Hyper-phosphorylated retinoblastoma protein suppresses telomere elongation
Hyper-phosphorylated retinoblastoma protein suppresses telomere elongation
复制标题
DOI：
10.1271/bbb.70715
复制
发表时间：
2008-02-01
影响因子：
1.6
通讯作者：
Yoshida, Shonen
中科院分区：
文献类型：
--
作者：
Takemura, Masaharu;Sugimura, Kazuto;Yoshida, Shonen
永生化细胞系通过表达端粒酶或通过另一种被称为端粒延长(ALT)的机制来维持端粒。虽然DNA聚合酶a被认为是端粒维持所必需的，但它在端粒维持中的关键作用还没有确定。我们利用端粒纤维FISH研究了视网膜母细胞瘤蛋白(PRB)和Pola在调节端粒长度中的作用。在HeLa细胞中，端粒长度的变化取决于细胞内Pola或pRb的丰度。部分超磷酸化pRb(PpRb)分子定位于HeLa细胞中的端粒DNA复制位点。因此，POL-α可能有助于端粒的维持，并可能受ppRb的调节。
Immortalized cell lines maintain telomeres by the expression of telomerase or by a mechanism designated alternative lengthening of telomeres (ALT). Although DNA polymerase a (pol-alpha) is reported to be required for telomere maintenance, the critical role of pol-a in telomere maintenance has not been firmly determined. We examined the role of retinoblastoma protein (pRb) and pol-a in the regulation of telomere length, using telomere-fiber FISH. Telomere length varied dependent on the intracellular abundance of pol-a or pRb in HeLa cells. A proportion of hyper-phosphorylated pRb (ppRb) molecules localized to sites of telomeric DNA replication in HeLa cells. Pol-alpha might thus contribute to telomere maintenance, and might be regulated by ppRb.