| First Author | Vigil D | Year | 2010 |
| Journal | Nat Rev Cancer | Volume | 10 |
| Issue | 12 | Pages | 842-57 |
| PubMed ID | 21102635 | Mgi Jnum | J:166993 |
| Mgi Id | MGI:4866958 | Doi | 10.1038/nrc2960 |
| Citation | Vigil D, et al. (2010) Ras superfamily GEFs and GAPs: validated and tractable targets for cancer therapy?. Nat Rev Cancer 10(12):842-57 |
| abstractText | 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. |
