The SH2-containing adapter protein GRB10 interacts with BCR-ABL

Bcr-Abl is an oncogenic tyrosine kinase expressed in tumor cells of CML and a subset of ALL which in its unregulated and activated state is thought to cause cell transformation and leukemia. Bcr-Abl contains several autophosphorylation sites which serve as potential docking sites for SH2-containing...

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Veröffentlicht in:	Oncogene 1998-08, Vol.17 (8), p.941-948
Hauptverfasser:	REN YUAN BAI, JAHN, T, SCHREM, S, MUNZERT, G, WEIDNER, K. M, WANG, J. Y. J, DUYSTER, J
Format:	Artikel
Sprache:	eng
Schlagworte:	Absorption Adapter proteins BCR-ABL protein Binding sites Biological and medical sciences Cell Line Cell physiology Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes Cell Transformation, Neoplastic - genetics Dimerization Enzyme Activation Fibroblasts Fundamental and applied biological sciences. Psychology Fusion protein Fusion Proteins, bcr-abl - genetics Fusion Proteins, bcr-abl - metabolism Genetic Vectors - metabolism GRB10 Adaptor Protein Grb2 protein Humans Immunoprecipitation Interleukin 3 Kinases Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism Molecular and cellular biology Mutants Mutation Myeloid cells Phosphotyrosine Protein Binding Protein-tyrosine kinase Protein-Tyrosine Kinases - metabolism Proteins - metabolism Receptor, Epidermal Growth Factor - metabolism Saccharomyces cerevisiae - genetics src Homology Domains Transfection Tumor cells Tumor Cells, Cultured
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