Hyper-Phosphorylated Retinoblastoma Protein Suppresses Telomere Elongation | Zendy

Masaharu Takemura | Zendy; Kazuto Sugimura | Zendy; Katsuzumi Okumura | Zendy; Siripan Limsirichaikul | Zendy; Motoshi Suzuki | Zendy; Yoshiji Yamada | Zendy; Shonen Yoshida | Zendy

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Hyper-Phosphorylated Retinoblastoma Protein Suppresses Telomere Elongation

Author(s) -

Masaharu Takemura,

Kazuto Sugimura,

Katsuzumi Okumura,

Siripan Limsirichaikul,

Motoshi Suzuki,

Yoshiji Yamada,

Shonen Yoshida

Publication year - 2008

Publication title -

bioscience biotechnology and biochemistry

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.509

H-Index - 116

eISSN - 1347-6947

pISSN - 0916-8451

DOI - 10.1271/bbb.70715

Subject(s) - telomere , telomerase , telomere binding protein , microbiology and biotechnology , biology , hela , dna polymerase , dna replication , retinoblastoma protein , dna damage , cell cycle , dna , cell culture , genetics , cell , dna binding protein , gene , transcription factor

Immortalized cell lines maintain telomeres by the expression of telomerase or by a mechanism designated alternative lengthening of telomeres (ALT). Although DNA polymerase alpha (pol-alpha) is reported to be required for telomere maintenance, the critical role of pol-alpha in telomere maintenance has not been firmly determined. We examined the role of retinoblastoma protein (pRb) and pol-alpha in the regulation of telomere length, using telomere-fiber FISH. Telomere length varied dependent on the intracellular abundance of pol-alpha 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.

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