title: Coupling kinase activation to substrate recognition in SRC-family tyrosine kinases.
abstract: Signal transduction molecules translate extracellular inputs into their corresponding intracellular responses. Given the complexity and number of signaling pathways present in the eukaryotic cell, it is not surprising that the functions of signaling molecules are often tightly regulated. Autoinhibition is a prevalent mechanism for governing the function of signaling molecules. The relationship between the viral, oncogenic form of Src (v-Src) and the corresponding cellular proto-oncogene (c-Src) highlights the importance of inhibitory intramolecular interactions. Src provides an example of the dramatic cellular consequences arising from the loss of autoregulation.
authors.affiliation: Laboratories of Molecular Biophysics and Howard Hughes Medical Institute, The Rockefeller University, 1230 York Avenue, New York, NY 10021, USA.
authors.forename: Patricia
authors.initials: P
authors.lastname: Pellicena
authors.forename: W Todd
authors.initials: WT
authors.lastname: Miller
mesh_terms: D000818:Animals; D004789:Enzyme Activation / Q000502:physiology; D006801:Humans; D000090063:Proto-Oncogene Mas; D013379:Substrate Specificity; D019061:src-Family Kinases / Q000737:chemistry / Q000378:metabolism* / Q000502:physiology
chemical_list: C000715470:MAS1 protein, human; D000090063:Proto-Oncogene Mas; D019061:src-Family Kinases