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Genomes and Genes | Min ChenSummaryAffiliation: National Institutes of Health Country: USA Publications
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Publications
Absence of the glucagon-like peptide-1 receptor does not affect the metabolic phenotype of mice with liver-specific G(s)? deficiencyMin 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....- G(s)alpha deficiency in skeletal muscle leads to reduced muscle mass, fiber-type switching, and glucose intolerance without insulin resistance or deficiencyMin 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... - Central nervous system imprinting of the G protein G(s)alpha and its role in metabolic regulationMin 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.... - G(s)alpha deficiency in adipose tissue leads to a lean phenotype with divergent effects on cold tolerance and diet-induced thermogenesisMin 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... - Effects of deficiency of the G protein Gs? on energy and glucose homeostasisMin 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.... - Severe obesity and insulin resistance due to deletion of the maternal Gsalpha allele is reversed by paternal deletion of the Gsalpha imprint control regionTao 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.... - Alternative Gnas gene products have opposite effects on glucose and lipid metabolismMin 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... - Increased glucose tolerance and reduced adiposity in the absence of fasting hypoglycemia in mice with liver-specific Gs alpha deficiencyMin 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... - Pancreas-specific Gsalpha deficiency has divergent effects on pancreatic alpha- and beta-cell proliferationTao 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... - Renal failure in mice with Gsalpha deletion in juxtaglomerular cellsLimeng 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... - Increased insulin sensitivity in paternal Gnas knockout mice is associated with increased lipid clearanceMin 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... - Impaired glucose tolerance in the absence of adenosine A1 receptor signalingRobert 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... - Skeletal abnormalities and extra-skeletal ossification in mice with restricted Gsalpha deletion caused by a renin promoter-Cre transgeneHayo 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... - Deficiency of the G-protein alpha-subunit G(s)alpha in osteoblasts leads to differential effects on trabecular and cortical boneAkio 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... - Stimulation of renin secretion by angiotensin II blockade is Gsalpha-dependentLimeng 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.... - Genetic background (C57BL/6J versus FVB/N) strongly influences the severity of diabetes and insulin resistance in ob/ob miceMartin 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.... - Identification of the control region for tissue-specific imprinting of the stimulatory G protein alpha-subunitJie 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... - Beta cell-specific deficiency of the stimulatory G protein alpha-subunit Gsalpha leads to reduced beta cell mass and insulin-deficient diabetesTao 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... - Studies of the regulation and function of the Gs alpha gene Gnas using gene targeting technologyLee 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... - Chondrocyte-specific knockout of the G protein G(s)alpha leads to epiphyseal and growth plate abnormalities and ectopic chondrocyte formationAkio 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... - Minireview: GNAS: normal and abnormal functionsLee 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... - Regulation of renin in mice with Cre recombinase-mediated deletion of G protein Gsalpha in juxtaglomerular cellsLimeng 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... - Tissue-specific imprinting of the G protein Gsalpha is associated with tissue-specific differences in histone methylationAkio 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.... - Genetic diseases associated with heterotrimeric G proteinsLee 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... - Phase I trial of 17-dimethylaminoethylamino-17-demethoxygeldanamycin (17-DMAG), a heat shock protein inhibitor, administered twice weekly in patients with advanced malignanciesShivaani Kummar
Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA
Eur J Cancer 46:340-7. 2010.... - Wnt/?-catenin signaling is differentially regulated by G? proteins and contributes to fibrous dysplasiaJean 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 G? proteins are playing physiologically significant roles during both skeletal development and disease by modulating Wnt/?-catenin signaling strength... - Gs(alpha) mutations and imprinting defects in human diseaseLee 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...