Conditional expression of Smad7 in pancreatic beta cells disrupts TGF-beta signaling and induces reversible diabetes mellitus - Test2 - elhamkhani - TriplyDB

Conditional expression of Smad7 in pancreatic beta cells disrupts TGF-beta signaling and induces reversible diabetes mellitus

Conditional expression of Smad7 in pancreatic beta cells disrupts TGF-beta signaling and induces reversible diabetes mellitus

http://www.wikidata.org/entity/Q25256996

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Oscillations, intercellular coupling, and insulin secretion in pancreatic beta cells.Connective tissue growth factor (CTGF) inactivation leads to defects in islet cell lineage allocation and beta-cell proliferation during embryogenesis Human β-cell proliferation and intracellular signaling: part 3 Activin B receptor ALK7 is a negative regulator of pancreatic beta-cell function Effects of activin A on survival, function and gene expression of pancreatic islets from non-diabetic and diabetic human donors Relative roles of the different Pax6 domains for pancreatic alpha cell development.Integrating pathway analysis and genetics of gene expression for genome-wide association studies Trigenic neural crest-restricted Smad7 over-expression results in congenital craniofacial and cardiovascular defects.Primary cilia in pancreatic development and disease.METABOLIC FUNCTIONS OF MYOSTATIN AND GDF11.Genetic variations in SMAD7 are associated with colorectal cancer risk in the colon cancer family registry.Nodal and lefty signaling regulates the growth of pancreatic cells Bone morphogenetic protein 3 controls insulin gene expression and is down-regulated in INS-1 cells inducibly expressing a hepatocyte nuclear factor 1A-maturity-onset diabetes of the young mutation.Overcoming Insulin Insufficiency by Forced Follistatin Expression in β-cells of db/db Mice.Wnt signaling regulates pancreatic beta cell proliferation Unraveling the biological functions of Smad7 with mouse models.Activin A levels are associated with abnormal glucose regulation in patients with myocardial infarction: potential counteracting effects of activin A on inflammation Differential synthesis and action of TGFß superfamily ligands in mouse and rat islets β-catenin is selectively required for the expansion and regeneration of mature pancreatic acinar cells in mice.Leukocyte function-associated antigen-1/intercellular adhesion molecule-1 interaction induces a novel genetic signature resulting in T-cells refractory to transforming growth factor-β signaling Activin B regulates islet composition and islet mass but not whole body glucose homeostasis or insulin sensitivity Transient Suppression of TGFβ Receptor Signaling Facilitates Human Islet Transplantation Inhibition of TGF-β Signaling Promotes Human Pancreatic β-Cell Replication.TGF-β Signaling Regulates Pancreatic β-Cell Proliferation through Control of Cell Cycle Regulator p27 Expression.Smad signaling pathways regulate pancreatic endocrine development.Formation and regeneration of the endocrine pancreas.Transforming growth factor-beta/Smad3 signaling regulates insulin gene transcription and pancreatic islet beta-cell function On the origin of the beta cell.The biology of activin: recent advances in structure, regulation and function The transcriptional response of the islet to pregnancy in mice.Abnormal glucose metabolism in heterozygous mutant mice for a type I receptor required for BMP signaling.A smad signaling network regulates islet cell proliferation A Pdx-1-Regulated Soluble Factor Activates Rat and Human Islet Cell Proliferation.Pancreas cell fate.M2 macrophages promote beta-cell proliferation by up-regulation of SMAD7.Antipsychotics activate the TGFβ pathway effector SMAD3 Systemic Activin signaling independently regulates sugar homeostasis, cellular metabolism, and pH balance in Drosophila melanogaster.Bone morphogenetic protein 4 inhibits insulin secretion from rodent beta cells through regulation of calbindin1 expression and reduced voltage-dependent calcium currents.The role of noggin in regulation of high glucose-induced apoptosis and insulin secretion in INS-1 rat beta cells.Proper activation of MafA is required for optimal differentiation and maturation of pancreatic β-cells

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P2860

Conditional expression of Smad7 in pancreatic beta cells disrupts TGF-beta signaling and induces reversible diabetes mellitus

http://www.wikidata.org/entity/Q25256996

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2006 nî lūn-bûn

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2006 թուականի Յունուարին հրատարակուած գիտական յօդուած

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2006年の論文

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Conditional expression of Smad ...... s reversible diabetes mellitus

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Conditional expression of Smad ...... s reversible diabetes mellitus

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Conditional expression of Smad ...... s reversible diabetes mellitus

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Conditional expression of Smad ...... s reversible diabetes mellitus

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Conditional expression of Smad ...... s reversible diabetes mellitus

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Conditional expression of Smad ...... s reversible diabetes mellitus

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Conditional expression of Smad ...... s reversible diabetes mellitus

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Conditional expression of Smad ...... s reversible diabetes mellitus

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Asa A Apelqvist

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Erin B Harmon

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James N Topper

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Nora G Smart

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Raymond J MacDonald

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Seung K Kim

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Xueying Gu

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P2860

Role of transcription factor KLF11 and its diabetes-associated gene variants in pancreatic beta cell function

Regulation of anterior/posterior patterning of the axial skeleton by growth/differentiation factor 11

Inactivation of menin, a Smad3-interacting protein, blocks transforming growth factor type beta signaling

Menin is required for bone morphogenetic protein 2- and transforming growth factor beta-regulated osteoblastic differentiation through interaction with Smads and Runx2

MafA is a glucose-regulated and pancreatic beta-cell-specific transcriptional activator for the insulin gene

Vascular MADs: two novel MAD-related genes selectively inducible by flow in human vascular endothelium

Menin and MLL cooperatively regulate expression of cyclin-dependent kinase inhibitors

Identification of beta-cell-specific insulin gene transcription factor RIPE3b1 as mammalian MafA.

Tight control of gene expression in mammalian cells by tetracycline-responsive promoters

The MafA transcription factor appears to be responsible for tissue-specific expression of insulin

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10.1371/JOURNAL.PBIO.0040039

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16435884

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1351925

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