Genetic cooperation between p21Cip1 and INK4 inhibitors in cellular senescence and tumor suppression. (Q53544041)

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1 January 2020

title

Genetic cooperation between p21Cip1 and INK4 inhibitors in cellular senescence and tumor suppression (English)

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1 January 2020

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1

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1 January 2020

Amancio Carnero

4

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1 January 2020

author name string

Martinalbo J

2

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1 January 2020

Dubus P

3

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1 January 2020

Malumbres M

5

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1 January 2020

language of work or name

English

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publication date

18 June 2007

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1 January 2020

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https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:17599058%20AND%20SRC:MED&resulttype=core&format=json

1 January 2020

volume

26

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1 January 2020

issue

55

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1 January 2020

page(s)

7665-7674

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Differential roles for cyclin-dependent kinase inhibitors p21 and p16 in the mechanisms of senescence and differentiation in human fibroblasts

1 January 2020

cites work

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Involvement of the cyclin-dependent kinase inhibitor p16 (INK4a) in replicative senescence of normal human fibroblasts

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Oncogene-Induced Senescence: Putting the Brakes on Tumor Development

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

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Radiation-induced cell cycle arrest compromised by p21 deficiency

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Loss-of-function genetics in mammalian cells: the p53 tumor suppressor model

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The p21(Cip1) and p27(Kip1) CDK 'inhibitors' are essential activators of cyclin D-dependent kinases in murine fibroblasts

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Ablation of the retinoblastoma gene family deregulates G(1) control causing immortalization and increased cell turnover under growth-restricting conditions

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Gfi1 coordinates epigenetic repression of p21Cip/WAF1 by recruitment of histone lysine methyltransferase G9a and histone deacetylase 1

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CDK inhibitors p18(INK4c) and p27(Kip1) mediate two separate pathways to collaboratively suppress pituitary tumorigenesis

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Functional collaboration between different cyclin-dependent kinase inhibitors suppresses tumor growth with distinct tissue specificity

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MaRX: an approach to genetics in mammalian cells.

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THE LIMITED IN VITRO LIFETIME OF HUMAN DIPLOID CELL STRAINS

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Stem-cell ageing modified by the cyclin-dependent kinase inhibitor p16INK4a

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E2F-Rb complexes regulating transcription of genes important for differentiation and development

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Loss of p16Ink4a confers susceptibility to metastatic melanoma in mice

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p16INK4a induces an age-dependent decline in islet regenerative potential

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Limited overlapping roles of P15(INK4b) and P18(INK4c) cell cycle inhibitors in proliferation and tumorigenesis

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Rb family proteins as modulators of gene expression and new aspects regarding the interaction with chromatin remodeling enzymes

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

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Mammalian cyclin-dependent kinases

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Cellular response to oncogenic ras involves induction of the Cdk4 and Cdk6 inhibitor p15(INK4b)

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7 January 2021

Mammalian cells cycle without the D-type cyclin-dependent kinases Cdk4 and Cdk6

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7 January 2021

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