Genomes and Genes
Mehboob A Hussain
Affiliation: Johns Hopkins University
- Brn-4 transcription factor expression targeted to the early developing mouse pancreas induces ectopic glucagon gene expression in insulin-producing beta cellsMehboob A Hussain
Laboratory of Molecular Endocrinology, Massachusetts General Hospital, Howard Hughes Medical Institute, Harvard Medical School, Boston, Massachusetts 02114, USA gt
J Biol Chem 277:16028-32. 2002..The early developmental expression of Brn-4 appears to be a dominant regulator of the glucagon expressing alpha cell lineage, even in the context of the beta cell lineage...
- Increased pancreatic beta-cell proliferation mediated by CREB binding protein gene activationMehboob A Hussain
Metabolism Division, Department of Pediatrics and Medicine, Johns Hopkins University, 600 N Wolfe Street, CMSC 10 113, Baltimore, MD 21287, USA
Mol Cell Biol 26:7747-59. 2006..In these beta cells, however, glucose-stimulated insulin secretion was diminished, resulting from concomitant CREB-CBP-mediated pgc1a gene activation...
- Exendin-4 stimulation of cyclin A2 in beta-cell proliferationWoo Jin Song
Metabolism Division, Departments of Pediatrics and Medicine, Johns Hopkins University, Baltimore, Maryland, USA
Diabetes 57:2371-81. 2008..We have examined effects, in particular those mediated through intracellular cAMP signaling, of the incretin hormone analog exendin-4 on cell cycle regulation in beta-cells...
- There is Kisspeptin - And Then There is KisspeptinMehboob A Hussain
Divisions of Metabolism and Pediatric Endocrinology, Departments of Medicine, Pediatrics, Biological Chemistry and Physiology, Johns Hopkins University, Baltimore, MD, USA Electronic address
Trends Endocrinol Metab 26:564-72. 2015..This review highlights these recent observations on the role of kisspeptin in metabolism as well as several key questions that need to be addressed in the future. ..
- Prkar1a in the regulation of insulin secretionM A Hussain
Department of Pediatrics, Medicine and Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
Horm Metab Res 44:759-65. 2012....
- Tsc2 is a molecular checkpoint controlling osteoblast development and glucose homeostasisRyan C Riddle
Department of Orthopaedic Surgery, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
Mol Cell Biol 34:1850-62. 2014..Together, these findings suggest that Tsc2 serves as a key checkpoint in the osteoblast that is required for proper insulin signaling and acts to ensure normal bone acquisition and energy homeostasis. ..
- Pancreatic β-cell response to increased metabolic demand and to pharmacologic secretagogues requires EPAC2AWoo Jin Song
Department of Pediatrics, Johns Hopkins University, Baltimore, Maryland, USA
Diabetes 62:2796-807. 2013..Our findings advance the rationale for developing EPAC2A-selective pharmacologic activators for β-cell-targeted pharmacotherapy in type 2 diabetes. ..
- Glucagon regulates hepatic kisspeptin to impair insulin secretionWoo Jin Song
Metabolism Division, Johns Hopkins University, CMSC Building 10 113, Baltimore, MD, 21287, USA Diabetes Institute, Johns Hopkins University, CMSC Building 10 113, Baltimore, MD, 21287, USA Department of Pediatrics, Johns Hopkins University, CMSC Building 10 113, Baltimore, MD, 21287, USA
Cell Metab 19:667-81. 2014..These observations indicate a hormonal circuit between the liver and the endocrine pancreas in glycemia regulation and suggest in T2DM a sequential link between hyperglucagonemia via hepatic kisspeptin1 to impaired insulin secretion...
- Snapin mediates incretin action and augments glucose-dependent insulin secretionWoo Jin Song
Department of Pediatrics, Metabolism Division, Johns Hopkins University, Baltimore, MD 21287, USA
Cell Metab 13:308-19. 2011..Thus, snapin is a critical node in GSIS regulation and provides a potential therapeutic target to improve β cell function in T2DM...
- Short telomeres compromise β-cell signaling and survivalNini Guo
Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America
PLoS ONE 6:e17858. 2011..They implicate telomere length as a determinant of β-cell function and diabetes pathogenesis...
- Metformin and insulin suppress hepatic gluconeogenesis through phosphorylation of CREB binding proteinLing He
Division of Metabolism, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
Cell 137:635-46. 2009..Our findings point to CBP phosphorylation at Ser436 by metformin as critical for its therapeutic effect, and as a potential target for pharmaceutical intervention...
- Increasing β-cell mass requires additional stimulation for adaptation to secretory demandProsenjit Mondal
Departments of Medicine M A H, Pediatrics P M, W J S, Y L, K S Y, M A H, and Biological Chemistry M A H, Johns Hopkins University, Baltimore, Maryland 21287
Mol Endocrinol 29:108-20. 2015..These observations indicate that increasing endogenous β-cell mass may not be sufficient to improve glycemic control in T2DM without additional strategies to increase β-cell stimulus secretion coupling. ..
- The dynamin-related GTPase Opa1 is required for glucose-stimulated ATP production in pancreatic beta cellsZhongyan Zhang
Department of Cell Biology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Mol Biol Cell 22:2235-45. 2011..Consequently, mice lacking Opa1 in beta cells develop hyperglycemia. The data suggest that the function of Opa1 in the maintenance of the electron transport chain is physiologically relevant in beta cells...
- Developmental and endocrine regulation of kisspeptin expression in mouse Leydig cellsSajad Salehi
Divisions of Endocrinology S S, i A, A W, S R and Metabolism B A H, F W, Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287 and Department of Biochemistry and Molecular Biology H C, B R Z, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland 21205
Endocrinology 156:1514-22. 2015..These data document kisspeptin expression in mouse Leydig cells, its secretion into peripheral serum, and its regulation by changes in reproductive neuroendocrine function. ..
- Glucose and weight control in mice with a designed ghrelin O-acyltransferase inhibitorBrad P Barnett
Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Science 330:1689-92. 2010..In addition to serving as a research tool for mapping ghrelin actions, GO-CoA-Tat may help pave the way for clinical targeting of GOAT in metabolic diseases...
- Insulin receptor signaling in osteoblasts regulates postnatal bone acquisition and body compositionKeertik Fulzele
Department of Orthopaedic Surgery, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Cell 142:309-19. 2010....
- The use of animal models to study stem cell therapies for diabetes mellitusWoo Jin Song
Metabolism Division, Department of Pediatrics, Johns Hopkins University, Baltimore, MD 21287, USA
ILAR J 51:74-81. 2009..Although there has been much progress in this area, further research is needed to enhance understanding and improve therapeutic strategies for this widespread disease...
- Exendin-4 as a stimulator of rat insulin I gene promoter activity via bZIP/CRE interactions sensitive to serine/threonine protein kinase inhibitor Ro 31-8220Oleg G Chepurny
Department of Physiology, New York University School of Medicine, New York, New York 10016, USA
Endocrinology 143:2303-13. 2002..It is concluded that the bZIP and CRE-mediated stimulation of RIP1 by Ex-4 explains, at least in part, how this insulinotropic hormone facilitates transcriptional activity of the rat insulin I gene...
- Endocrine pancreatic cell regeneration from bone marrowMehboob A Hussain; Fiscal Year: 2010..4) To identify the cell type within BM that contributes to the pancreatic endocrine cell population. The long-term goal of these studies is to evaluate transplantation of BM derived cells as a potential treatment for diabetes mellitus. ..