Growth factors differentially stimulate the phosphorylation of Shc proteins and their association with Grb2 in PC-12 pheochromocytoma cells. 1994

M Ohmichi, and K Matuoka, and T Takenawa, and A R Saltiel
Department of Physiology, University of Michigan School of Medicine, Ann Arbor 48109.

Growth factor receptor tyrosine kinases can form stable associations with intracellular proteins that contain src homology (SH) 2 domains, including two proteins, Shc and Grb2, that are thought to lie upstream from the ras protooncogene in a signaling cascade. The phosphorylation and molecular associations of these proteins were evaluated in PC-12 pheochromocytoma cells treated with nerve growth factor (NGF), epidermal growth factor (EGF), and insulin. Both NGF and EGF stimulated the tyrosine phosphorylation of Shc proteins and their subsequent association with the receptors. In contrast, insulin had no effect on Shc phosphorylation, despite the expression of functional insulin receptors in these cells at levels comparable to those observed for NGF and EGF. NGF and EGF also induced the association of Shc proteins with a Grb2 fusion protein or endogenous Grb2, whereas insulin had no effect. All of the tyrosine-phosphorylated Shc proteins associated with the Grb2 fusion protein, although only about half of the endogenous Shc was phosphorylated in response to NGF or EGF. However, all three hormones induced the association of several additional tyrosine phosphorylated proteins with Grb2, some of which also coprecipitated with antiserum against the 85-kDa subunit of phosphatidylinositol-3 kinase. Moreover, these growth factors stimulated the association of phosphatidylinositol-3 kinase activity with the Grb2 fusion protein, although this activity was not detected in anti-Shc immunoprecipitates. These results provide further evidence for the divergence of signaling pathways in insulin action, and suggest that Grb2 forms separate complexes with tyrosine-phosphorylated proteins in PC-12 cells.

UI MeSH Term Description Entries
D007328 Insulin A 51-amino acid pancreatic hormone that plays a major role in the regulation of glucose metabolism, directly by suppressing endogenous glucose production (GLYCOGENOLYSIS; GLUCONEOGENESIS) and indirectly by suppressing GLUCAGON secretion and LIPOLYSIS. Native insulin is a globular protein comprised of a zinc-coordinated hexamer. Each insulin monomer containing two chains, A (21 residues) and B (30 residues), linked by two disulfide bonds. Insulin is used as a drug to control insulin-dependent diabetes mellitus (DIABETES MELLITUS, TYPE 1). Iletin,Insulin A Chain,Insulin B Chain,Insulin, Regular,Novolin,Sodium Insulin,Soluble Insulin,Chain, Insulin B,Insulin, Sodium,Insulin, Soluble,Regular Insulin
D009414 Nerve Growth Factors Factors which enhance the growth potentialities of sensory and sympathetic nerve cells. Neurite Outgrowth Factor,Neurite Outgrowth Factors,Neuronal Growth-Associated Protein,Neuronotrophic Factor,Neurotrophic Factor,Neurotrophic Factors,Neurotrophin,Neurotrophins,Growth-Associated Proteins, Neuronal,Neuronal Growth-Associated Proteins,Neuronotrophic Factors,Neurotrophic Protein,Neurotrophic Proteins,Proteins, Neuronal Growth-Associated,Factor, Neurite Outgrowth,Factor, Neuronotrophic,Factor, Neurotrophic,Factors, Nerve Growth,Factors, Neurite Outgrowth,Factors, Neuronotrophic,Factors, Neurotrophic,Growth Associated Proteins, Neuronal,Growth-Associated Protein, Neuronal,Neuronal Growth Associated Protein,Neuronal Growth Associated Proteins,Outgrowth Factor, Neurite,Outgrowth Factors, Neurite,Protein, Neuronal Growth-Associated
D010750 Phosphoproteins Phosphoprotein
D010766 Phosphorylation The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety. Phosphorylations
D011506 Proteins Linear POLYPEPTIDES that are synthesized on RIBOSOMES and may be further modified, crosslinked, cleaved, or assembled into complex proteins with several subunits. The specific sequence of AMINO ACIDS determines the shape the polypeptide will take, during PROTEIN FOLDING, and the function of the protein. Gene Products, Protein,Gene Proteins,Protein,Protein Gene Products,Proteins, Gene
D011972 Receptor, Insulin A cell surface receptor for INSULIN. It comprises a tetramer of two alpha and two beta subunits which are derived from cleavage of a single precursor protein. The receptor contains an intrinsic TYROSINE KINASE domain that is located within the beta subunit. Activation of the receptor by INSULIN results in numerous metabolic changes including increased uptake of GLUCOSE into the liver, muscle, and ADIPOSE TISSUE. Insulin Receptor,Insulin Receptor Protein-Tyrosine Kinase,Insulin Receptor alpha Subunit,Insulin Receptor beta Subunit,Insulin Receptor alpha Chain,Insulin Receptor beta Chain,Insulin-Dependent Tyrosine Protein Kinase,Receptors, Insulin,Insulin Receptor Protein Tyrosine Kinase,Insulin Receptors
D004815 Epidermal Growth Factor A 6-kDa polypeptide growth factor initially discovered in mouse submaxillary glands. Human epidermal growth factor was originally isolated from urine based on its ability to inhibit gastric secretion and called urogastrone. Epidermal growth factor exerts a wide variety of biological effects including the promotion of proliferation and differentiation of mesenchymal and EPITHELIAL CELLS. It is synthesized as a transmembrane protein which can be cleaved to release a soluble active form. EGF,Epidermal Growth Factor-Urogastrone,Urogastrone,Human Urinary Gastric Inhibitor,beta-Urogastrone,Growth Factor, Epidermal,Growth Factor-Urogastrone, Epidermal,beta Urogastrone
D000818 Animals Unicellular or multicellular, heterotrophic organisms, that have sensation and the power of voluntary movement. Under the older five kingdom paradigm, Animalia was one of the kingdoms. Under the modern three domain model, Animalia represents one of the many groups in the domain EUKARYOTA. Animal,Metazoa,Animalia
D015398 Signal Transduction The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway. Cell Signaling,Receptor-Mediated Signal Transduction,Signal Pathways,Receptor Mediated Signal Transduction,Signal Transduction Pathways,Signal Transduction Systems,Pathway, Signal,Pathway, Signal Transduction,Pathways, Signal,Pathways, Signal Transduction,Receptor-Mediated Signal Transductions,Signal Pathway,Signal Transduction Pathway,Signal Transduction System,Signal Transduction, Receptor-Mediated,Signal Transductions,Signal Transductions, Receptor-Mediated,System, Signal Transduction,Systems, Signal Transduction,Transduction, Signal,Transductions, Signal
D016716 PC12 Cells A CELL LINE derived from a PHEOCHROMOCYTOMA of the rat ADRENAL MEDULLA. PC12 cells stop dividing and undergo terminal differentiation when treated with NERVE GROWTH FACTOR, making the line a useful model system for NERVE CELL differentiation. Pheochromocytoma Cell Line,Cell Line, Pheochromocytoma,Cell Lines, Pheochromocytoma,PC12 Cell,Pheochromocytoma Cell Lines

Related Publications

M Ohmichi, and K Matuoka, and T Takenawa, and A R Saltiel
March 1995, The Journal of biological chemistry,
M Ohmichi, and K Matuoka, and T Takenawa, and A R Saltiel
April 2002, Molecular and cellular endocrinology,
M Ohmichi, and K Matuoka, and T Takenawa, and A R Saltiel
January 1996, FEBS letters,
M Ohmichi, and K Matuoka, and T Takenawa, and A R Saltiel
April 1991, Proceedings of the National Academy of Sciences of the United States of America,
M Ohmichi, and K Matuoka, and T Takenawa, and A R Saltiel
October 1993, The Journal of biological chemistry,
M Ohmichi, and K Matuoka, and T Takenawa, and A R Saltiel
December 1998, Hypertension (Dallas, Tex. : 1979),
M Ohmichi, and K Matuoka, and T Takenawa, and A R Saltiel
October 1994, The Journal of biological chemistry,
M Ohmichi, and K Matuoka, and T Takenawa, and A R Saltiel
August 1988, Biochemical and biophysical research communications,
M Ohmichi, and K Matuoka, and T Takenawa, and A R Saltiel
January 1997, International journal of cancer,
M Ohmichi, and K Matuoka, and T Takenawa, and A R Saltiel
March 1999, Journal of leukocyte biology,
Copied contents to your clipboard!