Document Detail

Stress kinase signaling in cancer: fact or fiction?
MedLine Citation:
PMID:  15596290     Owner:  NLM     Status:  MEDLINE    
Cancer results from genetic alterations in intracellular signaling pathways, which normally orchestrate the execution of developmental programs and the organismic response to extrinsic factors. Mutations in upstream activators and components of the cytoplasmic (Ras-Raf MEK-ERK) cascade frequently occur in tumors. In vitro and in vivo studies have shown that isolated activation of this pathway is both, necessary and sufficient for transformation. During the last years two new groups of related kinases have joined the ranks of mitogen-activated protein kinases, stress-activated protein kinases/Jun N-terminal kinases and p38. Their activation not only occurs during cellular responses to unphysiological stimuli but also downstream of cytokine and pathogen receptors and has been observed in tumors. In this article we will review the role of stress kinases in cancer, and discuss the mechanisms through which they regulate the transformation process.
Ulrike Rennefahrt; Manickam Janakiraman; Robert Ollinger; Jakob Troppmair
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Cancer letters     Volume:  217     ISSN:  0304-3835     ISO Abbreviation:  Cancer Lett.     Publication Date:  2005 Jan 
Date Detail:
Created Date:  2004-12-14     Completed Date:  2005-03-03     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  7600053     Medline TA:  Cancer Lett     Country:  Ireland    
Other Details:
Languages:  eng     Pagination:  1-9     Citation Subset:  IM    
Institut für Medizinische Strahlenkunde und Zellforschung, University of Würzburg, Würzburg, Germany.
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MeSH Terms
Carrier Proteins / physiology*
Cell Transformation, Neoplastic*
Heat-Shock Proteins / physiology*
Neoplasms / enzymology*
Signal Transduction / physiology*
Reg. No./Substance:
0/Carrier Proteins; 0/Heat-Shock Proteins; 0/TP53INP1 protein, human

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

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