Acetylation of retinoblastoma-like protein-2 (Rbl2/p130): an additional check on cell proliferation?

Acetylation of retinoblastoma-like protein-2 (Rbl2/p130): an additional check on cell proliferation?

Authors

  • Muhammad Saeed Department of Biosciences, COMSATS Institute of Information Technology,

Keywords:

Acetylation, Retinoblastoma, Rbl2/p130, tumor suppressor, PTM, cell cycle.

Abstract

Pocket proteins are important regulator of cell cycle progression. The family includes three members namely: retinoblastoma protein (pRb/p105), the founding member of the family, retinoblastoma like protein-1 (Rb121/p107) and retinoblastoma like protein-2 (Rb12/p130). Pocket proteins exert their role by binding with the members of E2F family of transcription proteins, thus making them unavailable for transcription of gene required for the entry into S-phase of cell cycle. The Functional activity of pocket proteins is regulated by phosphorylation. Once phosphorylated, Rb-E2F complex is disrupted. The abrogation of Rb functions, leads to unchecked G1-S phase transition and uncontrolled cell division. The ultimate impact is tumor formation. Recently, we have demonstrated that Rbl2/p130 is also subject to posttranslational acetylation. The exact role of Rbl2/p130 acetylation in cell cycle control and tumor genesis remains elusive. This review discusses acetylation being a prerequisite for phosphorylation and investigates a possible role of Rbl2/p130 acetylation in regulating G1/S phase of cell cycle.

Author Biography

Muhammad Saeed, Department of Biosciences, COMSATS Institute of Information Technology,

Assistant Professor Department of Biosciences

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Published

2015-11-15

How to Cite

1.
Saeed M. Acetylation of retinoblastoma-like protein-2 (Rbl2/p130): an additional check on cell proliferation?. Eur J Oncol Env Hea [Internet]. 2015 Nov. 15 [cited 2025 Apr. 6];20(2):100-8. Available from: https://mattioli1885journals.com/index.php/EJOEH/article/view/3621