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Literature DB >> 17662938

Cellular senescence in cancer and aging.

Manuel Collado¹, Maria A Blasco, Manuel Serrano.

Abstract

Cellular senescence, a state of irreversible growth arrest, can be triggered by multiple mechanisms including telomere shortening, the epigenetic derepression of the INK4a/ARF locus, and DNA damage. Together these mechanisms limit excessive or aberrant cellular proliferation, and so the state of senescence protects against the development of cancer. Recent evidence suggests that cellular senescence also may be involved in aging.

Entities: Disease Gene

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Year: 2007 PMID： 17662938 DOI： 10.1016/j.cell.2007.07.003

Source DB: PubMed Journal: Cell ISSN： 0092-8674 Impact factor: 41.582

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Cited

634 in total

1. Overexpression of the pituitary tumor transforming gene induces p53-dependent senescence through activating DNA damage response pathway in normal human fibroblasts.

Authors: Yi-Hsin Hsu; Li-Jen Liao; Chuan-Hang Yu; Chun-Pin Chiang; Jing-Ru Jhan; Lien-Cheng Chang; Yann-Jang Chen; Pei-Jen Lou; Jing-Jer Lin
Journal: J Biol Chem Date: 2010-05-07 Impact factor: 5.157

2. Age-dependent cardiomyopathy in mitochondrial mutator mice is attenuated by overexpression of catalase targeted to mitochondria.

Authors: Dao-Fu Dai; Tony Chen; Jonathan Wanagat; Michael Laflamme; David J Marcinek; Mary J Emond; Calvin P Ngo; Tomas A Prolla; Peter S Rabinovitch
Journal: Aging Cell Date: 2010-04-29 Impact factor: 9.304

3. CCAAT/Enhancer-binding protein beta DNA binding is auto-inhibited by multiple elements that also mediate association with p300/CREB-binding protein (CBP).

Authors: Sook Lee; Maria Miller; Jon D Shuman; Peter F Johnson
Journal: J Biol Chem Date: 2010-05-07 Impact factor: 5.157

10. Oxidative Stress Increases the Number of Stress Granules in Senescent Cells and Triggers a Rapid Decrease in p21waf1/cip1 Translation.

Authors: Xian Jin Lian; Imed-Eddine Gallouzi
Journal: J Biol Chem Date: 2009-01-28 Impact factor: 5.157

Cellular senescence in cancer and aging.

1. Overexpression of the pituitary tumor transforming gene induces p53-dependent senescence through activating DNA damage response pathway in normal human fibroblasts.

2. Age-dependent cardiomyopathy in mitochondrial mutator mice is attenuated by overexpression of catalase targeted to mitochondria.

3. CCAAT/Enhancer-binding protein beta DNA binding is auto-inhibited by multiple elements that also mediate association with p300/CREB-binding protein (CBP).

4. Primary biliary cirrhosis: bad genes, bad luck.

Review 5. Trithorax group proteins: switching genes on and keeping them active.

6. A set of miRNAs participates in the cellular senescence program in human diploid fibroblasts.

7. Aging genetics and aging.

8. Oncogene-induced senescence results in marked metabolic and bioenergetic alterations.

9. p53 in stem cells.

10. Oxidative Stress Increases the Number of Stress Granules in Senescent Cells and Triggers a Rapid Decrease in p21waf1/cip1 Translation.