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Assignment 6 (°èÅë¼ö±×¸®±â) ¸¦ 12¿ù 9ÀÏ (¿ù) 6:00PM ±îÁö adanson2000@hotmail.comÀ¸·Î ¸ÞÀÏ·Î Á¦ÃâÇ϶ó°í ÇÏ¿´´Âµ¥, ¸¹Àº ÇлýµéÀÌ ¾ÆÁ÷ Á¦ÃâÇÏÁö ¾Ê¾Ò½À´Ï´Ù. ¸¶Áö¸· ¸®Æ÷Æ®·Î¼ ¹èÁ¡ÀÌ Å©´Ù°í °øÁöÇÑ ¹Ù ÀÖ½À´Ï´Ù. 2Â÷ ¸¶°¨ÀÏÀ» ÁöÁ¤ÇÏ´Ï ´Ê°Ô¶óµµ Á¦ÃâÇϵµ·Ï Çϼ¼¿ä. 2Â÷ ¸¶°¨ÀÏÀº 16ÀÏ 6:00PM ±îÁöÀÔ´Ï´Ù. adanson2000@hotmail.comÀ¸·Î ¸ÞÀÏ·Î Á¦Ãâ Çϼ¼¿ä. Á¦ÃâÇÏÁö ¾Ê¾Æµµ µÈ´Ù°í °øÁöÇÑ °ÍÀº Assignment 7 (Genome assembly) ÀÔ´Ï´Ù.
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6. 2013³â 11¿ù 25ÀÏ: Ưº°¼¼¹Ì³ª 4:30ºÎÅÍ B540 °ÀÇ½Ç DNA SINGLE STRAND BREAK REPAIR, NEURODEVELOPMENT AND BRAIN TUMOR. ¾ÆÁÖ´ëÇб³ ÀÇ°ú´ëÇÐ À¯Àüü ºÒ¾ÈÁ¤¼º Á¦¾î ¿¬±¸ ¼¾ÅÍ ÀÌ¿µ¼ö ±³¼ö Defects in DNA strand break repair can lead to human syndromes such as Ataxia Telangiectasia (A-T), A-T like disorder (A-TLD), Ataxia with Oculomotor Apraxia 1 (AOA1) or Spinocerebellar Ataxia with Axonal Neuropathy 1 (SCAN1). Neurodegeneration is one of the major clinical phenotypes in these genetic syndromes. While A-T is considered a defect in the response to DNA double-strand breaks (DSB), AOA1 and SCAN1 result from defects in the DNA single strand break repair (SSBR) pathway. In order to understand how SSBR during brain development and maintenance prevents neurodegeneration, Xrcc1 was selectively inactivated in the nervous system. Xrcc1 is a scaffolding protein that recruits several proteins involved in SSBR to DNA breaks. Xrcc1 deficiency induced an accumulation of DNA breaks throughout the nervous system, indicating that genomic instability was widespread in these mice. In the cerebellum, Xrcc1 inactivation triggered two different outcomes; apoptosis in the external germinal layer (EGL), and cell cycle arrest in the white matter (WM) progenitor cells resulting in loss of interneurons in the cerebellum. Concomitant p53 inactivation in the Xrcc1 animals restored cerebellar interneurons. We also found that Atm deficiency exacerbated neurological phenotypes observed in Xrcc1 null animals. Dual inactivation of Xrcc1 and Atm showed a pronounced effect in the cerebellum where disruption of granule cell genesis resulted in disorganization and ectopic distribution of Purkinje cells, causing severe ataxia. However, Atm deficiency did not rescue interneuron loss in the Xrcc1 null cerebellum. This study provides new insight into Atm function after DNA damage that appears distinct from p53 signaling when SSBR is inactivated during neuronal development. ¼¼¹Ì³ªÈÄ °úÁ¦(Assignment 5): ¼¼¹Ì³ª¿¡ ³ª¿Â ³»¿ë Áß ÀÚ½ÅÀÌ ¸ð¸£´Â ¿ë¾î, °³³ä, Áú¹® µîÀ» 3°¡Áö ¼±Á¤ÇÏ¿© °¢°¢ 1/3ÆäÀÌÁö¾¿ ¼¼ú, Á¤¸®ÇÏ¿© Á¦Ãâ.
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