| Molecular signaling and genetic pathways of senescence: Its role in tumorigenesis and aging. | |
| | |
MedLine Citation:
|
PMID: 17133363 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
|
In response to progressive telomere shortening in successive cell divisions, normal somatic cells enter senescence, during which they cease to proliferate irreversibly and undergo dramatic changes in gene expression. Senescence can also be activated by various types of stressful stimuli, including aberrant oncogenic signaling, oxidative stress, and DNA damage. Because of the limited proliferative capacity imposed by senescence, as well as the ability of senescent cells to influence neighboring non-senescent cells, senescence has been proposed to play an important role in tumorigenesis and to contribute to aging. Considerable effort has been put into elucidating the molecular mechanisms of senescence, including the signals that trigger senescence, the molecular pathways by which cells enter senescence, and evidence that supports its role in tumorigenesis and aging. |
| | |
Authors:
|
Hong Zhang |
Related Documents
:
|
11986943 - A novel mechanism of retinoic acid resistance in acute promyelocytic leukemia cells thr... 10619313 - The relationships of animal age and caloric intake to cellular replication in vivo and ... 2444023 - Gangliocytic paraganglioma of the duodenum: case report. |
Publication Detail:
|
Type: Journal Article; Review |
Journal Detail:
|
Title: Journal of cellular physiology Volume: 210 ISSN: 0021-9541 ISO Abbreviation: J. Cell. Physiol. Publication Date: 2007 Mar |
Date Detail:
|
Created Date: 2007-01-02 Completed Date: 2007-03-08 Revised Date: - |
Medline Journal Info:
|
Nlm Unique ID: 0050222 Medline TA: J Cell Physiol Country: United States |
Other Details:
|
Languages: eng Pagination: 567-74 Citation Subset: IM |
Copyright Information:
|
Copyright 2006 Wiley-Liss, Inc. |
Affiliation:
|
Department of Cell Biology, University of Massachusetts Medical School, Worcester, Massachusetts 01655, USA. hong.zhang@umassmed.edu |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
Aging
/
genetics*,
physiology* Cell Proliferation Cell Transformation, Neoplastic / genetics, pathology* Cyclin-Dependent Kinase Inhibitor p16 / genetics, physiology Cyclin-Dependent Kinase Inhibitor p21 / genetics, physiology Humans Retinoblastoma Protein / genetics, physiology Signal Transduction / genetics*, physiology* Telomere Tumor Suppressor Protein p53 / genetics, physiology |
| Chemical | |
Reg. No./Substance:
|
0/Cyclin-Dependent Kinase Inhibitor p16; 0/Cyclin-Dependent Kinase Inhibitor p21; 0/Retinoblastoma Protein; 0/Tumor Suppressor Protein p53 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Potent stimulation of large-conductance Ca2+-activated K+ channels by rottlerin, an inhibitor of pro...
Next Document: Features that determine telomere homolog oligonucleotide-induced therapeutic DNA damage-like respons...