Cellular Senescence: Molecular Mechanisms,In VivoSignificance, and Redox Considerations-Reference-Cited by-同舟云学术

Cellular Senescence: Molecular Mechanisms,In VivoSignificance, and Redox Considerations

Published:2009-01 Issue:1 Volume:11 Page:59-98
ISSN:1523-0864
Container-title:Antioxidants & Redox Signaling
language:en
Short-container-title:Antioxidants & Redox Signaling

Author:

Muller Michael¹

Affiliation:

1. Centre for Education and Research on Ageing, ANZAC Research Institute, University of Sydney, Concord RG Hospital, Concord, Sydney, Australia.

Publisher

Mary Ann Liebert Inc

Subject

Cell Biology,Clinical Biochemistry,Molecular Biology,Physiology,Biochemistry,Cell Biology,Clinical Biochemistry,Molecular Biology,Physiology,Biochemistry

Link

http://www.liebertpub.com/doi/pdf/10.1089/ars.2008.2104

Reference472 articles.

1. Increased gene expression of Alzheimer disease beta-amyloid precursor protein in senescent cultured fibroblasts.

2. Investigation of the Role of G1/S Cell Cycle Mediators in Cellular Senescence

3. Diminished Responsiveness of Senescent Normal Human Fibroblasts to TNF-Dependent Proliferation and Interleukin Production is Not Due to Its Effect on the Receptors or on the Activation of a Nuclear Factor NF- B

4. Telomere Reduction in Human Liver Tissues with Age and Chronic Inflammation

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

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