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- W2023673608 endingPage "413" @default.
- W2023673608 startingPage "402" @default.
- W2023673608 abstract "The nonreceptor tyrosine kinases Abl and Arg are among the most well-characterized tyrosine kinases in the human genome. The activation of Abl by N-terminal fusions with Bcr (Bcr-Abl) or Gag (v-Abl) is responsible for chronic myeloid leukemia or Ph+ acute lymphoblastic leukemia and mouse leukemia virus, respectively. In addition, aberrant Abl and Arg activation downstream of several oncogenic growth factor receptors contributes to the development and progression of a variety of human cancers, often associated with poor clinical outcome, drug resistance, and tumor invasion and metastasis. Abl activation can occur by a variety of mechanisms that include domain interactions involving structural remodeling of autoinhibited conformations as well as direct phosphorylation by upstream kinases and phosphatases. Constitutive activation of Abl plays a significant role in regulating the actin cytoskeleton by modulating cell adhesion, motility, and invadopodia. This review addresses the role of Abl and Arg in tumor progression with particular emphasis on the roles of Crk and Abi1 adapter proteins as distinct molecular switches for Abl transactivation. These insights, combined with new insights into the structure of these kinases, provide the rationale to envision that Crk and Abi1 fine-tune Abl regulation to control signaling to the cytoskeleton." @default.
- W2023673608 created "2016-06-24" @default.
- W2023673608 creator A5001842568 @default.
- W2023673608 creator A5016218082 @default.
- W2023673608 creator A5020964256 @default.
- W2023673608 creator A5047985322 @default.
- W2023673608 creator A5063809151 @default.
- W2023673608 date "2012-05-01" @default.
- W2023673608 modified "2023-10-03" @default.
- W2023673608 title "Crk and Abi1: Binary Molecular Switches That Regulate Abl Tyrosine Kinase and Signaling to the Cytoskeleton" @default.
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