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Contact inhibition and high cell density deactivate the mammalian target of rapamycin pathway, thus suppressing the senescence program

Proceedings of the National Academy of Sciences - PNAS, 2014-06, Vol.111 (24), p.8832-8837

2014

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Growth stimulation leads to cellular senescence when the cell cycle is blocked

Cell cycle (Georgetown, Tex.), 2008-11, Vol.7 (21), p.3355-3361

2008

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Paradoxical suppression of cellular senescence by p53

Proceedings of the National Academy of Sciences - PNAS, 2010-05, Vol.107 (21), p.9660-9664

2010

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Hypoxia suppresses conversion from proliferative arrest to cellular senescence

Proceedings of the National Academy of Sciences - PNAS, 2012-08, Vol.109 (33), p.13314-13318

2012

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Rapamycin decelerates cellular senescence

Cell cycle (Georgetown, Tex.), 2009-06, Vol.8 (12), p.1888-1895

2009

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The purpose of the HIF-1/PHD feedback loop: To limit mTOR-induced HIF-1α

Cell cycle (Georgetown, Tex.), 2011-05, Vol.10 (10), p.1557-1562

2011

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At concentrations that inhibit mTOR, resveratrol suppresses cellular senescence

Cell cycle (Georgetown, Tex.), 2009-06, Vol.8 (12), p.1901-1904

2009

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The choice between p53-induced senescence and quiescence is determined in part by the mTOR pathway

Aging (Albany, NY.), 2010-06, Vol.2 (6), p.344-352

2010

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Pseudo-DNA damage response in senescent cells

Cell cycle (Georgetown, Tex.), 2009-12, Vol.8 (24), p.4112-4118

2009

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Hyper-mitogenic drive coexists with mitotic incompetence in senescent cells

Cell cycle (Georgetown, Tex.), 2012-12, Vol.11 (24), p.4642-4649

2012

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Exploring long-term protection of normal human fibroblasts and epithelial cells from chemotherapy in cell culture

Oncotarget, 2011-03, Vol.2 (3), p.222-233

2011

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Dual mTORC1/C2 inhibitors suppress cellular geroconversion (a senescence program)

Oncotarget, 2015-09, Vol.6 (27), p.23238-23248

2015

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Elimination of proliferating cells unmasks the shift from senescence to quiescence caused by rapamycin

PloS one, 2011-10, Vol.6 (10), p.e26126-e26126

2011

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Pharmacologic inhibition of MEK and PI-3K converges on the mTOR/S6 pathway to decelerate cellular senescence

Cell cycle (Georgetown, Tex.), 2009-06, Vol.8 (12), p.1896-1900

2009

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Quantifying pharmacologic suppression of cellular senescence: prevention of cellular hypertrophy versus preservation of proliferative potential

Aging (Albany, NY.), 2009-12, Vol.1 (12), p.1008-1016

2009

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Rapamycin for life: A step to immortality

Cell cycle (Georgetown, Tex.), 2011-12, Vol.10 (24), p.4206-4206

Demidenko, Zoya N.

2011

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Recent discoveries in the cycling, growing and aging of the p53 field

Aging (Albany, NY.), 2012-12, Vol.4 (12), p.887-893

2012

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S6K in geroconversion

Cell cycle (Georgetown, Tex.), 2013-10, Vol.12 (20), p.3249-3252

2013

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Flavopiridol induces p53 via initial inhibition of Mdm2 and p21 and, independently of p53, sensitizes apoptosis-reluctant cells to tumor necrosis factor

Cancer research (Chicago, Ill.), 2004-05, Vol.64 (10), p.3653-3660

2004

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Cellular quiescence caused by the Mdm2 inhibitor Nutlin-3A

Cell cycle (Georgetown, Tex.), 2009-11, Vol.8 (22), p.3777-3781

2009

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The Regulation of Hypoxic Genes by Calcium Involves c-Jun/AP-1, Which Cooperates with Hypoxia-Inducible Factor 1 in Response to Hypoxia

Molecular and Cellular Biology, 2002-03, Vol.22 (6), p.1734-1741

2002

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Chronological lifespan in stationary culture: from yeast to human cells

Aging (Albany, NY.), 2011-11, Vol.3 (11), p.1041-1042

Demidenko, Zoya N

2011

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Depletion of mutant p53 and cytotoxicity of histone deacetylase inhibitors

Cancer research (Chicago, Ill.), 2005-08, Vol.65 (16), p.7386-7392

2005

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Contact inhibition and high cell density deactivate the mammalian target of rapamycin pathway, thus suppressing the senescence program

Growth stimulation leads to cellular senescence when the cell cycle is blocked

Paradoxical suppression of cellular senescence by p53

Hypoxia suppresses conversion from proliferative arrest to cellular senescence

Rapamycin decelerates cellular senescence

The purpose of the HIF-1/PHD feedback loop: To limit mTOR-induced HIF-1α

At concentrations that inhibit mTOR, resveratrol suppresses cellular senescence

The choice between p53-induced senescence and quiescence is determined in part by the mTOR pathway

Pseudo-DNA damage response in senescent cells

Hyper-mitogenic drive coexists with mitotic incompetence in senescent cells

Exploring long-term protection of normal human fibroblasts and epithelial cells from chemotherapy in cell culture

Dual mTORC1/C2 inhibitors suppress cellular geroconversion (a senescence program)

Elimination of proliferating cells unmasks the shift from senescence to quiescence caused by rapamycin

Pharmacologic inhibition of MEK and PI-3K converges on the mTOR/S6 pathway to decelerate cellular senescence

Quantifying pharmacologic suppression of cellular senescence: prevention of cellular hypertrophy versus preservation of proliferative potential

Rapamycin for life: A step to immortality

Recent discoveries in the cycling, growing and aging of the p53 field

S6K in geroconversion

Flavopiridol induces p53 via initial inhibition of Mdm2 and p21 and, independently of p53, sensitizes apoptosis-reluctant cells to tumor necrosis factor

Cellular quiescence caused by the Mdm2 inhibitor Nutlin-3A

Deregulation of the EGFR/PI3K/PTEN/Akt/mTORC1 pathway in breast cancer: possibilities for therapeutic intervention

The Regulation of Hypoxic Genes by Calcium Involves c-Jun/AP-1, Which Cooperates with Hypoxia-Inducible Factor 1 in Response to Hypoxia

Chronological lifespan in stationary culture: from yeast to human cells

Advances in targeting signal transduction pathways

Depletion of mutant p53 and cytotoxicity of histone deacetylase inhibitors

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