Mechanisms of Activation of Abl Family Kinases

摘要: Evidence that has accumulated over the last years points to c-Abl and Arg (ABL1 ABL2) as being particular forms of Src family kinases. Just much or even more than kinases, Abl members are built be able couple protein-protein interaction with protein tyrosine kinase catalytic output. This stems from constant competition between self-inhibitory intramolecular interactions (mostly via SH3 SH2 domains) generally activating intermolecular ligands. Ligand engagement both regulates and, in turn, is regulated by level activity domain. A series post-translational modifications act on this balance allows integration activity, localization multiprotein complex assembly functions. Most excitingly, majority principles appearing govern still operational Bcr-Abl oncogenic counterpart affect efficacy small molecular ATP-competitors.