proteinknown as p12 activates infected T cellsand causes them to become sticky andadhere to other T cells.

The greater stickiness happensbecause the p12 viral protein causesspecial adherence proteins found onthe surface of T cells to cluster in largegroups—something that normallyhappens when T cells touch to com-municate with one another during animmune response.

The findings also suggest that a drugthat inhibits the p12 protein might alsohelp prevent HTLV-1 transmission.

The research, published in the Mayissue of the Journal of Immunology, wasled by scientists with The Ohio StateUniversity Comprehensive CancerCenter and the OSU College of Veteri-nary Medicine.

“This study indicates that the p12protein plays an important role in pro-gramming infected cells for cell-to-celltransmission,” says principal investiga-tor Michael D. Lairmore.

“It shows that this virus takes advan-tage of something that T cells do nor-mally; but, in this case, the virus isstimulating the interaction with otherT cells rather than a normal immuneresponse.”

HTLV-1 infects an estimated 15 to 25million people worldwide. About 5 per-

Viral Protein Helps Infected T-cel ls St ickto Uninfected CellsN

ASBMB member Michael D. Lair-more is currently Chairperson of theDepartment of Veterinary Bio-sciences and the Associate Director ofBasic Sciences for The Ohio StateUniversity, Comprehensive CancerCenter. He earned his D.V.M. fromthe University of Missouri (1981) andhis Ph.D. from Colorado State Uni-versity (1987).His studies led to his appoint-ment to theNational Centersfor Disease Con-trol (CDC) inAtlanta, Georgiain 1987. Lairmore joined the OSUfaculty in 1990, and rose to the rankof full professor while establishing an

international reputation as a researcherand educator. He has authored or co-authored over 121 scientific publica-tions on topics that include novelvaccine approaches to overcome barri-ers to effective immune responsesagainst retroviruses, clarification ofwhich target cells express the CD4AIDS receptor in the human placenta,and the first report of an infectiousmolecular clone of HTLV-1. Lairmoreis the recipient of numerous acade-mic awards including the PfizerAward for Research Excellence,National Omega Tau Sigma CareerAward, Phi Zeta Honor Society andResearch Award, and the DavidWhite Research Award. He is a mem-ber of several editorial boards includ-ing The Journal of Virology.

Dr. Michael Lairmore


liver and is responsible for breakingdown heme, a molecule that consists ofan iron atom surrounded by a largering of other atoms. Further evidenceof the connection between heme oxy-genase-1 and the Kaposi’s sarcoma viruscame when elevated levels of the pro-tein were detected in biopsy tissue fromoral AIDS-Kaposi’s sarcoma lesions.

“Taking into account the predomi-nant function of vGPCR in Kaposi’ssarcoma and the elevated expression ofheme oxygenase-1 observed inKaposi’s sarcoma lesions, we decided tostudy whether vGPCR could increaseheme oxygenase-1 expression and ifso, to explore the putative role of theenzyme in vGPCR-dependent transfor-mation,” explains study author MariaJulia Marinissen of the UniversidadAutonoma de Madrid.

Marinissen and her colleagues foundthat vGPCR does indeed increase pro-duction of the heme oxygenase-1 pro-tein and the RNA that codes for it. Theyalso discovered that mice with tumorsthat were given specific pharmacologi-

cal inhibitors that blocked heme oxyge-nase-1 activity showed a significantreduction in vGPCR-induced tumorgrowth without apparent side effects.

“Considering that heme oxygenase-1is overexpressed in human Kaposi’s sar-coma lesions, the inhibition of intratu-moral heme oxygenase-1 activity bycurrently available drugs can representa new anticancer tactic in the treat-ment of Kaposi’s sarcoma and may beof potential clinical interest after moreextensive investigation,” says Marinis-sen. “The inhibitor that we used in thisstudy is a tin-protoporphyrin. A recentclinical trial showed that the inhibitorcan be administered to newborns atany time point in the progression ofpostnatal hyperbilirubinemia to rapidlyand predictably block heme degrada-tion and prevent severe jaundice with-out significant short- or long-term sideeffects. This is very important becauseit shows that the inhibitor has beensuccessfully used in human clinical tri-als to treat diseases in which heme oxy-genase-1 is involved.”

report in the April 21 issueJournal of Biological Chemistry(281, 11332-11346) shows

that inhibition of heme oxygenase-1,an enzyme involved in iron metabo-lism, reduces Kaposi sarcoma tumorgrowth. This discovery, which was fea-tured as a Paper of the Week, couldresult in the production of new drugsto treat this and other viral cancers.

Kaposi sarcoma is the most frequenttumor in AIDS patients and is causedby infection of the patients with theKaposi sarcoma-associated herpesvirus. The Kaposi sarcoma virusgenome contains sequence thatencodes for a protein called viral Gprotein-coupled receptor (vGPCR) thatplays a key role in the development oftumoral lesions.

Interestingly, a study done in early2004 showed that the cellular produc-tion of a protein called heme oxyge-nase-1 could be turned on by theKaposi’s sarcoma-associated her-pesvirus. Heme oxygenase-1 is anenzyme that is expressed in spleen and

A

Inhibit ion of Iron-Metabolizing EnzymeReduces Tumor Growth

By N ico le Kresge , Staf f Sc ience Wr i ter

UAB’s 12 schools and the Joint HealthSciences Departments. Each facultymember so honored receives a cashaward and a Steuben apple that standsas a symbol of his or her achievement.Students, faculty and alumni make thenominations for the award.

According to the UAB Reporter, Benoshas demonstrated a commitment toteaching that ranges from the elemen-tary classroom to students pursuing doc-toral degrees. He is credited withexcellence in teaching, research and

service, and alsocommended forhis ability andwillingness to helpdevelop coursesthat address spe-cific needs duringhis nearly 21 yearsat UAB.

Benos, who hasbeen an ASBMB member since 1998, isalso currently an Associate Editor forthe Journal of Biological Chemistry.

his past May, ASBMB memberDale J. Benos, Professor andChair, Department of Physiol-

ogy and Biophysics at the University ofAlabama at Birmingham (UAB), wasawarded the 2006 UAB PresidentialAward for Excellence in Teaching.

The President's Awards for Excel-lence in Teaching were established byformer UAB President Charles A.McCallum in 1990 to recognize excep-tional accomplishments in teaching.Recipients are chosen from each of

Dale J. Benos Receives UAB Teaching AwardT

Dr. Dale J. Benos

S P O T L I G H T O N A S B M B M E M B E R S


bacterial virus (phage). Unlike animalviruses that infect mammalian cells,bacterial viruses have evolved to infectonly bacterial hosts. The paper showshow particles of the hybrid virus, calledAAV phage or AAVP, can serve as avehicle for targeted delivery of genes toexperimental tumors in mice and tothe tumors' blood vessel supply, provid-ing a strategy for finding tumors andgenetically marking them for imagingon a clinic-ready body scanner.

The AAVP hybrid combines the abilityof the bacterial virus to target specific tis-sues with the capability of the mam-malian virus to deliver genes to cells. Thecrucial vehicles, or vectors, in the AAVPhybrid retained the properties of theirrespective parental viruses, which theresearchers called a surprising outcome.

“This is only a proof-of-concept, andalthough we have yet to translate thesehybrid viruses for use in humans, wehope that this new system will havefuture clinical applications,” says

Wadih Arap, M.D., the co-leader of thestudy and professor of Medicine andCancer Biology. “In addition to theobvious biological interest, when thevector is refined for patient use, it couldperhaps help us diagnose, monitor andtreat human tumors more accurately.”

The finding is the latest in a series ofstudies by Pasqualini and Arap that arebuilt around their discovery that thehuman vasculature system containsunique molecular addresses. Organsand specialized tissues also have specific“zip codes” on their blood vessels, as dotumor blood vessels. Knowing this,Pasqualini and Arap designed, con-structed, evaluated, and validated thetargeted AAVP system over the past sev-eral years. Amin Hajitou, Ph.D., a post-doctoral fellow in the Arap/Pasqualinilaboratory and first author of the Cellstudy says, “we were pleased by thestrong effects of gene transfer in mousemodels of common diseases such asbreast and prostate cancer.”

Their next step was to work closelywith the team of M. D. Andersonresearcher Juri Gelovani, M.D., Ph.D.,chair of the Department of Experimen-tal Diagnostic Imaging, a pioneer indevelopment of molecular-geneticimaging tools.

“We could see by using positronemission tomography that the reporterand therapeutic genes were beingexpressed throughout the tumors inthe animals,” Gelovani says. “This isan example of the so-called ‘theragnos-tic’ approach, a combination of thewords therapeutic and diagnostic.”

The international collaborativeresearch team plans to evaluate the safetyand efficacy of other hybrid vectors inanimal models. The ultimate goal is toadapt and optimize the AAVP-based tar-geting prototype for use in patients.

esearchers at The Universityof Texas M. D. Anderson Can-cer Center have created a new

class of hybrid virus and demonstratedits ability to find, highlight, anddeliver genes to tumors in mice.

Researchers say the advance, reportedin the April 21 issue of the journal Cell,is potentially an important step inmaking human cancer both more visi-ble and accessible to treatment.

“In tumor-bearing mice, we showthat this hybrid virus can target tumorssystemically to deliver an imaging ortherapeutic gene,” says co-leader of thestudy, Renata Pasqualini, Ph.D., profes-sor of Medicine and Cancer Biology.“The signal is specific only to tumors,so one can monitor drug effectivenessat the molecular level.”

The team created and characterizedthe hybrid viruses by combininggenetic elements and biological attrib-utes of an animal virus (adeno-associ-ated virus, or AAV) with those of a

New Hybrid Virus Provides Targe tedMolecular Imaging of CancerR

ASBMB member Renata Pasqualini isprofessor of medicine at The Universityof Texas M. D. AndersonCancer Center. Her researchexploits the molecular diver-sity of blood vessels todevelop targeted therapiesand imaging agents for can-cer and other debilitating dis-eases. Pasqualini received herdoctorate in biochemistryfrom the Ludwig Institute for CancerResearch at the University of Sao Paulo,Brazil, in 1990. She completed post-doctoral research fellowships at Har-vard Medical School, Dana FarberCancer Institute and The BurnhamInstitute in La Jolla, Calif.

Pasqualini is principal investigator fora large interdisciplinary study titled

“The Human Vascular Map Project,”which focuses on developing a road

map with “zip codes” of themolecular anatomy of bloodvessels in human organs andtissues. Pasqualini and WadihArap, M.D., an attendingphysician and professor ofmedicine and cancer biologyat M. D. Anderson, have pio-neered the “zip code” tech-

nique to identify proteins specific todifferent tissues, including prostate andbreast cancer. Their group also has iden-tified homing ligands that target whitefat vasculature in mice. Their ongoingwork aims to develop ways to destroyblood vessels that support fat accumu-lation, a strategy that could eventuallybe applied to human obesity treatment.

Dr. Renata Pasqualini


control system. These proteins couldbe rescued with pharmacologicalchaperones, or “pharmacoperones,”and restored to function.

“Clearly, production of misfoldedproteins is an important etiology ofdisease,” says Conn. “This replaces theview that mutants are always function-ally defective and leads to new thera-peutic approaches.”

Now Conn and his colleagues haveshown that this approach is alsoexploited as a means of controllingrouting in normal function ofhealthy cells. The study appears inthe March 31 issue of the Journal ofBiological Chemistry (281: 8417-8425)and shows a motif of four non-adja-cent amino acids that allows this tooccur in the human GnRHR.

The researchers discovered that theprimate GnRHR contains a lysineresidue at position 191 that restricts itsexpression at the plasma membrane,causing it to be retained in the endo-plasmic reticulum and then degraded.Deletion of this amino acid dramati-cally increased its expression at theplasma membrane, and rodents thatnormally do not contain Lys191expressed the synthesized receptor atmuch higher levels.

Conn and his colleagues showedthat Lys191 in the human GnRHreceptor destabilizes a specific Cys-Cys bridge that is essential for cre-ation of a properly folded receptor.When they expressed the humanplasmid in host cells, the bridgeformed about half the time, resultingin about half the receptor being prop-erly trafficked and the other halfbeing retained in the endoplasmicreticulum and destroyed.

The view that Lys191 causes thereceptors to be misrouted was alsosupported by the observation that apharmacoperone that enabledmutants to pass through the cellular

everal years ago, P. MichaelConn, associate director ofthe Oregon National Primate

Research Center (Oregon Health andSciences University), showed thatmost disease causing mutants of thehuman gonadotropin-releasing recep-tor (GnRHR) were actually competentproteins that had become misroutedand retained by the cellular quality

S

Protein Folding Controls Cellular Rout ingBy N ico le Kresge , Staf f Sc ience Wr i ter

Correct protein folding is required for accuratesubcellular routing of receptors, ion channelsand enzymes. GPRCs use engagement with thecellular quality control apparatus to regulateplasma membrane expression of receptors as apart of normal cellular function. Image by JoelIto and P. Michael Conn, Oregon NationalPrimate Research Center, OHSU.


which proteins, by interacting withchaperones, can rapidly respond toneed without protein synthesis.”

In the JBC paper, Conn’s lab alsoprovides evidence that other proteinsemploy this mechanism as well andthat this is a more common mecha-nism than is currently recognized.

“These studies explain how verymodest changes in DNA sequencemake possible major differences inprotein processing and cellular traf-ficking and present a mechanism bywhich cells can control functionalprotein levels without the require-ment for transcription or translation,”concludes Conn.

quality control system also increasedthe plasma membrane expression ofthe human receptor but not the rat receptor.

“The creation of a receptor that isdelicately balanced between theplasma membrane and the endoplas-mic reticulum has resulted in a humanreceptor that is extremely sensitive tomutation,” explains Conn. “Tolera-tion, let alone strong and convergentevolutionary pressure for such muta-tional liability, along with the burdenof inefficient function, suggests thatthis post-translational regulation isextremely important in advancedmammals. It provides a mechanism by

ASBMB member P. Michael Conn isthe Associate Director and Senior Sci-entist of the Oregon National PrimateResearch Center, Special Assistant tothe President, and Professor of Physi-ology and Pharmacology and of CellBiology and Development at OregonHealth and Science University. Afterreceiving a B.S. degree and teachingcertification from the University ofMichigan (1971), a M.S. from NorthCarolina State University (1973), anda Ph.D. degree from Baylor College ofMedicine (1976), Conn did a fellow-ship at the National Institute of ChildHealth and Human Development,NIH, then joined the faculty in theDepartment of Pharmacology, DukeUniversity Medical Center where hewas promoted to Associate Professorin 1982. In 1984, he became Professorand Head of Pharmacology at theUniversity of Iowa College of Medi-cine, a position he held for elevenyears. Conn is the former Editor-in-Chief of Endocrinology, Molecular andCellular Neurosciences, Methods in Neu-roscience and Recent Progress in Hor-

mone Research and prior editor of J. Clinical Endocrinology and Metabo-lism; he is presently is the Editor-in-Chief of Endocrine, Methods, Contemporary Endocrinology, and Con-temporary Drug Therapy.

Conn, a vigorous supporter of thehumane use of animals in research isbest known for his research in thearea of the cellular and molecularbasis of action of gonadotropinreleasing hormone action in the pitu-itary and CNS. He has authored orco-authored nearly 300 publicationsin this area. The work of his labora-tory has been recognized with aMERIT award from the NIH, the J. J.Abel Award of the American Societyfor Pharmacology and ExperimentalTherapeutics, the Weitzman, Oppen-heimer and Ingbar Awards of theEndocrine Society, the National Sci-ence Medal of Mexico (the MiguelAleman Prize) and the StevensonAward of Canada. Conn is a formerPresident of the Endocrine Society,during which time he founded theHormone Foundation.

In an effort to incorporate moreclinical patient-oriented research,the Journal of Lipid Research is initi-ating a new category for submittedmanuscripts called “Patient-OrientedResearch Articles.” This category willinclude research articles containingstudies in which human subjectsplay an important role and at leastone of the authors has had directcontact with the subjects. The crite-ria for review will be similar to regu-lar research articles. To facilitatesubmission of these manuscripts, theonline system for JLR manuscriptsubmission now has a check box forpapers in the Patient-OrientedResearch category.

The new section will launch in theAugust 2006 issue of JLR. This issue willalso contain a new Thematic ReviewSeries devoted to patient-orientedresearch. The series will be edited byJLR Associate Editor Henry Ginsbergand will consist of several invitedreviews covering a broad range ofpatient-oriented research involvinglipids, lipoproteins, and arteriosclerosis.

For more information please visitthe JLR website at www.jlr.org.

New Pat ient-Oriented Research

Sect ion in J LR


S c i e n c e fr o m A S B M B J o u r n a l sBy N ico le Kresge , Staf f Sc ience Wr i ter

Mussels are able to thrive despite persistent surf and tides in part due totheir ability to adhere to surfaces via a holdfast structure called thebyssus. This fibrous extracellular structure consists of a bundle of threadseach of which is tipped distally by an adhesive plaque that bonds to min-eral and metal surfaces. Using direct laser desorption ionization massspectrometry, the authors of this manuscript analyze the “footprints”that were deposited onto glass coverslips by the California musselMytilus californianus. They find that the secretions contain variants of afamily of proteins known as M. californianus foot protein 3 (mcfp3).Purification of these proteins from plaques and foot tissue reveals thatmcfp3s are highly polar, dihydroxyphenylalanine-rich molecules. Thesefindings suggest that adhesion in the California mussel may be governedby novel interactions in addition to the usual noncovalent ones.

Mussel footprint plaques were analyzed by MALDI.

Probing the Adhesive Footprints ofMytilus californianus Byssus Hua Zhao, Nicholas B. Robertson, Scott A. Jewhurst, and J. Herbert Waite

J. Biol. Chem. 2006 281: 11090-11096

Formins Regulate Actin Filament Flexibilitythrough Long Range Allosteric InteractionsBeáta Bugyi, Gábor Papp, Gábor Hild, Dénes Lôrinczy, Elisa M. Nevalainen, Pekka Lappalainen, Béla Somogyi, and Miklós Nyitrai

J. Biol. Chem. 2006 281: 10727-10736

Formins are proteins that nucleate actin filaments and play essentialroles in the regulation of the actin cytoskeleton. In this paper, the authorsdescribe the effects of a formin fragment from mice (mDia1-FH2) on theconformation of actin filaments using a temperature-dependent fluores-cence resonance energy transfer method. Their results reveal that forminfragments increase the flexibility of actin filaments. The magnitude of thiseffect depends on the formin:actin concentration ratio. The characteristicsof this concentration dependence indicate that more than one mecha-nism is involved in the formin effects. From their findings, the authorspropose a model in which formin binding to barbed ends of actin makesthe filaments more flexible through long range allosteric interactionswhile formin binding to the sides of the filaments stabilizes the protomer-protomer interactions. A model showing how formin affects the

dynamic properties of actin filaments.

AS BM B Bio Bits


S c i e n c e fr o m A S B M B J o u r n a l s

In most mammalian tissues, the synthesis of triglyceridesinvolves the sequential addition of fatty acids to a glycerol back-bone, with unique enzymes catalyzing each step. The 1-acylglyc-erol-3-phosphate O-acyltransferase (AGPAT) is involved in anintermediate acylation step. To date, seven AGPAT genes havebeen identified, but their physiological functions remain elusive.In this study, the authors generate a mouse model deficient inAGPAT6 and find that the mice have a 25% reduction in bodyweight. The mice are also resistant to both diet-induced andgenetically-induced obesity. Among other things, this reductionin body weight is associated with increased energy expenditure,reduced triglyceride accumulation in adipose tissue, and a lack ofadipose tissue in the subdermal region.

Mice without AGPAT6 lack a subdermal fat cell layer.

Agpat6 Deficiency Causes SubdermalLipodystrophy and Resistance to ObesityLaurent Vergnes, Anne P. Beigneux, Ryan Davis, Steven M. Watkins, Stephen G. Young, and Karen Reue

J. Lipid Res. 2006 47: 745-754.

Phosphorylation is a fundamental post-translationalmodification that is used to regulate the function, local-ization, and binding specificity of proteins. However,abnormal protein phosphorylation can lead to carcino-genesis and neuropathogenesis. Thus, methods for deter-mining the phosphorylation state of proteins areimportant with respect to evaluating biological andpathological processes. Here, the authors introduce twomethods for the visualization of phosphorylated proteinsusing alkoxide-bridged dinuclear metal complexes asnovel phosphate-binding tag (Phos-tag) molecules. Thefirst method uses electroblotting to analyze protein phos-phorylation status by phosphate-selective ECL signals.The second method is based on the mobility shift ofphosphorylated proteins in SDS-PAGE with a poly-acrylmide-bound Mn2+-Phos-tag.

Visualization of phosphorylated proteins on a blotting membrane.

Phosphate-binding Tag, a New Tool toVisualize Phosphorylated ProteinsEiji Kinoshita, Emiko Kinoshita-Kikuta, Kei Takiyama, and Tohru Koike

Mol. Cell . Proteomics 2006 5: 749-757

B I O T E C H B U S I N E S S N E W S


of it in facilities owned by public enti-ties like the State of Illinois.

By comparison, the areas aroundBoston and San Francisco, theacknowledged leaders in the field, eachhave more than 11 million square feet.But even much smaller cities like Madi-son, Wisconsin and Raleigh-Durham,North Carolina outperform Chicago inthis respect.

“The lack of space has been a stum-bling block,” said David Miller, Presi-dent of the Illinois Biotech IndustryOrganization, “What has happened inthe past is that a scientist could usuallyget a few thousand square feet of spacefrom a university or a corporation topursue a promising idea, but theminute he or she got bigger andneeded 10,000 or 20,000 square feet itwas a problem.”

Scott Brandwein, Senior ManagingDirector of the life sciences group ofCB Richard Ellis, the national realestate services firm, which is assistingForest City in leasing the Skokie center,agrees. “There are very few options forcompanies coming into the market,”he said. “There’s never been a specula-tive market here.”

What speculative space is availablegenerally leases for $20 to $30 a squarefoot, but Forest City is hoping to dobetter than that — about $30 to $40 asquare foot — for at least some of thenewer space in the complex.

“We’re targeting three types of ten-ants,” said Michael Rosen, senior vicepresident for new business develop-ment for the center. “The first is inter-national companies in need of spacefor a U.S. headquarters, the second iscompanies that provide services to thepharmaceutical industry on a contractbasis, and the third is new companies

that are ready to leave the incubators.”One company looking at the project

is Midwest BioResearch, a biotech start-up based in an incubator facilityowned by Northwestern University innearby Evanston. “Our initial need isfor 10,000 square feet but we coulddouble that in a fairly short period oftime,” said Mark Weston, a businessconsultant who is advising the firm onreal estate and financial issues.

Mr. Weston added that, “From thestandpoint of networking, productinnovation and creating new business,I think having a cluster of businesses inone location is important.” The draw-back, predictably, is rent. “I think,” saidMr. Weston, “that both the lessee andthe lessor will have to come together inthe beginning to get tenants in.”

The acquisition and subsequentredevelopment of a former Pfizerpharmaceutical research facility byForest City, a Cleveland-based devel-oper, promises to quadruple theamount of speculative office spaceavailable for biotechnology companiesin the Chicago area.

Forest City bought the one-million-square-foot complex last spring for $43million. Since then, the company hasdemolished 9 of the 13 buildings onthe 23-acre campus, leaving about700,000 square feet of offices and labo-ratories. The company plans to buildan additional 1.3 million square feet ofnew space, also for offices and labs,over the next 10 years. Overall, theproject is expected to cost more than$500 million.

The goal, according to Gayle Blake-ley Farris, President of the Science andTechnology Group of Forest City, is tocreate something that the companysays is long overdue in Chicago: abiotech cluster similar to those in thehigh-tech bastions operating in themetropolitan areas around Boston andSan Francisco.

“We think there’s an opportunity forChicago to become the third coast forthe biotech industry,” Farris said.“There are a number of major institu-tions here—such as the University ofChicago, the University of Illinois andNorthwestern University—whereimportant research is going on. But upuntil now, there hasn’t been a criticalmass of space available for companiesseeking to capitalize on that research.”

According to a recent study commis-sioned by Forest City, there is a short-age of speculative biotech office andlaboratory space in Chicago. The cityhas about 500,000 square feet, much

Making Space for a Biotech Center in the Chicago Area

‘Florida Research Coast’Touted in Chicago

The goal of Florida development offi-cials at the BIO 2006 conference inChicago this April was to marketFlorida’s Research Coast and form rela-tionships that could bring biotechnol-ogy-related business or investments tothe region. After spending several dayspromoting local assets at what is consid-ered the world’s largest biotech industrygathering, the Research Coast’s threerepresentatives said they think theyachieved their goals.

The three said high-skill jobs associ-ated with biotechnology are needed tooffset the low-wage employment baseand high home prices. TammySimoneau of the Economic Council ofMartin County said agricultural biotech-nology, for example, could be a great fit.“We can’t continue to survive strictly asa service-based industry,” she declared.

by John D . Thompson , Ed i tor

F o r Yo u r L a b / F o r Yo u r L a b / F o r Yo u r L a b


The information in For Your Lab has been provided by manufacturers and suppliers of

laboratory equipment. For further information about any of these products l isted

contacts are l isted at the bottom of each panel. When contacting any of these

companies, please mention that you saw their product in AS BM B Today . Please note

that a l isting in AS BM B Today does not imply an endorsement by the American Society

for Biochemistry and Molecular Biology or by any of its members or staff.

Manufacturers and suppliers, to include your products in For Your Lab contact

Molly at [email protected] or 301-634-7157 (direct) or 1-800-433-2732 ext. 7157.

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B I O T E C H B U S I N E S S N E W S


by John D . Thompson , Ed i tor

Demand for pharmaceuticals inChina is projected to increase 13.6percent annually to 375 billion yuan(U.S. $46.29 billion) in 2010, accord-ing to a new study from The Freedo-nia Group, a U.S.-based industryresearch firm.

The report says that Western pro-prietary prescription drugs will gen-erate the strongest growth based onnew products, especially for cardio-vascular, neurological, cancer andantiviral indications that are nottreated effectively by currently avail-able therapies. However, Westerngeneric medicines will continue tohold the largest share of the Chinesepharmaceutical market. The bestgrowth opportunities for these drugswill emerge in newly off-patent cho-lesterol-reducing, antipsychotic andsecond generation antihistaminepreparations.

Based on proven efficacy overthousands of years and sustainedprofitability among older residents,

traditional Chinese medicines willcontinue to form a large segment ofChina’s pharmaceutical industry.However, due to the lack of propri-etary products and sharper pricingcompetition, these preparations willsee somewhat slower growth thanWestern drugs.

Regulatory and commercialreforms will open up distributionsystems to a wider range of propri-etary and generic drugs. Theresearch report sees several therapeu-tic classes of medication, includingantiviral, anticancer, psychothera-peutic, and neurological agents asunderserved in China and the causeof major imbalances in the overallquality of health care.

Western over-the-counter (OTC)medication will increasingly penetratethe Chinese market as the govern-ment promotes the expansion of theretail drug sector to improve the acces-sibility of basic medicines to residentsof rural and overcrowded urban areas.

China’s Demand for Pharmaceut icalsMay Reach $46.29 Bil l ion

biotech companies needing cash, man-ufacturing skills, and marketing musclefrom the big drug companies.

Despite big gains in revenue, thebiotech industry overall still lostmoney last year as it spent heavily todevelop new products, the report said.However, the industry’s revenue hasbeen growing at annual double-digitrates for nearly two decades, morethan twice as fast as the traditionalpharmaceutical industry, thanks to 58

biotech products at the FDA awaitingapproval and hundreds more in latestages of testing.

Though losses continue, they arenarrowing rapidly. The loss for publiclytraded biotech companies in theUnited States shrank to $2.1 billion lastyear from the $4.9 billion of 2004,largely due to cost-cutting. The indus-try appears to be on track to achieveoverall profitability by the end of thedecade, Ernst & Young said.

The American biotechnology indus-try has surpassed pharmaceutical com-panies for the third straight year as theprimary source of new medicines,helping biotech revenue jump nearly16 percent last year to a record $50.7billion, according to an Ernst & Youngreport released last month.

Biotechnology companies still spendconsiderably less on research thantheir rivals in the traditional pharma-ceutical industry, the report said, about$20 billion a year compared with morethan $60 billion for the establisheddrug giants. But the biotech companiesget more results for their money, sur-passing pharmaceutical companies forthe first time in 2003 in getting noveltypes of medicines approved by theFood and Drug Administration.

“This is an independent, self-sustain-ing industry that is growing at morethan twice the rate of the pharmaceuti-cal industry,” said Scott Morrison, apartner at Ernst & Young LLP.

Biotech firms have lately become themain source of innovation in U.S. med-icine, including treatments for ailmentssuch as cancer and heart disease. Aprime example is Exubera, the inhaledinsulin for which Pfizer Inc. won FDAapproval early this year. Hailed as amilestone in the lives of diabetics, Exu-bera is the first new way to get insulininto the body since that hormone wasdiscovered in 1921. However, it wasn’tinvented at Pfizer, it was developed byNektar Therapeutics, a small biotechcompany in San Carlos, California,which may benefit handsomely ifExubra is a success in the marketplace.

“The pharmaceutical sector is clearlylooking at biotech as the innovationleader,” Morrison said, noting that thedependency runs both ways, with

Biotech’s Gains Again Outstrip Drug Giants


IFOM-IEO CAMPUS For MolecularOncology, MILAN, ITALY

HEAD OF PROTEOMICS

Two of the main Cancer researchInstitutions in Italy, the FIRC Instituteof Molecular Oncology (IFOM) and theEuropean Institute of Oncology (IEO)have expanded and integrated theirresearch activities into a common cam-pus. The IFOM-IEO Campus is alsohome to the PhD program of theEuropean School of Molecular Medicine(www.semm.it). Central services includeAnimal Facilities (mouse, zebrafish andC. elegans), Imaging, Protein andAntibody Production, DNA and TissueMicroarrays, DNA Sequencing, Real-time PCR, Bioinformatics. Open struc-ture laboratories foster communicationbetween groups. We are now calling forapplications for the position of Head ofProteomics.

The successful candidate will manageboth his/her own research group andthe Proteomics Facility in the Campus.Commensurate packages will be provid-ed for each activity, including equip-ment and personnel. As a Group Leaderin the Campus, the candidate will beexpected to develop an internationallycompetitive line of research in any areapertinent to cancer biology, diagnosticsor therapy. As a Facility Director, thecandidate will guarantee access to pro-teomics-based solutions to otherresearch groups in the Campus. TheFacility is expected to maintain a state-of-the-art technological infrastructureover time. The Campus provides a vastpotential for scientific interactions.Candidates should have extensive expe-rience in proteomics and a proventrack-record in running a competitiveresearch group.

DEADLINE FOR APPLICATIONS: June 30, 2006.

Applications should be sent by e-mailonly to [email protected] and should include: CV, pub-

C a r e e r O p p o r t u n i t i e s

UMCP

ASSISTANT PROFESSOR IN APPLIEDNUTRITION AND NUTRIGENOMICS

The Department of Nutrition andFood Science, University of Maryland,invites applications for a 9.5-month,tenure track research/teaching position.Applicants must have a PhD in Nutritionor related research discipline. Status as aRegistered Dietitian with practical clini-cal experience is desirable.

Responsibilities include: 1.) teachingundergraduate and graduate courses inclinical nutrition, nutritional assessment,advanced nutrition, and other relatedareas as needed; 2.) establishing an inde-pendent, innovative, competitivelyfunded research program in the area ofapplied nutrition/nutrigenomics.

A strong commitment to teaching atthe undergraduate and graduate levels,the ability to obtain outside funding tosupport research and a demonstrated abil-ity to publish in peer-reviewed journalsare essential elements of this position.

The scientist in this position is encour-aged to develop interdisciplinaryresearch with other faculty in the depart-ment and other campus units.

Applicants should send a statement ofteaching and research interests and howthey will extend and complement that ofthe current faculty, a complete CV, repre-sentative publications, official transcripts,and the contact information (mail, email,phone, fax) for 3 references to:

Dr. Robert Jackson, Chair , Search andScreening CommitteeDepartment of Nutrition and FoodScience0112 Skinner Building, College Park, MD20742

Applications will be accepted until asuccessful candidate is selected. For bestconsideration, apply by June 15, ‘06. TheUniversity of Maryland is an EO, AAemployer.

lication list, statement of Achievementsand Interests (max. 2 pages), names ande-mail addresses of 4-5 referees.Applicants should also ask their refereesto directly send their letters to the samee-mail address.

The IFOM-IEO campus is an equalopportunity employer. We encourageapplications from women and willimplement measures required to place allscientists in a situation of equal competi-tiveness.

www.ifom-ieo-campus.it

Florida Int’l Univ.

Applied Research Center at FloridaInternational University (Miami, FL)

MOLECULAR BIOLOGY RESEARCHER

The ARC at Florida InternationalUniversity (FIU) in Miami, FL has animmediate opening for a MolecularBiologist to lead a research programjointly performed by FIU-ARC and theNational Renewable Energy Laboratory(NREL). The program constitutes cut-ting-edge biological hydrogen researchconsisting of gene cloning, regulation,and expression in E. coli, DNA and pep-tide sequencing, and hydrogenaseenzyme purification and activity studies.A Ph.D. in Molecular Biology or relatedfields is required, along with strongexperience in vector construction andanalysis, bacterial expression systems,western blots, and sequencing. The ARCis a leading research institution in ener-gy and the environment(www.arc.fiu.edu). NREL is the premierrenewable energy laboratory of theDepartment of Energy (www.nrel.gov).

A competitive compensation packagewill be provided. FIU is an EqualOpportunity Employer. Submit your cvand three reference contacts to Dr. GeorgePhilippidis, Applied Research Center,Florida International University, 10555 W.Flagler St., EC 2100, Miami, FL 33174 orto [email protected].

C a l e n d a r o f S c i e n t i f i c M e e t i n g s


17th International Symposium on Plant Lipids

July 16–21 • Michigan State University Campus, East LansingOrganizer: Christoph BenningFor registration information, preliminary program, instruc-tions for submitting abstracts, and for information on finan-cial aid available for young scientists to attend the meeting, goto: www.ispl2006.msu.edu/. Members of underrepresentedgroups are especially encouraged to apply for financial aid.

Bioscience 2006: Bioscience for the 21st Century

July 23–27 • Glasgow, ScotlandAbstract Submission Deadline: April 13, 2006Early Registration Deadline: May 22, 2006For information: www.BioScience2006.org

Biochemical Journal SymposiumLiterature, Legacy, Life

July 24 • Glasgow, ScotlandCelebrating 100 Years of BiochemistryFor information: www.BioScience2006.org

A U G U S T 2 0 0 6

ISPMB 2006 – 8th International Congress of PlantMolecular Biology

August 20–25 • Adelaide Convention Centre, South AustraliaAbstract and Early Registration Deadline: Friday, March 3.Online registration and abstract submission pages:www.sallyjayconferences.com.au/ispmb2006/registration.htm www.sallyjayconferences.com.au/ispmb2006/abstract.htmAbstracts cannot be accepted without registration and pay-ment. All abstracts must be submitted online, abstracts sent asattachments will not be accepted.www.sallyjayconferences.com.au/ispmb2006/program.htm

S E P T E M B E R 2 0 0 6

5th European Congress of Biogerontology

September 16-20 • Istanbul, TurkeyTel: +90 216 347 35 35 Pbx; Fax: +90 216 347 78 50Email: [email protected]; Website: www.symcon.com.tr Congress President Prof. Serif Akman, Etlik, Ankara , Turkey Tel: +90 312 304 3306; Fax: +90 312 304 3300 E-mail: [email protected]

The 33rd Annual Conference of the Federation ofAnalytical Chemistry and Spectroscopy Societies(FACSS)

September 24–28 • Disney’s Contemporary Resort, LakeBuena Vista, FLContact: FACSS, PO Box 24379, Santa Fe, NM 87502Phone: 505-820-1648; Fax: 505-989-1073Email: [email protected]; Web Page: www.facss.org

J U N E 2 0 0 6

20th IUBMB International Congress of Biochemistryand Molecular Biology and 11th FAOBMB Congress inconjunction with 79th Annual Meeting of the JapaneseBiochemical Society and 29th Annual Meeting of theMolecular Biology Society of Japan

June 16–23 • Kyoto, JapanDeadline for On-line Registration: May 18, 2006Website: www.congre.co.jp/iubmb/registration.html

Bacterial Cell SurfacesA Gordon Research Conference

June 25–30 • Colby-Sawyer College New London, New HampshireChairs: Ry Young and Arnold J. Driessen Vice Chairs: Anne H. Delcour and Jeff Errington

4th Annual Meeting of the International Society forStem Cell Research

June 29–July 1 • Metro Toronto Convention Centre Toronto, Ontario, CanadaFor information on the ISSCR Annual Meeting, contact ISSCRHeadquarters: Ph: 847-509-1944; E-mail: [email protected] Administrator: Deb Pederson [email protected] Press Inquiries: Heather Gagnon [email protected] Conference Director: Liz Freyn [email protected]

J U LY 2 0 0 6

Third Annual World Congress on IndustrialBiotechnology and Bioprocessing

July 11–14 • Toronto, CanadaSponsored by the Biotechnology Industry Organization (BIO),American Chemical Society (ACS), National AgricultureBiotechnology Council (NABC), Agri-Food Innovation Forum,and BIOTECanada.Email: [email protected]; Ph: 202-962-9200

ASCB 2006 Summer Meeting: Stem Cell Niches

July 15-18 • Boston UniversityOrganized by Sean Morrison, HHMI/University of MichiganKeynote: Allan Spradling, Carnegie Institute ofWashington/HHMISession 4: Hematopoietic Stem Cell Niches (Cont.) Session Chair: Fiona DoetschSession 5: New Niches for Stem Cells Session Chair: David Scadden

American Society for Biochemistry and MolecularBiology Annual Meeting in Conjunction with EB2007

April 28 – May 2 • Washington, DCContact: ASBMB 2007, 9650 Rockville Pike, Bethesda, MD20814-3008Ph: 301-634-7145Email: [email protected]: www.asbmb.org/meetings

O C T O B E R 2 0 0 7

34th Annual Conference of the Federation ofAnalytical Chemistry and Spectroscopy Societies(FACSS)

October 12–18 • Memphis Convention Center, Memphis, TNContact: FACSS, PO Box 24379, Santa Fe, NM 87502.Ph: 505-820-1648; Fax: (505) 989-1073Email: [email protected]; Web Page: www.facss.org

O C T O B E R 2 0 0 6

International Conference of Immunogenomics andImmunomics

October 8–12 • Budapest, HungaryA joint meeting of 2nd Basic and Clinical Immunogenomicsand 3rd Immunoinformatics (Immunomics) ConferencesEmail: [email protected] Website: www.bcii2006.org

4th International Conference on Structural Genomics

October 22 – 26 • Beijing, ChinaWebsite: http://www.sino-meetings.com/icsg2006/

N O V E M B E R 2 0 0 6

Transcriptional Regulation by Chromatin and RNAPolymerase I I

November 2–6 • Kiawah Island, South CarolinaOrganizer: Ali Shilatifard, Saint Louis, University School ofMedicine, Email: [email protected]

Annual meeting of the Society for Glycobiology

November 15-18 • Los AngelesContacts: Linda Baum, President; [email protected] Moremen, Secretary; [email protected]: www.glycobiology.org

A P R I L 2 0 0 7

Second Workshop on Biophysics of Membrane-activePeptides

April 1 – 4 • Lisbon Science Museum, PortugalThe Lisbon Science Museum includes a 19th century lab andlecture room. Conference call for papers: special theme issueof J Pep Sci. Symposia: Membrane-translocating peptides / Cellpenetrating peptides, Membrane-permeabilizing peptides /Antimicrobial peptides, Fusogenic peptides, and Structure andDynamics in peptide-membrane interaction, Plenary lectures:Jöel Schneide: Bio-active properties of peptide surfaces. RobertHancock: Antimicrobial peptides. Stuart McLaughlin:Electrostatic interaction of basic peptides with acidic lipids inmembranes. Abstract submission, January 15, 2007, Early registration,January 15, 2007, Faculty of Sciences, University of Lisbon,Miguel Castanho, Ph.D.For Further information: www.biophysicsmap.com

– an outstanding new onlinereference work from one ofthe world's leading experts

Professor Sir Michael J Berridge(Cambridge)Shaw Laureate in Life Science and Medicine 2005

This major new contribution to the field of cellsignalling biology provides researchers, teachers andstudents alike with an essential online resource.Emerging information on cell signalling pathways isintegrated and presented within the context of specificcell types and processes.

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Contents1 Introduction2 Generation of second messengers3 Ion channels4 Sensors and effectors5 Off reactions6 Cellular processes7 Spatial and temporal aspects of signalling8 Development9 Proliferation10 Neuronal signalling11 Cell stress, inflammatory response(s) and cell death12 Signalling defects and disease

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Contents1 Introduction2 Generation of second messengers3 Ion channels4 Sensors and effectors5 Off reactions6 Cellular processes7 Spatial and temporal aspects of signalling8 Development9 Proliferation10 Neuronal signalling11 Cell stress, inflammatory response(s) and cell death12 Signalling defects and disease

Visit www.cellsignallingbiology.orgto register your interest in this exciting new product

Subscriptions available from July 2006

cell_ad_us.qxd 4/24/06 11:04 AM Page 1

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