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壓婰偵傛傝擄尋僙儈僫乕傪奐嵜偟傑偡偺偱丄懡悢屼棃挳壓偝偄丅
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丂丂 暯惉18擭11寧7擔乮壩乯17:00乣19:00
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| 丂応丂強丂 |
| 丂丂 乵弜壨戜抧嬫乶擄帯幘姵尋媶強俀俥乮俀僛儈乯 |
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| 丂墘丂幰丂 |
丂丂 Razq Hakem攷巑
丂丂丂Dept. Med. Biophysics, University of Toronto, Canada |
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| 丂墘丂戣丂 |
| 丂丂 To Repair Or To Die: That Is The Question |
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| 丂梫丂巪丗丂 |
丂丂Defective repair of damaged DNA contributes to the accumulation of genomic instability and increases the risk for cancer. Similarly, compromised cell death facilitates several human pathologies including cancer and immunodeficiency. Using mouse models we have studied diseases associated with specific defects in the DNA repair or apoptosis processes. We have characterized the mechanisms that lead to cancer development in the presence of mutation of tumor suppressors such as BRCA1, Mus81 and P53. We have also characterized the in vivo functions of caspases and have identified a novel role for caspase 8 in maintaining survival and homeostasis.
嬈愌丗Human Molecular Genetics. 15: 831-838, 2006, J Exp Med, 202: 727-732, 2005, Science, 304: 1822-1826, 2004, Embo J, 23: 3677-3688, 2004, Genes Dev, 18: 1144-1153, 2004, Embo J, 22: 6137-6147, 2003, Genes Dev, 17: 883-895, 2003
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| 丂楢丂棈丂愭 |
| 丂丂丂恗壢 攷巎 nishina.dbio@mri.tmd.ac.jp丂乮敪惗嵞惗惗暔妛暘栰丂撪慄4659乯 |
| 丂丂丂嵶朎惂屼妛暘栰乮嶳棞 桾巌嫵庼丂撪慄5814乯偲偺嫟嵜偱偡丅 |
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