71 2198

P1-1824

24 4 6 8 11

2

4

8

4 119

2

3 4

P1-19

: Outcome-based Education OBE

2014OBE

OBE

3 4

GP

OBE

11

170 1992013 4

P1-20

SNAPPS six micro skills

3

4

R.

SNAPPSsix micro skills

SNAPPS six micro skills

SNAPPSsix micro skills

SNAPPS 21 six micro skills 12SNAPPS six micro skills

SD6.76 1.786 6.92 1.881

3.95 2.312 2.08 2.065 8.293.304 6.42 2.021 2.00 1.000

1.17 1.030unpaired t test P

0.819 0.086

0.0270.030

SNAPPS six mi-cro skills

P2-21SH3BP5 is essential for Humanin-mediated pro-tection against Alzheimer’s disease-relevant toxic-ity

3

Humanin HN inhibits Alzheimer’s disease AD -

relevant neuronal death by binding to the specific cell surface receptor complex, composed of CNTFR , WSX-

1, and gp130, and by activating the JAK2/STAT3 intra-cellular prosurvival signaling axis. In this study, we have attempted to identify HN’s essential downstream effectors, usig a differential display screening. Among genes the expression of which was induced by HN in SHSY5Y human neuroblastoma line cells, we focused on SH3BP5 that has been known as a Bruton’s tyrosine ki-nase and c-Jun N-terminal kinase JNK interactor. Quantitative RT-PCR and speci c immunocytochemical staining analysis showed that both the levels of SH3BP5 mRNA and protein expression were upregulated by treat-ment with S14G-HN, a potent HN derivative. The overexpression of SH3BP5 inhibited SHSY5Y cell death, induced by familial AD-linked V642I-APP. Recipro-cally, the siRNA-mediated reduction of expression di-minished the HN neuroprotection against the V642I-

APP-induced cell death. The overexpression of SH3BP5 also inhibited both constitutive-active JNK and apoptosis signaling kinase 1-induced death of SHSY5Y

12