Document Detail

Cell cycle control by anchorage signaling.
MedLine Citation:
PMID:  22522183     Owner:  NLM     Status:  Publisher    
Virtually all the cells constituting solid organs in adult animals require anchorage to the extracellular matrix for their proliferation and survival. When deprived of anchorage, those cells arrest in G(1) phase of the cell cycle and die of apoptosis known as anoikis. However, if malignantly transformed, cells no longer require such an anchorage to proliferate and survive, and it is generally thought that the acquirement of this ability underlies the tumorigenic and metastatic capability of malignant cells. Therefore, for the past two decades, great efforts have been devoted to uncovering the nature of the anchorage signal and the mechanism by which this signal controls the G(1)-S transition in the cell cycle with little progress. However, several critical findings were recently made on anchorage signaling and the control of the cell cycle and cell death by this signaling. This review focuses on the newly emerging understanding and perspective of this highly important cell cycle and cell death regulation.
Hiroto Okayama
Related Documents :
22843843 - The histidine kinase pdhs controls cell cycle progression of the pathogenic alphaproteo...
14731493 - The oligodendrocyte and its many cellular processes.
15154083 - Stage-specific localization of transforming growth factor beta1 and beta3 and their rec...
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-4-13
Journal Detail:
Title:  Cellular signalling     Volume:  -     ISSN:  1873-3913     ISO Abbreviation:  -     Publication Date:  2012 Apr 
Date Detail:
Created Date:  2012-4-23     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8904683     Medline TA:  Cell Signal     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2012. Published by Elsevier Inc.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Molecular mechanisms of feedback inhibition of protein kinase A on intracellular cAMP accumulation.
Next Document:  Clinical nutrition, body composition and oncology: A critical literature review of the synergies.