Premium
Association of the Abl tyrosine kinase with the Trk nerve growth factor receptor
Author(s) -
Yano Hiroko,
Cong Feng,
Birge Raymond B.,
Goff Stephen P.,
Chao Moses V.
Publication year - 2000
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(20000201)59:3<356::aid-jnr9>3.0.co;2-g
Subject(s) - tropomyosin receptor kinase a , low affinity nerve growth factor receptor , receptor tyrosine kinase , microbiology and biotechnology , trk receptor , tropomyosin receptor kinase c , tyrosine kinase , tyrosine phosphorylation , nerve growth factor , biology , chemistry , abl , phosphorylation , platelet derived growth factor receptor , cancer research , signal transduction , receptor , biochemistry , growth factor
Nerve growth factor (NGF) initiates the majority of its biological effects by promoting the dimerization and activation of the tyrosine kinase receptor TrkA. In addition to rapid increases in the phosphorylation of phosphatidylinositol 3′‐kinase (PI 3‐kinase) and phospholipase C‐γ and increased ras activity, phosphorylation of c‐Crk and paxillin proteins has been observed upon TrkA activation. The c‐Abl tyrosine kinase is involved in the control of the axonal cytoskeleton and is known to interact with c‐Crk proteins. Here we have tested the possibility that TrkA receptors might form an association with the c‐Abl protein. After transfection in 293T cells, TrkA and c‐Abl kinases could be coimmunoprecipitated. This interaction did not require TrkA receptors to be autophosphorylated. Mapping analysis indicated that the region of c‐Abl association was confined to the juxtamembrane region of TrkA. The interaction of c‐Abl with TrkA was also observed in differentiated pheochromocytoma PC12 cells. These results suggest that c‐Abl may be recruited to the NGF receptor complex and be involved in regulating specific phosphorylation events that occur during neuronal differentiation. J. Neurosci. Res. 59:356–364, 2000 © 2000 Wiley‐Liss, Inc.