Emerging role of the MORF/MRG gene family in various biological processes, including aging.
Emerging role of the MORF/MRG gene family in various biological processes, including aging.
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DOI：
10.1111/j.1749-6632.2010.05197.x
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发表时间：
2010-06
影响因子：
5.2
通讯作者：
Pereira-Smith OM
中科院分区：
文献类型：
--
作者：
Chen M;Tominaga K;Pereira-Smith OM
细胞衰老是长生不老的主要表型。在我们鉴定衰老相关基因的研究中，我们克隆了在肿瘤细胞亚群中诱导衰老的Morf4。Morf4是一个由7个基因组成的家族中的一员，在染色体15 （Mrg15）和X （MrgX）上也表达Morf相关基因（Mrg）。与MORF4相反，MRG15和MRGX是细胞分裂的正调节因子。这三种蛋白与组蛋白乙酰化酶（hat）和乙酰转移酶（hdac）相互作用，表明它们在染色质动力学调节中起作用。Mrg15基因敲除小鼠是胚胎致死性的，与野生型相比，来自Mrg15基因缺失胚胎的mef增殖能力差，进入衰老期快，DNA修复受损。Mrg15缺失的胚胎神经干细胞/祖细胞的增殖和分化能力也下降。需要进一步的研究来确定该基因家族在包括神经干/祖细胞衰老在内的各种生物过程中的功能。
Cellular senescence is the dominant phenotype over immortality. In our studies to identify senescence related genes we cloned Morf4 that induced senescence in a subset of tumor cells. Morf4 is a member of a family of 7 genes, and the Morf related genes (Mrg) on chromosomes 15 (Mrg15) and X (MrgX) are also expressed. In contrast to MORF4, MRG15 and MRGX are positive regulators of cell division. All three proteins interact with histone acetylases (HATs) and acetyltransferase (HDACs), suggesting they function in regulation of chromatin dynamics. Mrg15 knockout mice are embryonic lethal, and MEFs derived from Mrg15 null embryos proliferate poorly, enter senescence rapidly and have impaired DNA repair compared to wild type. Mrg15 null embryonic neural stem/progenitor cells also have a decreased capacity for proliferation and differentiation. Further studies are needed to determine the function of this gene family in various biological processes including neural stem/progenitor cell aging.
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影响因子：
3.7
作者：
HAYFLICK, L;MOORHEAD, PS
通讯作者：
MOORHEAD, PS
DOI：
10.1073/pnas.92.20.9363
发表时间：
1995-09-26
影响因子：
11.1
作者：
DIMRI, GP;LEE, XH;CAMPISI, J
通讯作者：
CAMPISI, J
影响因子：
4.4
作者：
Bertram, MJ;Bérubé, NG;Pereira-Smith, OM
通讯作者：
Pereira-Smith, OM
影响因子：
7.8
作者：
Bandyopadhyay D;Curry JL;Lin Q;Richards HW;Chen D;Hornsby PJ;Timchenko NA;Medrano EE
通讯作者：
Medrano EE
影响因子：
64.5
作者：
Barlow, C;Hirotsune, S;WynshawBoris, A
通讯作者：
WynshawBoris, A