By Anthony Koleske
Abl kinfolk Kinases in improvement and sickness offers an outline of the capabilities of Abl kinfolk kinases in improvement and illness. This new name discusses the biochemical, genetic, and phone organic facts that elucidate the mobile roles for those kinases in those approaches.
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Additional resources for Abl Family Kinases in Development and Disease (Molecular Biology Intelligence Unit)
Puma and Noxa, by p53 in response to DNA damage. Indeed, IR-induced apoptosis in the developing central nervous system (CNS) is abrogated in yl77\
Verfaillie C M , McCarthy JB, McGlave PB. Mechanisms underlying abnormal trafficking of malignant progenitors in chronic myelogenous leukemia. Decreased adhesion to stroma and fibronectin but increased adhesion to the basement membrane components laminin and collagen type IV. J Clin Invest 1992; 90(4):1232-124l. 17. Bhatia R, M u n t h e HA, Verfaillie C M . Role of abnormal integrin-cytoskeletal interactions in impaired betal integrin function in chronic myelogenous leukemia hematopoietic progenitors.
Abl in DNA Damage-Induced Apoptosis Activation of the Abl tyrosine kinase by DNA damage has been linked in mammalian cells to the induction of apoptosis. ^ '^^'^^ Abl and Cell Death 29 Table 1. ABL-interacting proteins relevant to the control of cell death Name* Gene I D * Molecular Function ATM 472 Protein kinase belonging to the PI-3 kinase super-family involved in D N A damage signal transduction ATR 545 ATM-related protein kinase involved in D N A damage signal transduction and D N A replication BRCA1 672 A nuclear scaffolding protein w i t h E3-ligase activity and involved in D N A repair and D N A damage signal transduction Function Relative to ABL Ref.
Abl Family Kinases in Development and Disease (Molecular Biology Intelligence Unit) by Anthony Koleske