Dok1 mediates high-fat diet–induced adipocyte hypertrophy and obesity through modulation of PPAR-γ phosphorylation
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Masato Kasuga | Yasushi Matsuki | Wataru Ogawa | Hiroshi Sakaue | Y. Matsuki | R. Hiramatsu | M. Kasuga | M. Lazar | W. Ogawa | Takehiro Nakamura | K. Kotani | H. Sakaue | Y. Yamanashi | H. Inoue | Hiroshi Inoue | Ryuji Hiramatsu | Ko Kotani | Mashito Sakai | T. Yasuda | Mitchell A Lazar | Yuji Yamanashi | Tomoharu Yasuda | Tetsuya Hosooka | Tetsuya Noguchi | Takehiro Nakamura | Kazutoshi Tobimatsu | Kazuo Takazawa | Mashito Sakai | T. Hosooka | T. Noguchi | Kazuo Takazawa | K. Tobimatsu | Yasushi Matsuki
[1] M. Kasuga,et al. Inhibition of the Motility and Growth of B16F10 Mouse Melanoma Cells by Dominant Negative Mutants of Dok-1 , 2001, Molecular and Cellular Biology.
[2] A. Hevener,et al. Deletion of Gab1 in the liver leads to enhanced glucose tolerance and improved hepatic insulin action , 2005, Nature Medicine.
[3] C. Kahn,et al. Adipose tissue selective insulin receptor knockout protects against obesity and obesity-related glucose intolerance. , 2002, Developmental cell.
[4] S. Tafuri,et al. Regulation of Peroxisome Proliferator-activated Receptor γ Activity by Mitogen-activated Protein Kinase* , 1997, The Journal of Biological Chemistry.
[5] D. Baltimore,et al. Role of the rasGAP-associated docking protein p62(dok) in negative regulation of B cell receptor-mediated signaling. , 2000, Genes & development.
[6] Y. Nakaya,et al. Increased insulin sensitivity and hypoinsulinemia in APS knockout mice. , 2003, Diabetes.
[7] B. Spiegelman,et al. Molecular regulation of adipogenesis. , 2000, Annual review of cell and developmental biology.
[8] M. Kasuga,et al. Tyrosine phosphorylation of p62Dok induced by cell adhesion and insulin: possible role in cell migration , 1999, EMBO Journal.
[9] D. Baltimore,et al. Identification of the Abl- and rasGAP-Associated 62 kDa Protein as a Docking Protein, Dok , 1997, Cell.
[10] J. Auwerx,et al. Peroxisome proliferator‐activated receptor‐γ: too much of a good thing causes harm , 2004 .
[11] R. Kesterson,et al. Deletion of PPARγ in adipose tissues of mice protects against high fat diet-induced obesity and insulin resistance , 2005, Proceedings of the National Academy of Sciences of the United States of America.
[12] K. Kaestner,et al. Genetic Modulation of PPARγ Phosphorylation Regulates Insulin Sensitivity , 2003 .
[13] M. White. Insulin Signaling in Health and Disease , 2003, Science.
[14] Bruce M. Spiegelman,et al. Inhibition of Adipogenesis Through MAP Kinase-Mediated Phosphorylation of PPARγ , 1996, Science.
[15] Fenglin Liu,et al. Insulin Receptor-mediated p62dok Tyrosine Phosphorylation at Residues 362 and 398 Plays Distinct Roles for Binding GTPase-activating Protein and Nck and Is Essential for Inhibiting Insulin-stimulated Activation of Ras and Akt* , 2001, The Journal of Biological Chemistry.
[16] 窪田 直人. PPAR γ mediates high-fat diet-induced adipocyte hypertrophy and insulin resistance , 2001 .
[17] Y. Iwakura,et al. Dok-1 and Dok-2 are negative regulators of lipopolysaccharide-induced signaling , 2005, The Journal of experimental medicine.
[18] Satoshi Tanaka,et al. PPARγ Mediates High-Fat Diet–Induced Adipocyte Hypertrophy and Insulin Resistance , 1999 .
[19] 野口 哲也. Tyrosine phosphorylation of p62Dok induced by cell adhesion and insulin : Possible role in cell migration , 2002 .
[20] M. Kasuga,et al. Characterization of a 60-kilodalton substrate of the insulin receptor kinase. , 1994, The Journal of biological chemistry.
[21] P. Pandolfi,et al. P62dok, a Negative Regulator of Ras and Mitogen-Activated Protein Kinase (Mapk) Activity, Opposes Leukemogenesis by P210bcr-abl , 2001, The Journal of experimental medicine.
[22] R. Kobayashi,et al. p62 dok : A Constitutively Tyrosine-Phosphorylated, GAP-Associated Protein in Chronic Myelogenous Leukemia Progenitor Cells , 1997, Cell.
[23] M. Lazar,et al. Transcriptional Activation by Peroxisome Proliferator-activated Receptor γ Is Inhibited by Phosphorylation at a Consensus Mitogen-activated Protein Kinase Site* , 1997, The Journal of Biological Chemistry.
[24] W. Wahli,et al. Transcriptional regulation of metabolism. , 2006, Physiological reviews.
[25] R. Evans,et al. Improved insulin-sensitivity in mice heterozygous for PPAR-γ deficiency , 2000 .
[26] J. Auwerx,et al. Compensation by the muscle limits the metabolic consequences of lipodystrophy in PPARγ hypomorphic mice , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[27] M. Lazar,et al. Interdomain communication regulating ligand binding by PPAR-gamma. , 1998, Nature.
[28] M. Goalstone,et al. Hyperinsulinemia potentiates activation of p21Ras by growth factors. , 1997, Endocrinology.
[29] J. Auwerx,et al. Peroxisome proliferator-activated receptor-gamma: too much of a good thing causes harm. , 2004, EMBO reports.
[30] M. White,et al. Disruption of the SH2-B Gene Causes Age-Dependent Insulin Resistance and Glucose Intolerance , 2004, Molecular and Cellular Biology.
[31] C. M. Adams,et al. Interactions between Subunits of the Human Epithelial Sodium Channel* , 1997, The Journal of Biological Chemistry.
[32] M. Lazar,et al. Interdomain communication regulating ligand binding by PPAR-γ , 1998, Nature.
[33] Weimin He,et al. Adipose-specific peroxisome proliferator-activated receptor γ knockout causes insulin resistance in fat and liver but not in muscle , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[34] Y. Matsuki,et al. Skp2 Controls Adipocyte Proliferation during the Development of Obesity* , 2007, Journal of Biological Chemistry.
[35] P. Withers,et al. c-Cbl-deficient mice have reduced adiposity, higher energy expenditure, and improved peripheral insulin action. , 2004, The Journal of clinical investigation.