大衛·安德魯·辛克萊 (Chinese Wikipedia)

Analysis of information sources in references of the Wikipedia article "大衛·安德魯·辛克萊" in Chinese language version.

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bbc.co.uk

Stop, rewind: the scientists slowing the ageing process. BBC News. January 26, 2011 [2017-05-15]. （原始内容存档于2020-11-11）.

Mills KD, Sinclair DA, Guarente L. MEC1-dependent redistribution of the Sir3 silencing protein from telomeres to DNA double-strand breaks.. Cell (Print). May 28, 1999, 97 (5): 609–20. PMID 10367890. doi:10.1016/S0092-8674(00)80772-2. The yeast Sir2/3/4p complex is found in abundance at telomeres, where it participates in the formation of silent heterochromatin and telomere maintenance. Here, we show that Sir3p is released from telomeres in response to DNA double-strand breaks (DSBs), binds to DSBs, and mediates their repair, independent of cell mating type. Sir3p relocalization is S phase specific and, importantly, requires the DNA damage checkpoint genes MEC1 and RAD9. MEC1 is a homolog of ATM, mutations in which cause ataxia telangiectasia (A-T), a disease characterized by various neurologic and immunologic abnormalities, a predisposition for cancer, and a cellular defect in repair of DSBs. This novel mode by which preformed DNA repair machinery is mobilized by DNA damage sensors may have implications for human diseases resulting from defective DSB repair
Sinclair, David A. Declining NAD+ Induces a Pseudohypoxic State Disrupting Nuclear-Mitochondrial Communication during Aging. Cell. 19 December 2013, 155 (7): 1624–1638 [14 April 2015]. PMC 4076149 . PMID 24360282. doi:10.1016/j.cell.2013.11.037. （原始内容存档于2019-09-23）.

Cameron, David. A New—and Reversible—Cause of Aging. Harvard Medical School. 19 December 2013 [14 April 2015]. （原始内容存档于2017-08-03）.

Mills KD, Sinclair DA, Guarente L. MEC1-dependent redistribution of the Sir3 silencing protein from telomeres to DNA double-strand breaks.. Cell (Print). May 28, 1999, 97 (5): 609–20. PMID 10367890. doi:10.1016/S0092-8674(00)80772-2. The yeast Sir2/3/4p complex is found in abundance at telomeres, where it participates in the formation of silent heterochromatin and telomere maintenance. Here, we show that Sir3p is released from telomeres in response to DNA double-strand breaks (DSBs), binds to DSBs, and mediates their repair, independent of cell mating type. Sir3p relocalization is S phase specific and, importantly, requires the DNA damage checkpoint genes MEC1 and RAD9. MEC1 is a homolog of ATM, mutations in which cause ataxia telangiectasia (A-T), a disease characterized by various neurologic and immunologic abnormalities, a predisposition for cancer, and a cellular defect in repair of DSBs. This novel mode by which preformed DNA repair machinery is mobilized by DNA damage sensors may have implications for human diseases resulting from defective DSB repair
Sinclair, David A. Declining NAD+ Induces a Pseudohypoxic State Disrupting Nuclear-Mitochondrial Communication during Aging. Cell. 19 December 2013, 155 (7): 1624–1638 [14 April 2015]. PMC 4076149 . PMID 24360282. doi:10.1016/j.cell.2013.11.037. （原始内容存档于2019-09-23）.

Stop, rewind: the scientists slowing the ageing process. BBC News. January 26, 2011 [2017-05-15]. （原始内容存档于2020-11-11）.
Sinclair, David A. Declining NAD+ Induces a Pseudohypoxic State Disrupting Nuclear-Mitochondrial Communication during Aging. Cell. 19 December 2013, 155 (7): 1624–1638 [14 April 2015]. PMC 4076149 . PMID 24360282. doi:10.1016/j.cell.2013.11.037. （原始内容存档于2019-09-23）.
Bellman, Gary. New Elixir of Youth? Researchers Develop a Drug That Can Reverse Aging in Animal Models. Male Anti-Aging Institute. [14 April 2015]. （原始内容存档于2017-04-14）.
Cameron, David. A New—and Reversible—Cause of Aging. Harvard Medical School. 19 December 2013 [14 April 2015]. （原始内容存档于2017-08-03）.