DOI: 10.1210/endo.141.6.7516. Persistent Activation of Phosphatidylinositol 3-Kinase Causes Insulin Resistance Due to Accelerated Insulin-Induced Insulin Receptor Substrate-1 Degradation in 3T3-L1 Adipocytes*

Persistent Activation of Phosphatidylinositol 3-Kinase Causes Insulin Resistance Due to Accelerated Insulin-Induced Insulin Receptor Substrate-1 Degradation in 3T3-L1 Adipocytes*

10.1210/endo.141.6.7516

Crossref journal-article

The Endocrine Society

Endocrinology (80)

Bibliography

Egawa, K., Nakashima, N., Sharma, P. M., Maegawa, H., Nagai, Y., Kashiwagi, A., Kikkawa, R., & Olefsky, J. M. (2000). Persistent Activation of Phosphatidylinositol 3-Kinase Causes Insulin Resistance Due to Accelerated Insulin-Induced Insulin Receptor Substrate-1 Degradation in 3T3-L1 Adipocytes*. Endocrinology, 141(6), 1930â1935.

Authors 8

Katsuya Egawa (first)
Naoki Nakashima (additional)
Prem M. Sharma (additional)
Hiroshi Maegawa (additional)
Yoshio Nagai (additional)
Atsunori Kashiwagi (additional)
Ryuichi Kikkawa (additional)
Jerrold M. Olefsky (additional)

References 21 Referenced 44

10.1074/jbc.272.34.21403 / J Biol Chem / A novel 160-kDa phosphotyrosine protein in insulin-treated embryonic kidney cells is a new member of the insulin receptor substrate family. by Lavan (1997)
10.1074/jbc.272.17.11439 / J Biol Chem / The 60-kDa phosphotyrosine protein in insulin-treated adipocytes is a new member of the insulin receptor substrate family. by Lavan (1997)
10.1016/S0021-9258(17)42297-6 / J Biol Chem / The insulin signaling system. by White (1994)
10.1128/MCB.14.11.7466 / Mol Cell Biol / Microinjection of the SH2 domain of the 85-kilodalton subunit of phosphatidylinositol 3-kinase inhibits insulin-induced DNA synthesis and c-fos expression. by Jhun (1994)
10.1073/pnas.91.2.797 / Proc Natl Acad Sci USA / Insulin receptor substrate 1 is required for insulin-mediated mitogenic signal transduction. by Rose (1994)
10.1074/jbc.274.20.14306 / J Biol Chem / Membrane-targeted phosphatidylinositol 3-kinase mimics insulin actions and induces a state of cellular insulin resistance. by Egawa (1999)
10.1016/S0021-9258(17)32042-2 / J Biol Chem / The phosphatidylinositol 3-kinase serine kinase phosphorylates IRS-1. by Lam (1994)
10.1126/science.271.5249.665 / Science / IRS-1-mediated inhibition of insulin receptor tyrosine kinase activity in TNF-alpha- and obesity-induced insulin resistance. by Hotamisligil (1996)
10.1128/MCB.17.12.7386 / Mol Cell Biol / Adenovirus-mediated overexpression of IRS-1 interacting domains abolishes insulin-stimulated mitogenesis without affecting glucose transport in 3T3–L1 adipocytes. by Sharma (1997)
{'key': '2019041121252576400_R10', 'first-page': '187', 'article-title': 'Helper-free adenovirus type- 5 vectors', 'author': 'Gluzman', 'year': '1982', 'journal-title': 'In: Gluzman Y (ed) Eucaryotic Viral Vectors. Cold Spring Harbor Laboratory, Cold Spring Harbor, NY, pp'} / In: Gluzman Y (ed) Eucaryotic Viral Vectors. Cold Spring Harbor Laboratory, Cold Spring Harbor, NY, pp / Helper-free adenovirus type- 5 vectors by Gluzman (1982)
10.1016/0042-6822(88)90302-9 / Virology / A simple technique for the rescue of early region I mutations into infectious human adenovirus type 5. by McGrory (1988)
10.1073/pnas.87.4.1411 / Proc Natl Acad Sci USA / Activation of phosphatidylinositol 3-kinase by insulin. by Ruderman (1990)
10.1016/0303-7207(96)03875-0 / Mol Cell Endocrinol / The insulin-induced down-regulation of IRS-1 in 3T3–L1 adipocytes is mediated by a calcium-dependent thiol protease. by Smith (1996)
10.1021/bi971157f / Biochemistry / Protein kinase C modulation of insulin receptor substrate-1 tyrosine phosphorylation requires serine 612. by DeFea (1997)
10.1074/jbc.272.50.31400 / J Biol Chem / Modulation of insulin receptor substrate-1 tyrosine phosphorylation and function by mitogen-activated protein kinase. by DeFea (1997)
10.1006/bbrc.1993.1143 / Biochem Biophys Res Commun / Insulin stimulates the degradation of IRS-1 in 3T3–L1 adipocytes. by Rice (1993)
10.1074/jbc.271.30.17605 / J Biol Chem / Activated phosphatidylinositol 3-kinase is sufficient to mediate actin rearrangement and GLUT4 translocation in 3T3–L1 adipocytes. by Martin (1996)
10.1128/MCB.17.1.190 / Mol Cell Biol / Differential effects of constitutively active phosphatidylinositol 3-kinase on glucose transport, glycogen synthase activity, and DNA synthesis in 3T3–L1 adipocytes. by Frevert (1997)
10.1006/bbrc.1993.1936 / Biochem Biophys Res Commun / The PKC-inhibitor RO 31–8220 selectively suppresses PMA- and diacylglycerol-induced fluid pinocytosis and actin polymerization in PMNs. by Keller (1993)
10.1042/bj3240981 / Biochem J / Increased flux through the hexosamine biosynthesis pathway inhibits glucose transport acutely by activation of protein kinase C. by Filippis (1977)
10.1006/bbrc.1999.1734 / Biochem Biophys Res Commun / Differential regulation of immediate early gene expression in preadipocyte cells through multiple signaling pathways. by Inuzuka (1999)

Dates

Type	When
Created	11 years, 7 months ago (Jan. 8, 2014, 11:11 a.m.)
Deposited	3 years, 5 months ago (March 21, 2022, 7:15 p.m.)
Indexed	1 year, 1 month ago (July 3, 2024, 9:58 a.m.)
Issued	25 years, 3 months ago (June 1, 2000)
Published	25 years, 3 months ago (June 1, 2000)
Published Print	25 years, 3 months ago (June 1, 2000)

Funders 0

None

BibTeX

@article{Egawa_2000, title={Persistent Activation of Phosphatidylinositol 3-Kinase Causes Insulin Resistance Due to Accelerated Insulin-Induced Insulin Receptor Substrate-1 Degradation in 3T3-L1 Adipocytes*}, volume={141}, ISSN={1945-7170}, url={http://dx.doi.org/10.1210/endo.141.6.7516}, DOI={10.1210/endo.141.6.7516}, number={6}, journal={Endocrinology}, publisher={The Endocrine Society}, author={Egawa, Katsuya and Nakashima, Naoki and Sharma, Prem M. and Maegawa, Hiroshi and Nagai, Yoshio and Kashiwagi, Atsunori and Kikkawa, Ryuichi and Olefsky, Jerrold M.}, year={2000}, month=jun, pages={1930–1935} }

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