Role of the Src homology 2 (SH2) domain and c-terminus tyrosine phosphorylation sites of SH2-containing inositol phosphatase (SHIP) in the regulation of insulin-induced mitogenesis

Endocrinology

Volumn 140, Issue 10, 1999, Pages 4585-4594

  Wada, T ^a   Sasaoka, T ^a   Ishiki, M ^a   Hori, H ^a   Haruta, T ^a   Ishihara, H ^a   Kobayashi, M ^a  

^a UNIVERSITY OF TOYAMA   (Japan)

Author keywords

[No Author keywords available]

Indexed keywords

INOSITOL; INSULIN; PHOSPHATASE; TYROSINE;

ANIMAL CELL; ARTICLE; DNA TRANSFECTION; GENETIC TRANSFECTION; MITOGENESIS; NONHUMAN; PRIORITY JOURNAL; PROTEIN ANALYSIS; PROTEIN BINDING; PROTEIN PHOSPHORYLATION; RAT; REGULATORY MECHANISM; SEQUENCE HOMOLOGY;

EID: 0033304860     PISSN: 00137227     EISSN: None     Source Type: Journal    
DOI: 10.1210/endo.140.10.7028     Document Type: Article

References (49)

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9. Human Sos1: A guanine nucleotide exchange factor for Ras that binds to Grb2
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13. The 145-kDa protein induced to associate with Shc by multiple cytokines is an inositol tetraphosphate and phosphatidylinositol 3,4,5-triphosphate 5-phosphatase
14. Multiple forms of an inositol polyphosphate 5-phosphatase form signaling complexes with Shc and Grb2
15. Cloning and characterization of human SHIP, the 145-kDa inositol 5-phosphatase that associates with Shc after cytokine stimulation
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17. Shc interaction with src homology 2 domain containing inositol phosphatase (SHIP) in vivo requires the Shc-phosphotyrosine binding domain and two specific phosphotyrosines on SHIP
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19. Negative signaling in B lymphocytes induces tyrosine phosphorylation of the 145-kDa inositol polyphosphate 5-phosphatase, SHIP
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21. Deletion of SHIP or SHP-1 reveals two distinct pathways for inhibitory signaling
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23. SIP/SHIP inhibits xenopus oocyte maturation induced by insulin and phosphatidylinositol 3-kinase
24. Phosphotyrosine-dependent interaction of Shc and insulin receptor substrate 1 with NPEY motif of the insulin receptor via a novel non-SH2 domain
25. A mutant insulin receptor with defective tyrosine kinase displays no biologic activity and does not undergo endocytosis
26. Evidence for a physical association between the Shc-PTB domain and the βc chain of the granulocyte-macrophage colony-stimulating factor receptor
27. Differential inhibition of signaling pathways by dominant-negative SH2/SH3 adapter proteins
28. Structure and ligand recognition of the phosphotyrosine binding domain of Shc
29. Mutation of the two carboxyl-terminal tyrosines results in an insulin receptor with normal metabolic signaling but enhanced mitogenic signaling properties
30. Multiple cytokines induce the tyrosine phosphorylation of Shc and its association with Grb2 in hemopoietic cells
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33. B cell antigen receptor cross-linking induces phosphorylation of the p21ras oncoprotein activators Shc and mSos1 as well as assembly of complexes containing Shc, Grb-2, mSos1, and a 145-kDa tyrosine-phosphoryla ted protein
34. Interaction of Shc with the ζ chain of the T cell receptor upon T cell activation
35. Multiple cytokines stimulate the binding of a common 145-kilodalton protein to Shc at the Grb2 recognition site of Shc
36. Insulin-stimulated MAP-2 kinase phosphorylates and activates ribosomal protein S6 kinase II
37. Identification of the regulatory phosphorylation sites in pp42/mitogen-activated protein kinase (MAP kinase)
38. Phosphatidylinositol 3-kinase activation is required for insulin stimulation of pp70 S6 kinase, DNA synthesis, and glucose transporter translocation
39. Phosphatidylinositol 3-kinase functions upstream of Ras and Raf in mediating insulin stimulation of c-fos transcription
40. Microinjection of the SH2 domain of the 85-kilodalton subunit of phosphatidylinositol 3-kinase inhibits insulin-induced DNA synthesis and c-fos expression
41. An SH2 domain-containing 5' inositolphosphatase inhibits insulin-induced Glut4 translocation and growth factor-induced actin filament rearrangement
42. Targeted disruption of SHIP leads to hemopoietic perturbations, lung pathology, and a shortened life span
43. Comparison of the insulin and insulin-like growth factor 1 mitogertic intracellular signaling pathways
44. The inositol 5'-phosphatase SHIP binds to immunoreceptor signaling motifs and responds to high affinity IgE receptor aggregation
45. The phosphatidylinositol polyphosphate 5-phosphatase SHIP and the protein tyrosine phosphatase SHP-2 form a complex in hematopoietic cells which can be regulated by BCR/ABL and growth factors
46. P85 subunit of PI3 kinase does not bind to human Flt3 receptor, but associates with SHP2, SHIP, and a tyrosine-phosphorylated 100-kDa protein in Flt3 ligand-stimulated hematopoietic cells
47. The SH2 domain-containing inositol 5'-phosphatase (SHIP) recruits the p85 subunit of phosphoinositide 3-kinase during FcγRIIb1-mediated inhibition of B cell receptor signaling
48. Identification of a second SH2-domain-containing protein closely related to the phosphatidylinositol polyphosphate 5-phosphatase SHIP
49. Growth factors and insulin stimulate tyrosine phosphorylation of the 51C/SHIP2 protein