| The Ras signal transduction pathway. | |
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MedLine Citation:
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PMID: 8143346 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Considerable progress has been made over the past year in elucidating the mechanisms by which extracellular signals are transduced via cell surface receptors to trigger changes in gene expression which determine the growth and differentiated state of a cell. In particular, Ras proteins have been implicated as key intermediates that mediate the signal from upstream tyrosine kinases to a downstream cascade of serine/threonine kinases, which then activate nuclear factors that control gene expression and protein synthesis. How Ras proteins function is regulated in this role as a molecular switch, and how the signal is transmitted between the various components of the pathway, are now being determined. Finally, the Rho family of Ras-related proteins, which regulate the actin cytoskeleton, have also been implicated as mediators of oncogenic Ras transformation. The brisk pace at which the key components of Ras-mediated signal transduction pathways are being identified hold great promise that new targets for therapeutic intervention in cancer may now be identified. |
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Authors:
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R Khosravi-Far; C J Der |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.; Review |
Journal Detail:
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Title: Cancer metastasis reviews Volume: 13 ISSN: 0167-7659 ISO Abbreviation: Cancer Metastasis Rev. Publication Date: 1994 Mar |
Date Detail:
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Created Date: 1994-05-05 Completed Date: 1994-05-05 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 8605731 Medline TA: Cancer Metastasis Rev Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 67-89 Citation Subset: IM |
Affiliation:
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Department of Pharmacology, School of Medicine, Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill 27599-7365. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Cell Differentiation Cell Division GTP-Binding Proteins / physiology Gene Expression Regulation* Genes, ras* Humans Mammals Mutation Neoplasms / genetics*, pathology* Oncogenes Proto-Oncogene Proteins p21(ras) / physiology* Proto-Oncogenes Receptors, Cell Surface / physiology* Signal Transduction* |
| Grant Support | |
ID/Acronym/Agency:
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CA42978/CA/NCI NIH HHS; CA52072/CA/NCI NIH HHS; CA55008/CA/NCI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Receptors, Cell Surface; EC 3.6.1.-/GTP-Binding Proteins; EC 3.6.5.2/HRAS protein, human; EC 3.6.5.2/Proto-Oncogene Proteins p21(ras) |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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