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Abl  (c-Abl) Tyrosine Kinase

 

A non-receptor tyrosine kinase of the src family but distinguished from other members by its large COOH terminal domain.  To forms of the normal protein exist which differ in the extreme N terminal.  One form (type IV/Ib) is myristoylated on the N-terminal glycine, the other normal form (I/Ia) in not. c-Abl contains both a G-actin binding site and an independent F-actin site. 

References:-

McWhirter, J.R., Wang, J.Y.J. (1991). "Activation of tyrosine kinase and microfilament-binding functions of c-abl by bcr sequences in bcr/abl fusion proteins." Mol.Cell.Biol. 11, 1785-1792.

McWhirter, J.R., Wang, J.Y.J. (1993). "An actin -binding function contributes to transformation by the Bcr-Abl oncoprotein of the Philadelphia chromosome-positive leukemias. EMBO J. 12, 1533-1546.

Van Etten, R.A., Jackson, P.K., Baltimore, D., Sander, M.C., Matsudaira, P.T. & Janmey, P.A. (1994). "The COOH terminus of the c-Abl tyrosine kinase contains distinct F-actin and G-actin binding domains with bundling activity." J.Cell Biol. 124, 325-340.

Wills, Z., Bateman, J., Korey, C. A., Comer, A. & Van Vactor, D. (1999) The tyrosine kinase Abl and its substrate enabled collaborate with the receptor phosphase Dlar to control motor axon guidance., Neuron. 22, 301-312.

Wills, Z., Marr, L., Zinn, K., Goodman, C. S. & Van Vactor, D. (1999) Profilin and the Abl tyrosine kinase are required for motor axon outgrowth in the Drosophila embryo., Neuron. 22, 291-299.

 
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