Histone deacetylase inhibitors induce a senescence-like state in human cells by a p16-dependent mechanism that is independent of a mitotic clock (Q40565411)

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scientific article published on May 2004

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English	Histone deacetylase inhibitors induce a senescence-like state in human cells by a p16-dependent mechanism that is independent of a mitotic clock	scientific article published on May 2004

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scholarly article

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Europe PubMed Central

PubMed publication ID

21 September 2017

Histone deacetylase inhibitors induce a senescence-like state in human cells by a p16-dependent mechanism that is independent of a mitotic clock (English)

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Europe PubMed Central

PubMed publication ID

21 September 2017

author name string

June Munro

1

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Europe PubMed Central

PubMed publication ID

21 September 2017

Nighean I Barr

2

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Europe PubMed Central

PubMed publication ID

21 September 2017

Hazel Ireland

3

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Europe PubMed Central

PubMed publication ID

21 September 2017

Vivienne Morrison

4

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Europe PubMed Central

PubMed publication ID

21 September 2017

E Kenneth Parkinson

5

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Europe PubMed Central

PubMed publication ID

21 September 2017

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publication date

1 May 2004

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Europe PubMed Central

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21 September 2017

Experimental Cell Research

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Europe PubMed Central

PubMed publication ID

21 September 2017

295

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Europe PubMed Central

PubMed publication ID

21 September 2017

2

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Europe PubMed Central

PubMed publication ID

21 September 2017

525-538

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Europe PubMed Central

PubMed publication ID

21 September 2017

THE LIMITED IN VITRO LIFETIME OF HUMAN DIPLOID CELL STRAINS

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The biology of replicative senescence

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Telomeres shorten during ageing of human fibroblasts

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Telomere reduction in human colorectal carcinoma and with ageing

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Specific Association of Human Telomerase Activity with Immortal Cells and Cancer

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Telomere states and cell fates

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The Shortest Telomere, Not Average Telomere Length, Is Critical for Cell Viability and Chromosome Stability

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Evidence that exposure of the telomere 3' overhang sequence induces senescence

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Telomerase contributes to tumorigenesis by a telomere length-independent mechanism

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Altered regulation of G1 cyclins in senescent human diploid fibroblasts: accumulation of inactive cyclin E-Cdk2 and cyclin D1-Cdk2 complexes

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Activation of telomerase in a human tumor

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ATM-dependent telomere loss in aging human diploid fibroblasts and DNA damage lead to the post-translational activation of p53 protein involving poly(ADP-ribose) polymerase.

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Different telomere damage signaling pathways in human and mouse cells

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Sensitivity and selectivity of the DNA damage sensor responsible for activating p53-dependent G1 arrest

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Agents that cause DNA double strand breaks lead to p16INK4a enrichment and the premature senescence of normal fibroblasts

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Posttranslational modifications of p53 in replicative senescence overlapping but distinct from those induced by DNA damage

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Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours

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Mice Lacking p21CIP1/WAF1 undergo normal development, but are defective in G1 checkpoint control

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Bypass of Senescence After Disruption of p21 CIP1/WAF1 Gene in Normal Diploid Human Fibroblasts

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INK4a-deficient human diploid fibroblasts are resistant to RAS-induced senescence

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p53 deficiency rescues the adverse effects of telomere loss and cooperates with telomere dysfunction to accelerate carcinogenesis

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p53- and ATM-dependent apoptosis induced by telomeres lacking TRF2

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Human keratinocytes that express hTERT and also bypass a p16(INK4a)-enforced mechanism that limits life span become immortal yet retain normal growth and differentiation characteristics

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Both Rb/p16INK4a inactivation and telomerase activity are required to immortalize human epithelial cells.

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Putative telomere-independent mechanisms of replicative aging reflect inadequate growth conditions

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Human fibroblast replicative senescence can occur in the absence of extensive cell division and short telomeres

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Evidence for a telomere-independent "clock" limiting RAS oncogene-driven proliferation of human thyroid epithelial cells

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A two-stage, p16(INK4A)- and p53-dependent keratinocyte senescence mechanism that limits replicative potential independent of telomere status

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Immortalisation and transformation revisited

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Effect of TERT over-expression on the long-term transplantation capacity of hematopoietic stem cells

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Tumor suppression at the mouse INK4a locus mediated by the alternative reading frame product p19ARF

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Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a

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The oncogene and Polycomb-group gene bmi-1 regulates cell proliferation and senescence through the ink4a locus

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Senescence bypass screen identifies TBX2, which represses Cdkn2a (p19(ARF)) and is amplified in a subset of human breast cancers.

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Downregulation of 14-3-3sigma prevents clonal evolution and leads to immortalization of primary human keratinocytes

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Opposing effects of Ets and Id proteins on p16INK4a expression during cellular senescence

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Expression of the p16INK4a tumor suppressor versus other INK4 family members during mouse development and aging.

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Strong effects of 5-azacytidine on the in vitro lifespan of human diploid fibroblasts.

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Human fibroblast commitment to a senescence-like state in response to histone deacetylase inhibitors is cell cycle dependent

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based on heuristic

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Telomere shortening associated with chromosome instability is arrested in immortal cells which express telomerase activity

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15 December 2024

https://opencitations.net/index/api/v1/citations/10.1002/J.1460-2075.1992.TB05245.X

Identifiers

10.1016/J.YEXCR.2004.01.017

1 reference

Europe PubMed Central

PubMed publication ID

21 September 2017

PubMed publication ID

1 reference

Europe PubMed Central

PubMed publication ID

21 September 2017

ResearchGate publication ID

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