Functional in vivo interactions between JNK1 and JNK2 isoforms in obesity and insulin resistance.
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[1] M. Karin,et al. The E3 Ubiquitin Ligase Itch Couples JNK Activation to TNFα-induced Cell Death by Inducing c-FLIPL Turnover , 2006, Cell.
[2] G. Hotamisligil. Role of endoplasmic reticulum stress and c-Jun NH2-terminal kinase pathways in inflammation and origin of obesity and diabetes. , 2005, Diabetes.
[3] B. Dahiyat,et al. JNK and Tumor Necrosis Factor-α Mediate Free Fatty Acid-induced Insulin Resistance in 3T3-L1 Adipocytes* , 2005, Journal of Biological Chemistry.
[4] D. Neuberg,et al. Disruption of the Jnk2 (Mapk9) gene reduces destructive insulitis and diabetes in a mouse model of type I diabetes. , 2005, Proceedings of the National Academy of Sciences of the United States of America.
[5] K. Wellen,et al. Inflammation, stress, and diabetes. , 2005, The Journal of clinical investigation.
[6] M. Karin,et al. From JNK to Pay Dirt: Jun Kinases, their Biochemistry, Physiology and Clinical Importance , 2005, IUBMB life.
[7] Y. Minemoto,et al. c-Jun N-Terminal Protein Kinase 1 (JNK1), but Not JNK2, Is Essential for Tumor Necrosis Factor Alpha-Induced c-Jun Kinase Activation and Apoptosis , 2004, Molecular and Cellular Biology.
[8] R. Flavell,et al. JNK potentiates TNF-stimulated necrosis by increasing the production of cytotoxic reactive oxygen species. , 2004, Genes & development.
[9] G. Sumara,et al. Requirement of JNK2 for Scavenger Receptor A-Mediated Foam Cell Formation in Atherogenesis , 2004, Science.
[10] L. Glimcher,et al. Endoplasmic Reticulum Stress Links Obesity, Insulin Action, and Type 2 Diabetes , 2004, Science.
[11] M. Karin,et al. Jun Turnover Is Controlled Through JNK-Dependent Phosphorylation of the E3 Ligase Itch , 2004, Science.
[12] H. Kaneto,et al. Possible novel therapy for diabetes with cell-permeable JNK-inhibitory peptide , 2004, Nature Medicine.
[13] E. Wagner,et al. Distinct roles for JNK1 and JNK2 in regulating JNK activity and c-Jun-dependent cell proliferation. , 2004, Molecular cell.
[14] Michael Karin,et al. A central role for JNK in obesity and insulin resistance , 2002, Nature.
[15] E. Van Obberghen,et al. SOCS-3 Inhibits Insulin Signaling and Is Up-regulated in Response to Tumor Necrosis Factor-α in the Adipose Tissue of Obese Mice* , 2001, The Journal of Biological Chemistry.
[16] Michael Karin,et al. Reversal of Obesity- and Diet-Induced Insulin Resistance with Salicylates or Targeted Disruption of Ikkβ , 2001, Science.
[17] E. Wagner,et al. C-Jun Nh2-Terminal Kinase (Jnk)1 and Jnk2 Have Similar and Stage-Dependent Roles in Regulating T Cell Apoptosis and Proliferation , 2001, The Journal of experimental medicine.
[18] R. Davis,et al. Signal Transduction by the JNK Group of MAP Kinases , 2000, Cell.
[19] Roger Davis,et al. The c-Jun NH2-terminal Kinase Promotes Insulin Resistance during Association with Insulin Receptor Substrate-1 and Phosphorylation of Ser307 * , 2000, The Journal of Biological Chemistry.
[20] G. Shulman,et al. On Diabetes: Insulin Resistance Cellular Mechanisms of Insulin Resistance , 2022 .
[21] E. Wagner,et al. JNK2 is required for efficient T-cell activation and apoptosis but not for normal lymphocyte development , 1999, Current Biology.
[22] R. Flavell,et al. Defective T cell differentiation in the absence of Jnk1. , 1998, Science.
[23] R. Flavell,et al. Differentiation of CD4+ T cells to Th1 cells requires MAP kinase JNK2. , 1998, Immunity.
[24] K. Uysal,et al. Protection from obesity-induced insulin resistance in mice lacking TNF-α function , 1997, Nature.
[25] Margaret S. Wu,et al. Targeted Disruption of the Tumor Necrosis Factor-α Gene: Metabolic Consequences in Obese and Nonobese Mice , 1997, Diabetes.
[26] G. Boden. Role of Fatty Acids in the Pathogenesis of Insulin Resistance and NIDDM , 1997, Diabetes.
[27] B. Spiegelman,et al. IRS-1-Mediated Inhibition of Insulin Receptor Tyrosine Kinase Activity in TNF-α- and Obesity-Induced Insulin Resistance , 1996, Science.
[28] M. Papa,et al. Tumor necrosis factor alpha-induced phosphorylation of insulin receptor substrate-1 (IRS-1). Possible mechanism for suppression of insulin-stimulated tyrosine phosphorylation of IRS-1. , 1995, The Journal of biological chemistry.
[29] M. Karin. The Regulation of AP-1 Activity by Mitogen-activated Protein Kinases (*) , 1995, The Journal of Biological Chemistry.
[30] M. Karin,et al. Identification of an oncoprotein- and UV-responsive protein kinase that binds and potentiates the c-Jun activation domain. , 1993, Genes & development.
[31] B. Spiegelman,et al. Adipose expression of tumor necrosis factor-alpha: direct role in obesity-linked insulin resistance. , 1993, Science.