L
Lynda Elghazi
Researcher at University of Michigan
Publications - 36
Citations - 3093
Lynda Elghazi is an academic researcher from University of Michigan. The author has contributed to research in topics: Insulin resistance & PI3K/AKT/mTOR pathway. The author has an hindex of 24, co-authored 34 publications receiving 2831 citations. Previous affiliations of Lynda Elghazi include St. Jude Children's Research Hospital & French Institute of Health and Medical Research.
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Journal ArticleDOI
Ghrelin cells replace insulin-producing β cells in two mouse models of pancreas development
TL;DR: It is proposed that insulin and ghrelin cells share a common progenitor and that Nkx2.2 and Pax4 are required to specify or maintain differentiation of the beta cell fate.
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Conditional gene targeting in mouse pancreatic β-cells: Analysis of ectopic Cre transgene expression in the brain
Barton Wicksteed,Marcela Brissova,Wenbo Yan,Darren M. Opland,Jennifer L. Plank,Rachel B. Reinert,Lorna M. Dickson,Natalia A. Tamarina,Louis H. Philipson,Alena Shostak,Ernesto Bernal-Mizrachi,Lynda Elghazi,Michael W. Roe,Patricia A. Labosky,Martin G. Myers,Maureen Gannon,Alvin C. Powers,Alvin C. Powers,Peter J. Dempsey +18 more
TL;DR: Cre-mediated gene manipulation using transgenic lines that express Cre under the control of the Ins2 and Pdx1 promoters are likely to alter gene expression in nutrient-sensing neurons.
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Akt Induces β-Cell Proliferation by Regulating Cyclin D1, Cyclin D2, and p21 Levels and Cyclin-Dependent Kinase-4 Activity
Szabolcs Fatrai,Lynda Elghazi,Norman Balcazar,Corentin Cras-Méneur,Irina Krits,Hiroaki Kiyokawa,Ernesto Bernal-Mizrachi +6 more
TL;DR: The experiments suggest that Akt induces beta-cell proliferation in a cdk4-dependent manner by regulation of cyclin D1, cyclinD2, and p21 levels, and indicate that alteration in levels of these cell cycle components could affect the maintenance of beta- cell mass in basal states and the adaptation of Beta-cells to pathological states resulting in diabetes.
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Disruption of Tsc2 in pancreatic β cells induces β cell mass expansion and improved glucose tolerance in a TORC1-dependent manner
Latif Rachdi,Norman Balcazar,Fernando Osorio-Duque,Lynda Elghazi,Aaron J. Weiss,Aaron P. Gould,Karen J. Chang-Chen,Michael J. Gambello,Ernesto Bernal-Mizrachi +8 more
TL;DR: A critical role is uncovered for the Tsc2/mTOR pathway in regulation of β cell mass and carbohydrate metabolism in vivo and inhibition of the mTOR/Raptor (TORC1) complex with rapamycin treatment suggests that TORC1 mediates proliferative and growth signals induced by deletion of T sc2 in β cells.
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Neurofibromatosis-1 Regulates Neuronal and Glial Cell Differentiation from Neuroglial Progenitors In Vivo by Both cAMP- and Ras-Dependent Mechanisms
Balazs Hegedus,Biplab Dasgupta,Jung Eun Shin,Ryan J. Emnett,Elizabeth K. Hart-Mahon,Lynda Elghazi,Ernesto Bernal-Mizrachi,David H. Gutmann +7 more
TL;DR: It is demonstrated that neurofibromin is required for normal glial and neuronal development involving separable Ras-dependent and cAMP-dependent mechanisms.