Journal
NATURE REVIEWS CANCER
Volume 10, Issue 12, Pages 842-857Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nrc2960
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Funding
- US National Institutes of Health [CA042978, CA129610, CA127152, CA67771, CA106991]
- American Cancer Society
- Centre National de la Recherche Scientifique, France
- Association pour la Recherche Contre le Cancer, France
- Agence Nationale de la Recherche, France
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There is now considerable and increasing evidence for a causal role for aberrant activity of the Ras superfamily of small GTPases in human cancers. These GTPases function as GDP-GTP-regulated binary switches that control many fundamental cellular processes. A common mechanism of GTPase deregulation in cancer is the deregulated expression and/or activity of their regulatory proteins, guanine nucleotide exchange factors (GEFs) that promote formation of the active GTP-bound state and GTPase-activating proteins (GAPs) that return the GTPase to its GDP-bound inactive state. In this Review, we assess the association of GEFs and GAPs with cancer and their druggability for cancer therapeutics.
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