127 related articles for article (PubMed ID: 8257690)
1. Deletion of exon 21 of the insulin receptor eliminates tyrosine kinase activity but preserves mitogenic signaling.
Rolband GC; Williams JF; Webster NJ; Hsu D; Olefsky JM
Biochemistry; 1993 Dec; 32(49):13545-50. PubMed ID: 8257690
[TBL] [Abstract][Full Text] [Related]
2. Insulin internalization in the absence of the insulin receptor tyrosine kinase domain is insufficient for mediating intracellular biological effects.
Schranz DB; Rohilla AM; Anderson C; Wood WM; Berhanu P
Biochem Biophys Res Commun; 1996 Oct; 227(2):600-7. PubMed ID: 8878559
[TBL] [Abstract][Full Text] [Related]
3. A domain of the insulin receptor required for endocytosis in rat fibroblasts.
Thies RS; Webster NJ; McClain DA
J Biol Chem; 1990 Jun; 265(17):10132-7. PubMed ID: 2161833
[TBL] [Abstract][Full Text] [Related]
4. Deletion of the insulin receptor beta-subunit acidic domain results in enhanced metabolic signaling.
Rolband GC; Williams JF; Webster NJ; Olefsky JM
Endocrinology; 1993 Sep; 133(3):1437-43. PubMed ID: 8396020
[TBL] [Abstract][Full Text] [Related]
5. Transmembrane signaling by an insulin receptor lacking a cytoplasmic beta-subunit domain.
Sasaoka T; Takata Y; Kusari J; Anderson CM; Langlois WJ; Olefsky JM
Proc Natl Acad Sci U S A; 1993 May; 90(10):4379-83. PubMed ID: 8506276
[TBL] [Abstract][Full Text] [Related]
6. Insulin signal transduction by a mutant human insulin receptor lacking the NPEY sequence. Evidence for an alternate mitogenic signaling pathway that is independent of Shc phosphorylation.
Berhanu P; Anderson C; Hickman M; Ciaraldi TP
J Biol Chem; 1997 Sep; 272(36):22884-90. PubMed ID: 9278451
[TBL] [Abstract][Full Text] [Related]
7. Mechanisms of enhanced transmembrane signaling by an insulin receptor lacking a cytoplasmic beta-subunit domain.
Sasaoka T; Langlois WJ; Rose DW; Olefsky JM
J Biol Chem; 1995 May; 270(18):10885-92. PubMed ID: 7738028
[TBL] [Abstract][Full Text] [Related]
8. Enhanced insulin-induced mitogenesis and mitogen-activated protein kinase activities in mutant insulin receptors with substitution of two COOH-terminal tyrosine autophosphorylation sites by phenylalanine.
Ando A; Momomura K; Tobe K; Yamamoto-Honda R; Sakura H; Tamori Y; Kaburagi Y; Koshio O; Akanuma Y; Yazaki Y
J Biol Chem; 1992 Jun; 267(18):12788-96. PubMed ID: 1618780
[TBL] [Abstract][Full Text] [Related]
9. Mutagenic structure/function analysis of the cytoplasmic cysteines of the insulin receptor.
Macaulay SL; Polites M; Frenkel MJ; Hewish DR; Ward CW
Biochem J; 1995 Mar; 306 ( Pt 3)(Pt 3):811-20. PubMed ID: 7702578
[TBL] [Abstract][Full Text] [Related]
10. C-terminus or juxtamembrane deletions in the insulin receptor do not affect the glucose-dependent inhibition of the tyrosine kinase activity.
Mosthaf L; Berti L; Kellerer M; Mushack J; Seffer E; Bossenmaier B; Coghlan M; Siddle K; Ullrich A; Häring HU
Eur J Biochem; 1995 Feb; 227(3):787-91. PubMed ID: 7867639
[TBL] [Abstract][Full Text] [Related]
11. Properties of a human insulin receptor with a COOH-terminal truncation. I. Insulin binding, autophosphorylation, and endocytosis.
McClain DA; Maegawa H; Levy J; Huecksteadt T; Dull TJ; Lee J; Ullrich A; Olefsky JM
J Biol Chem; 1988 Jun; 263(18):8904-11. PubMed ID: 2837467
[TBL] [Abstract][Full Text] [Related]
12. Augmented mitogenesis and impaired metabolic signaling mediated by a truncated insulin receptor.
Thies RS; Ullrich A; McClain DA
J Biol Chem; 1989 Aug; 264(22):12820-5. PubMed ID: 2753889
[TBL] [Abstract][Full Text] [Related]
13. The amino acid sequence GPLY is not necessary for normal endocytosis of the human insulin receptor B isoform.
Berhanu P; Anderson C; Paynter DR; Wood WM
Biochem Biophys Res Commun; 1995 Apr; 209(2):730-8. PubMed ID: 7537496
[TBL] [Abstract][Full Text] [Related]
14. Serine residues 1177/78/82 of the insulin receptor are required for substrate phosphorylation but not autophosphorylation.
Bossenmaier B; Strack V; Stoyanov B; Krützfeldt J; Beck A; Lehmann R; Kellerer M; Klein H; Ullrich A; Lammers R; Häring HU
Diabetes; 2000 Jun; 49(6):889-95. PubMed ID: 10866039
[TBL] [Abstract][Full Text] [Related]
15. Properties of a human insulin receptor with a COOH-terminal truncation. II. Truncated receptors have normal kinase activity but are defective in signaling metabolic effects.
Maegawa H; McClain DA; Freidenberg G; Olefsky JM; Napier M; Lipari T; Dull TJ; Lee J; Ullrich A
J Biol Chem; 1988 Jun; 263(18):8912-7. PubMed ID: 2837468
[TBL] [Abstract][Full Text] [Related]
16. Amino acid sequences Gly-Pro-Leu-Tyr and Asn-Pro-Glu-Tyr in the submembranous domain of the insulin receptor are required for normal endocytosis.
Rajagopalan M; Neidigh JL; McClain DA
J Biol Chem; 1991 Dec; 266(34):23068-73. PubMed ID: 1744103
[TBL] [Abstract][Full Text] [Related]
17. Intracellular signaling by a mutant human insulin receptor lacking the carboxyl-terminal tyrosine autophosphorylation sites.
Takata Y; Webster NJ; Olefsky JM
J Biol Chem; 1992 May; 267(13):9065-70. PubMed ID: 1577744
[TBL] [Abstract][Full Text] [Related]
18. Endocytosis of insulin receptors is not required for activation or deactivation of the hormone response.
McClain DA
J Biol Chem; 1990 Dec; 265(34):21363-7. PubMed ID: 2174444
[TBL] [Abstract][Full Text] [Related]
19. Phorbol ester-mediated protein kinase C interaction with wild-type and COOH-terminal truncated insulin receptors.
Anderson CM; Olefsky JM
J Biol Chem; 1991 Nov; 266(32):21760-4. PubMed ID: 1657981
[TBL] [Abstract][Full Text] [Related]
20. Transmembrane domain interactions are necessary for negative cooperativity of the insulin receptor.
Whittaker J; Garcia P; Yu GQ; Mynarcik DC
Mol Endocrinol; 1994 Nov; 8(11):1521-7. PubMed ID: 7877620
[TBL] [Abstract][Full Text] [Related]
[Next] [New Search]
