GCN5和PCAF基因敲低对端粒维持替代机制的相反作用。
Opposite effects of GCN5 and PCAF knockdowns on the alternative mechanism of telomere maintenance.
作者信息
Jeitany Maya, Bakhos-Douaihy Dalal, Silvestre David C, Pineda Jose R, Ugolin Nicolas, Moussa Angela, Gauthier Laurent R, Busso Didier, Junier Marie-Pierre, Chneiweiss Hervé, Chevillard Sylvie, Desmaze Chantal, Boussin François D
机构信息
Laboratoire de Radiopathologie, CEA, Institut de Radiobiologie Cellulaire et Moléculaire, Fontenay-aux-Roses, France.
INSERM UMR967, Fontenay-aux-Roses, France.
出版信息
Oncotarget. 2017 Apr 18;8(16):26269-26280. doi: 10.18632/oncotarget.15447.
Cancer cells can use a telomerase-independent mechanism, known as alternative lengthening of telomeres (ALT), to elongate their telomeres. General control non-derepressible 5 (GCN5) and P300/CBP-associated factor (PCAF) are two homologous acetyltransferases that are mutually exclusive subunits in SAGA-like complexes. Here, we reveal that down regulation of GCN5 and PCAF had differential effects on some phenotypic characteristics of ALT cells. Our results suggest that GCN5 is present at telomeres and opposes telomere recombination, in contrast to PCAF that may indirectly favour them in ALT cells.
癌细胞可以利用一种不依赖端粒酶的机制，即端粒替代延长（ALT），来延长其端粒。一般控制非抑制性5（GCN5）和P300/CBP相关因子（PCAF）是两种同源乙酰转移酶，它们是类SAGA复合物中相互排斥的亚基。在这里，我们揭示了GCN5和PCAF的下调对ALT细胞的某些表型特征有不同的影响。我们的结果表明，GCN5存在于端粒处并抑制端粒重组，而PCAF在ALT细胞中可能间接促进端粒重组。
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