Webster NJ - Search Results

1

GnRH activates ERK1/2 leading to the induction of c-fos and LHbeta protein expression in LbetaT2 cells.

Liu F, Austin DA, Mellon PL, Olefsky JM, Webster NJ. Liu F, et al. Among authors: webster nj. Mol Endocrinol. 2002 Mar;16(3):419-34. doi: 10.1210/mend.16.3.0791. Mol Endocrinol. 2002. PMID: 11875099

2

Intracellular signaling by a mutant human insulin receptor lacking the carboxyl-terminal tyrosine autophosphorylation sites.

Takata Y, Webster NJ, Olefsky JM. Takata Y, et al. Among authors: webster nj. J Biol Chem. 1992 May 5;267(13):9065-70. J Biol Chem. 1992. PMID: 1577744 Free article.

3

Mutation of the two carboxyl-terminal tyrosines results in an insulin receptor with normal metabolic signaling but enhanced mitogenic signaling properties.

Takata Y, Webster NJ, Olefsky JM. Takata Y, et al. Among authors: webster nj. J Biol Chem. 1991 May 15;266(14):9135-9. J Biol Chem. 1991. PMID: 2026614 Free article.

4

Relative expression of insulin receptor isoforms does not differ in lean, obese, and noninsulin-dependent diabetes mellitus subjects.

Anderson CM, Henry RR, Knudson PE, Olefsky JM, Webster NJ. Anderson CM, et al. Among authors: webster nj. J Clin Endocrinol Metab. 1993 May;76(5):1380-2. doi: 10.1210/jcem.76.5.7684396. J Clin Endocrinol Metab. 1993. PMID: 7684396

5

The insulin receptor C-terminus is involved in regulation of the receptor kinase activity.

Kaliman P, Baron V, Alengrin F, Takata Y, Webster NJ, Olefsky JM, Van Obberghen E. Kaliman P, et al. Among authors: webster nj. Biochemistry. 1993 Sep 21;32(37):9539-44. doi: 10.1021/bi00088a004. Biochemistry. 1993. PMID: 7690586

6

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. Rolband GC, et al. Among authors: webster nj. Biochemistry. 1993 Dec 14;32(49):13545-50. doi: 10.1021/bi00212a021. Biochemistry. 1993. PMID: 8257690

7

Deletion of the insulin receptor beta-subunit acidic domain results in enhanced metabolic signaling.

Rolband GC, Williams JF, Webster NJ, Olefsky JM. Rolband GC, et al. Among authors: webster nj. Endocrinology. 1993 Sep;133(3):1437-43. doi: 10.1210/endo.133.3.8396020. Endocrinology. 1993. PMID: 8396020

8

Association of the insulin receptor with phospholipase C-gamma (PLCgamma) in 3T3-L1 adipocytes suggests a role for PLCgamma in metabolic signaling by insulin.

Kayali AG, Eichhorn J, Haruta T, Morris AJ, Nelson JG, Vollenweider P, Olefsky JM, Webster NJ. Kayali AG, et al. Among authors: webster nj. J Biol Chem. 1998 May 29;273(22):13808-18. doi: 10.1074/jbc.273.22.13808. J Biol Chem. 1998. PMID: 9593725 Free article.

9

Inhibition of PLC-gamma1 activity converts nerve growth factor from an anti-mitogenic to a mitogenic signal in CHO cells.

Zapf-Colby A, Eichhorn J, Webster NJ, Olefsky JM. Zapf-Colby A, et al. Among authors: webster nj. Oncogene. 1999 Sep 2;18(35):4908-19. doi: 10.1038/sj.onc.1202861. Oncogene. 1999. PMID: 10490825

10

Stimulation of MAPK cascades by insulin and osmotic shock: lack of an involvement of p38 mitogen-activated protein kinase in glucose transport in 3T3-L1 adipocytes.

Kayali AG, Austin DA, Webster NJ. Kayali AG, et al. Among authors: webster nj. Diabetes. 2000 Nov;49(11):1783-93. doi: 10.2337/diabetes.49.11.1783. Diabetes. 2000. PMID: 11078444

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