Rb2/p130 is the dominating pocket protein in the p53-p21 DNA damage response pathway leading to senescence (Q39817833)

14 September 2017

Rb2/p130 is the dominating pocket protein in the p53-p21 DNA damage response pathway leading to senescence (English)

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14 September 2017

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H Helmbold

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14 September 2017

N Kömm

series ordinal

2

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14 September 2017

W Deppert

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3

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14 September 2017

W Bohn

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4

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14 September 2017

language of work or name

English

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publication date

3 August 2009

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28

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39

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3456-3467

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https://scigraph.springernature.com/pub.10.1038/onc.2009.222

14 September 2017

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cites work

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The DNA damage signaling pathway connects oncogenic stress to cellular senescence.

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The transcription factor E2F-1 mediates the autoregulation of RB gene expression

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Distinct recruitment of E2F family members to specific E2F-binding sites mediates activation and repression of the E2F1 promoter

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Reversal of human cellular senescence: roles of the p53 and p16 pathways

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Oncogene-induced senescence as an initial barrier in lymphoma development

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Bypass of senescence after disruption of p21CIP1/WAF1 gene in normal diploid human fibroblasts

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Requirement for p53 and p21 to sustain G2 arrest after DNA damage

31 March 2020

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p21Waf1/Cip1/Sdi1-induced growth arrest is associated with depletion of mitosis-control proteins and leads to abnormal mitosis and endoreduplication in recovering cells

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Crucial role of p53-dependent cellular senescence in suppression of Pten-deficient tumorigenesis

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Tumor-specific exon 1 mutations could be the 'hit event' predisposing Rb2/p130 gene to epigenetic silencing in lung cancer.

31 March 2020

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Cell cycle-specific association of E2F with the p130 E1A-binding protein

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Tumour biology: senescence in premalignant tumours

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Oncogene-induced senescence is a DNA damage response triggered by DNA hyper-replication

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A biomarker that identifies senescent human cells in culture and in aging skin in vivo

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Regulation of cellular senescence by Rb2/p130.

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Primary and compensatory roles for RB family members at cell cycle gene promoters that are deacetylated and downregulated in doxorubicin-induced senescence of breast cancer cells

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Cooperation between p53 and p130(Rb2) in induction of cellular senescence

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Cancer risk and the ATM gene: a continuing debate

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Identification of a p130 domain mediating interactions with cyclin A/cdk 2 and cyclin E/cdk 2 complexes

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Expression of Rb2/p130 protein correlates with the degree of malignancy in gliomas.

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To cycle or not to cycle: a critical decision in cancer.

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Rb-mediated heterochromatin formation and silencing of E2F target genes during cellular senescence

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The IARC TP53 database: new online mutation analysis and recommendations to users

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A Restriction Point for Control of Normal Animal Cell Proliferation

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Role of the retinoblastoma pathway in senescence triggered by repression of the human papillomavirus E7 protein in cervical carcinoma cells.

31 March 2020

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E2F integrates cell cycle progression with DNA repair, replication, and G(2)/M checkpoints

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A senescence program controlled by p53 and p16INK4a contributes to the outcome of cancer therapy

31 March 2020

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Expression of the retinoblastoma-related gene Rb2/p130 is downregulated in atypical endometrial hyperplasia and adenocarcinoma.

31 March 2020

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Mitogenic signalling and the p16INK4a-Rb pathway cooperate to enforce irreversible cellular senescence

31 March 2020

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Genetic and epigenetic alterations of RB2/p130 tumor suppressor gene in human sporadic retinoblastoma: implications for pathogenesis and therapeutic approach

31 March 2020

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Uncoupling of S phase and mitosis induced by anticancer agents in cells lacking p21

31 March 2020

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The E7 proteins of low- and high-risk human papillomaviruses share the ability to target the pRB family member p130 for degradation

31 March 2020

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Exit from G1 and S phase of the cell cycle is regulated by repressor complexes containing HDAC-Rb-hSWI/SNF and Rb-hSWI/SNF

31 March 2020

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Inhibition of cell proliferation by p107, a relative of the retinoblastoma protein

31 March 2020

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31 March 2020

Identifiers

DOI

10.1038/ONC.2009.222

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14 September 2017

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