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251 related items for PubMed ID: 3101064
1. Replacement of lysine residue 1030 in the putative ATP-binding region of the insulin receptor abolishes insulin- and antibody-stimulated glucose uptake and receptor kinase activity. Ebina Y, Araki E, Taira M, Shimada F, Mori M, Craik CS, Siddle K, Pierce SB, Roth RA, Rutter WJ. Proc Natl Acad Sci U S A; 1987 Feb; 84(3):704-8. PubMed ID: 3101064 [Abstract] [Full Text] [Related]
2. Human insulin receptors mutated at the ATP-binding site lack protein tyrosine kinase activity and fail to mediate postreceptor effects of insulin. Chou CK, Dull TJ, Russell DS, Gherzi R, Lebwohl D, Ullrich A, Rosen OM. J Biol Chem; 1987 Feb 05; 262(4):1842-7. PubMed ID: 3100537 [Abstract] [Full Text] [Related]
3. Tyrosine kinase-defective insulin receptors undergo decreased endocytosis but do not affect internalization of normal endogenous insulin receptors. Grako KA, Olefsky JM, McClain DA. Endocrinology; 1992 Jun 05; 130(6):3441-52. PubMed ID: 1317784 [Abstract] [Full Text] [Related]
4. Biologic activities of naturally occurring human insulin receptor mutations. Evidence that metabolic effects of insulin can be mediated by a kinase-deficient insulin receptor mutant. Moller DE, Benecke H, Flier JS. J Biol Chem; 1991 Jun 15; 266(17):10995-1001. PubMed ID: 1645719 [Abstract] [Full Text] [Related]
12. Ala1048-->Asp mutation in the kinase domain of insulin receptor causes defective kinase activity and insulin resistance. Haruta T, Takata Y, Iwanishi M, Maegawa H, Imamura T, Egawa K, Itazu T, Kobayashi M. Diabetes; 1993 Dec 15; 42(12):1837-44. PubMed ID: 8243830 [Abstract] [Full Text] [Related]
13. Cytoplasmic juxtamembrane region of the insulin receptor: a critical role in ATP binding, endogenous substrate phosphorylation, and insulin-stimulated bioeffects in CHO cells. Backer JM, Schroeder GG, Cahill DA, Ullrich A, Siddle K, White MF. Biochemistry; 1991 Jul 02; 30(26):6366-72. PubMed ID: 1647198 [Abstract] [Full Text] [Related]
14. Substitution of glutamic acid for alanine 1135 in the putative "catalytic loop" of the tyrosine kinase domain of the human insulin receptor. A mutation that impairs proteolytic processing into subunits and inhibits receptor tyrosine kinase activity. Cama A, de la Luz Sierra M, Quon MJ, Ottini L, Gorden P, Taylor SI. J Biol Chem; 1993 Apr 15; 268(11):8060-9. PubMed ID: 8096518 [Abstract] [Full Text] [Related]
19. Mutation in a conserved motif next to the insulin receptor key autophosphorylation sites de-regulates kinase activity and impairs insulin action. Formisano P, Sohn KJ, Miele C, Di Finizio B, Petruzziello A, Riccardi G, Beguinot L, Beguinot F. J Biol Chem; 1993 Mar 05; 268(7):5241-8. PubMed ID: 8383132 [Abstract] [Full Text] [Related]