Literature DB >> 21465484

The switch from pRb/p105 to Rb2/p130 in DNA damage and cellular senescence.

Heike Helmbold1, Umberto Galderisi, Wolfgang Bohn.   

Abstract

Cellular senescence is a response to genotoxic stress that results in an irreversible cell cycle arrest. Activation of this pathway relies on the activity of the retinoblastoma proteins and proteins of the DNA damage response cascade. Here, we discuss the functional relevance of the switch from pRb/p105 to Rb2/p130 that becomes apparent when cells enter senescent arrest.
Copyright © 2011 Wiley Periodicals, Inc.

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Year:  2012        PMID： 21465484     DOI： 10.1002/jcp.22786

Source DB:  PubMed          Journal:  J Cell Physiol        ISSN： 0021-9541            Impact factor:   6.384


  14 in total

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Review 3.  Senescence suppressors: their practical importance in replicative lifespan extension in stem cells.

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4.  Mesenchymal stromal cells having inactivated RB1 survive following low irradiation and accumulate damaged DNA: Hints for side effects following radiotherapy.

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7.  Timing of transcription during the cell cycle: Protein complexes binding to E2F, E2F/CLE, CDE/CHR, or CHR promoter elements define early and late cell cycle gene expression.

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8.  Gene expression profiling identifies different sub-types of retinoblastoma.

Authors:  G Kapatai; M-A Brundler; H Jenkinson; P Kearns; M Parulekar; A C Peet; C M McConville
Journal:  Br J Cancer       Date:  2013-06-11       Impact factor: 7.640

9.  Cell senescence in myxoid/round cell liposarcoma.

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10.  How does ethanol induce apoptotic cell death of SK-N-SH neuroblastoma cells.

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