Min Chen

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. pmc Absence of the glucagon-like peptide-1 receptor does not affect the metabolic phenotype of mice with liver-specific G(s)α deficiency
    Min Chen
    Metabolic Diseases Branch, Building 10 Room 8C101, National Institute for Diabetes, Digestive, and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 1752, USA
    Endocrinology 152:3343-50. 2011
  2. pmc Central nervous system imprinting of the G protein G(s)alpha and its role in metabolic regulation
    Min Chen
    Signal Transduction Section, Metabolic Diseases Branch, National Institute of Diabetes, Digestive, and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Cell Metab 9:548-55. 2009
  3. pmc G(s)alpha deficiency in skeletal muscle leads to reduced muscle mass, fiber-type switching, and glucose intolerance without insulin resistance or deficiency
    Min Chen
    Metabolic Diseases Branch, National Institute of Diabetes, Digestive, and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 1752, USA
    Am J Physiol Cell Physiol 296:C930-40. 2009
  4. pmc G(s)alpha deficiency in adipose tissue leads to a lean phenotype with divergent effects on cold tolerance and diet-induced thermogenesis
    Min Chen
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Cell Metab 11:320-30. 2010
  5. pmc Effects of deficiency of the G protein Gsα on energy and glucose homeostasis
    Min Chen
    Signal Transduction Section, National Institute of Diabetes and Digestive, and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Eur J Pharmacol 660:119-24. 2011
  6. pmc Severe obesity and insulin resistance due to deletion of the maternal Gsalpha allele is reversed by paternal deletion of the Gsalpha imprint control region
    Tao Xie
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases National Institutes of Health, Building 10, Room 8C101, Bethesda, Maryland 20892 1752, USA
    Endocrinology 149:2443-50. 2008
  7. pmc Alternative Gnas gene products have opposite effects on glucose and lipid metabolism
    Min Chen
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 102:7386-91. 2005
  8. pmc Increased glucose tolerance and reduced adiposity in the absence of fasting hypoglycemia in mice with liver-specific Gs alpha deficiency
    Min Chen
    Metabolic Diseases Branch, NIDDK, NIH, Bethesda, Maryland 20892 1752, USA
    J Clin Invest 115:3217-27. 2005
  9. ncbi request reprint Increased insulin sensitivity in paternal Gnas knockout mice is associated with increased lipid clearance
    Min Chen
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases National Institutes of Health, Building 10, Room 8C101, Bethesda, Maryland 20892 1752, USA
    Endocrinology 145:4094-102. 2004
  10. pmc Renal failure in mice with Gsalpha deletion in juxtaglomerular cells
    Limeng Chen
    National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD, USA
    Am J Nephrol 32:83-94. 2010

Detail Information

Publications30

  1. pmc Absence of the glucagon-like peptide-1 receptor does not affect the metabolic phenotype of mice with liver-specific G(s)α deficiency
    Min Chen
    Metabolic Diseases Branch, Building 10 Room 8C101, National Institute for Diabetes, Digestive, and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 1752, USA
    Endocrinology 152:3343-50. 2011
    ....
  2. pmc Central nervous system imprinting of the G protein G(s)alpha and its role in metabolic regulation
    Min Chen
    Signal Transduction Section, Metabolic Diseases Branch, National Institute of Diabetes, Digestive, and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Cell Metab 9:548-55. 2009
    ....
  3. pmc G(s)alpha deficiency in skeletal muscle leads to reduced muscle mass, fiber-type switching, and glucose intolerance without insulin resistance or deficiency
    Min Chen
    Metabolic Diseases Branch, National Institute of Diabetes, Digestive, and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 1752, USA
    Am J Physiol Cell Physiol 296:C930-40. 2009
    ..MGsKO mice are a valuable model for future studies of the role of G(s)alpha signaling pathways in skeletal muscle adaptation and their effects on whole body metabolism...
  4. pmc G(s)alpha deficiency in adipose tissue leads to a lean phenotype with divergent effects on cold tolerance and diet-induced thermogenesis
    Min Chen
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Cell Metab 11:320-30. 2010
    ..In normal mice, high-fat diet raised sympathetic nerve activity in muscle, but not in BAT. Our results show that cold- and diet-induced thermogenesis may occur in separate tissues, especially when BAT function is impaired...
  5. pmc Effects of deficiency of the G protein Gsα on energy and glucose homeostasis
    Min Chen
    Signal Transduction Section, National Institute of Diabetes and Digestive, and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Eur J Pharmacol 660:119-24. 2011
    ....
  6. pmc Severe obesity and insulin resistance due to deletion of the maternal Gsalpha allele is reversed by paternal deletion of the Gsalpha imprint control region
    Tao Xie
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases National Institutes of Health, Building 10, Room 8C101, Bethesda, Maryland 20892 1752, USA
    Endocrinology 149:2443-50. 2008
    ....
  7. pmc Alternative Gnas gene products have opposite effects on glucose and lipid metabolism
    Min Chen
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 102:7386-91. 2005
    ..Differences between E1m-/+ and E1+/p- mice presumably result from differential effects on G(s)alpha expression in tissues where G(s)alpha is normally imprinted...
  8. pmc Increased glucose tolerance and reduced adiposity in the absence of fasting hypoglycemia in mice with liver-specific Gs alpha deficiency
    Min Chen
    Metabolic Diseases Branch, NIDDK, NIH, Bethesda, Maryland 20892 1752, USA
    J Clin Invest 115:3217-27. 2005
    ..Our results define novel roles for hepatic G(s)-signaling pathways in glucose and lipid regulation, which may prove useful in designing new therapeutic targets for diabetes and obesity...
  9. ncbi request reprint Increased insulin sensitivity in paternal Gnas knockout mice is associated with increased lipid clearance
    Min Chen
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases National Institutes of Health, Building 10, Room 8C101, Bethesda, Maryland 20892 1752, USA
    Endocrinology 145:4094-102. 2004
    ..Further studies will clarify whether XLalphas deficiency is responsible for these effects and if so, the mechanism by which XLalphas deficiency leads to this metabolic phenotype...
  10. pmc Renal failure in mice with Gsalpha deletion in juxtaglomerular cells
    Limeng Chen
    National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD, USA
    Am J Nephrol 32:83-94. 2010
    ..In the present study we have determined the long-term effect on renal function, blood pressure, and renal pathology in this low renin and diuretic mouse model...
  11. pmc Pancreas-specific Gsalpha deficiency has divergent effects on pancreatic alpha- and beta-cell proliferation
    Tao Xie
    Signal Transduction Section, Metabolic Diseases Branch, National Institute of Diabetes, Digestive, and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Endocrinol 206:261-9. 2010
    ..In addition, PGsKO mice show morphological changes in exocrine pancreas and evidence for malnutrition and dehydration, indicating an important role for G(s)alpha in the exocrine pancreas as well...
  12. pmc Impaired glucose tolerance in the absence of adenosine A1 receptor signaling
    Robert Faulhaber-Walter
    National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA
    Diabetes 60:2578-87. 2011
    ..The role of adenosine (ADO) in the regulation of glucose homeostasis is not clear. In the current study, we used A1-ADO receptor (A1AR)-deficient mice to investigate the role of ADO/A1AR signaling for glucose homeostasis...
  13. ncbi request reprint Deficiency of the G-protein alpha-subunit G(s)alpha in osteoblasts leads to differential effects on trabecular and cortical bone
    Akio Sakamoto
    Metabolic Diseases Branch, NIDDK, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Biol Chem 280:21369-75. 2005
    ..Osteoblast-specific G(s)alpha deficiency leads to reduced bone turnover...
  14. ncbi request reprint Skeletal abnormalities and extra-skeletal ossification in mice with restricted Gsalpha deletion caused by a renin promoter-Cre transgene
    Hayo Castrop
    National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA
    Cell Tissue Res 330:487-501. 2007
    ..Nevertheless, the present report reaffirms the importance of Gs alpha signaling for bone development and the suppression of ectopic ossification...
  15. pmc Stimulation of renin secretion by angiotensin II blockade is Gsalpha-dependent
    Limeng Chen
    National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, 9000 Rockville Pike, Building 31, Room 2B11, Bethesda, MD 20892, USA
    J Am Soc Nephrol 21:986-92. 2010
    ....
  16. ncbi request reprint Genetic background (C57BL/6J versus FVB/N) strongly influences the severity of diabetes and insulin resistance in ob/ob mice
    Martin Haluzik
    Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    Endocrinology 145:3258-64. 2004
    ....
  17. pmc Identification of the control region for tissue-specific imprinting of the stimulatory G protein alpha-subunit
    Jie Liu
    Metabolic Diseases Branch and Genetics of Development and Disease Branch, National Institute of Diabetes, Digestive, and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 102:5513-8. 2005
    ..The 1A region is a maternal imprint mark that contains one or more methylation-sensitive cis-acting elements that suppress G(s)alpha expression from the paternal allele in a tissue-specific manner...
  18. pmc Activation of Hedgehog signaling by loss of GNAS causes heterotopic ossification
    Jean B Regard
    1 National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland, USA 2
    Nat Med 19:1505-12. 2013
    ....
  19. pmc Gsα deficiency in the paraventricular nucleus of the hypothalamus partially contributes to obesity associated with Gsα mutations
    Min Chen
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases National Institutes of Health, Bethesda, Maryland 20892 1752, USA
    Endocrinology 153:4256-65. 2012
    ....
  20. pmc Beta cell-specific deficiency of the stimulatory G protein alpha-subunit Gsalpha leads to reduced beta cell mass and insulin-deficient diabetes
    Tao Xie
    Metabolic Disease Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 104:19601-6. 2007
    ..These results show that G(s)alpha/cAMP pathways are critical regulators of beta cell function and proliferation that can work through IRS2-independent mechanisms...
  21. ncbi request reprint Chondrocyte-specific knockout of the G protein G(s)alpha leads to epiphyseal and growth plate abnormalities and ectopic chondrocyte formation
    Akio Sakamoto
    Metabolic Diseases Branch, National Institute of Diabetes, Digestive, and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Bone Miner Res 20:663-71. 2005
    ..These results show that G(s)alpha negatively regulates chondrocyte differentiation and is the critical signaling mediator of the PTH/PTH-rP receptor in growth plate chondrocytes...
  22. pmc Studies of the regulation and function of the Gs alpha gene Gnas using gene targeting technology
    Lee S Weinstein
    Metabolic Diseases Branch, National Institute of Diabetes, Digestive, and Kidney Diseases, National Institutes of Health, Bethesda, MD 20854, USA
    Pharmacol Ther 115:271-91. 2007
    ..Our present knowledge gleaned from various Gnas gene targeting models are discussed in relation to the pathogenesis of human disorders with mutation or abnormal imprinting of the human orthologue GNAS...
  23. ncbi request reprint Tissue-specific imprinting of the G protein Gsalpha is associated with tissue-specific differences in histone methylation
    Akio Sakamoto
    Metabolic Diseases Branch, National Institute of Diabetes, Digestive, and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Hum Mol Genet 13:819-28. 2004
    ....
  24. ncbi request reprint Regulation of renin in mice with Cre recombinase-mediated deletion of G protein Gsalpha in juxtaglomerular cells
    Limeng Chen
    National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 1370, USA
    Am J Physiol Renal Physiol 292:F27-37. 2007
    ..We conclude that Gsalpha-mediated signal transduction is essential and nonredundant in the control of renin synthesis and release...
  25. ncbi request reprint Minireview: GNAS: normal and abnormal functions
    Lee S Weinstein
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    Endocrinology 145:5459-64. 2004
    ..Mouse knockout models show that G(s)alpha and the alternative G(s)alpha isoform XLalphas that is expressed from the paternal GNAS allele may have opposite effects on energy metabolism in mice...
  26. pmc Wnt/β-catenin signaling is differentially regulated by Gα proteins and contributes to fibrous dysplasia
    Jean B Regard
    National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 108:20101-6. 2011
    ..Our data suggest that activated Gα proteins are playing physiologically significant roles during both skeletal development and disease by modulating Wnt/β-catenin signaling strength...
  27. ncbi request reprint Genetic diseases associated with heterotrimeric G proteins
    Lee S Weinstein
    Metabolic Diseases Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Trends Pharmacol Sci 27:260-6. 2006
    ..g. hypertension and metabolic syndrome). To date, no other G proteins have been implicated directly in human disease...
  28. pmc Phase I trial of 17-dimethylaminoethylamino-17-demethoxygeldanamycin (17-DMAG), a heat shock protein inhibitor, administered twice weekly in patients with advanced malignancies
    Shivaani Kummar
    Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA
    Eur J Cancer 46:340-7. 2010
    ....
  29. ncbi request reprint Gs(alpha) mutations and imprinting defects in human disease
    Lee S Weinstein
    Metabolic Diseases Branch, National Institute of Diabetes, Digestive, and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    Ann N Y Acad Sci 968:173-97. 2002
    ..This GNAS1 imprinting defect is predicted to decrease Gs(alpha) expression in tissues where Gs(alpha) is normally imprinted and therefore to lead to renal parathyroid hormone resistance...
  30. ncbi request reprint Characterization and analysis of the proximal Janus kinase 3 promoter
    Martin Aringer
    Molecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 170:6057-64. 2003
    ..Thus, transcription factors that bind these sites, especially Ets family members, are likely to be important regulators of Jak3 expression...