Mehboob A Hussain

Summary

Affiliation: Johns Hopkins University
Country: USA

Publications

  1. ncbi request reprint Brn-4 transcription factor expression targeted to the early developing mouse pancreas induces ectopic glucagon gene expression in insulin-producing beta cells
    Mehboob 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
  2. pmc Increased pancreatic beta-cell proliferation mediated by CREB binding protein gene activation
    Mehboob 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
  3. pmc Exendin-4 stimulation of cyclin A2 in beta-cell proliferation
    Woo Jin Song
    Metabolism Division, Departments of Pediatrics and Medicine, Johns Hopkins University, Baltimore, Maryland, USA
    Diabetes 57:2371-81. 2008
  4. pmc Prkar1a in the regulation of insulin secretion
    M 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
  5. pmc Tsc2 is a molecular checkpoint controlling osteoblast development and glucose homeostasis
    Ryan C Riddle
    Department of Orthopaedic Surgery, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Mol Cell Biol 34:1850-62. 2014
  6. pmc Pancreatic β-cell response to increased metabolic demand and to pharmacologic secretagogues requires EPAC2A
    Woo Jin Song
    Department of Pediatrics, Johns Hopkins University, Baltimore, Maryland, USA
    Diabetes 62:2796-807. 2013
  7. pmc Snapin mediates incretin action and augments glucose-dependent insulin secretion
    Woo Jin Song
    Department of Pediatrics, Metabolism Division, Johns Hopkins University, Baltimore, MD 21287, USA
    Cell Metab 13:308-19. 2011
  8. pmc Short telomeres compromise β-cell signaling and survival
    Nini Guo
    Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America
    PLoS ONE 6:e17858. 2011
  9. pmc Metformin and insulin suppress hepatic gluconeogenesis through phosphorylation of CREB binding protein
    Ling He
    Division of Metabolism, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Cell 137:635-46. 2009
  10. pmc Increasing β-cell mass requires additional stimulation for adaptation to secretory demand
    Prosenjit 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

Research Grants

Collaborators

Detail Information

Publications17

  1. ncbi request reprint Brn-4 transcription factor expression targeted to the early developing mouse pancreas induces ectopic glucagon gene expression in insulin-producing beta cells
    Mehboob 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...
  2. pmc Increased pancreatic beta-cell proliferation mediated by CREB binding protein gene activation
    Mehboob 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...
  3. pmc Exendin-4 stimulation of cyclin A2 in beta-cell proliferation
    Woo 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...
  4. pmc Prkar1a in the regulation of insulin secretion
    M 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
    ....
  5. pmc Tsc2 is a molecular checkpoint controlling osteoblast development and glucose homeostasis
    Ryan 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. ..
  6. pmc Pancreatic β-cell response to increased metabolic demand and to pharmacologic secretagogues requires EPAC2A
    Woo 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. ..
  7. pmc Snapin mediates incretin action and augments glucose-dependent insulin secretion
    Woo 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...
  8. pmc Short telomeres compromise β-cell signaling and survival
    Nini 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...
  9. pmc Metformin and insulin suppress hepatic gluconeogenesis through phosphorylation of CREB binding protein
    Ling 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...
  10. pmc Increasing β-cell mass requires additional stimulation for adaptation to secretory demand
    Prosenjit 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. ..
  11. pmc The dynamin-related GTPase Opa1 is required for glucose-stimulated ATP production in pancreatic beta cells
    Zhongyan 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...
  12. pmc Glucose and weight control in mice with a designed ghrelin O-acyltransferase inhibitor
    Brad 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...
  13. pmc Insulin receptor signaling in osteoblasts regulates postnatal bone acquisition and body composition
    Keertik Fulzele
    Department of Orthopaedic Surgery, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Cell 142:309-19. 2010
    ....
  14. doi request reprint Developmental and endocrine regulation of kisspeptin expression in mouse leydig cells
    Sajad 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. ..
  15. pmc Glucagon regulates hepatic kisspeptin to impair insulin secretion
    Woo 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...
  16. ncbi request reprint The use of animal models to study stem cell therapies for diabetes mellitus
    Woo 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...
  17. pmc Exendin-4 as a stimulator of rat insulin I gene promoter activity via bZIP/CRE interactions sensitive to serine/threonine protein kinase inhibitor Ro 31-8220
    Oleg 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...

Research Grants1

  1. Endocrine pancreatic cell regeneration from bone marrow
    Mehboob 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. ..