beta-Cell-specific overexpression of glutathione peroxidase preserves intranuclear MafA and reverses diabetes in db/db mice. - Wikidata - awgldk - TriplyDB

beta-Cell-specific overexpression of glutathione peroxidase preserves intranuclear MafA and reverses diabetes in db/db mice.

beta-Cell-specific overexpression of glutathione peroxidase preserves intranuclear MafA and reverses diabetes in db/db mice.

http://www.wikidata.org/entity/Q37418222

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Pancreatic β Cell Mass Death Knowledge Gaps in Rodent Pancreas Biology: Taking Human Pluripotent Stem Cell-Derived Pancreatic Beta Cells into Our Own Hands Whole grains, type 2 diabetes, coronary heart disease, and hypertension: links to the aleurone preferred over indigestible fiber Redox homeostasis in pancreatic β cells Mitochondrial regulation of β-cell function: maintaining the momentum for insulin release Paradoxical Roles of Antioxidant Enzymes: Basic Mechanisms and Health Implications The B55α-containing PP2A holoenzyme dephosphorylates FOXO1 in islet β-cells under oxidative stress An islet in distress: β cell failure in type 2 diabetes.MicroRNA-7a regulates pancreatic β cell function.12-lipoxygenase promotes obesity-induced oxidative stress in pancreatic islets.Impacts of dietary selenium deficiency on metabolic phenotypes of diet-restricted GPX1-overexpressing mice Two tales of antioxidant enzymes on β cells and diabetes.Mafa expression enhances glucose-responsive insulin secretion in neonatal rat beta cells.Friendly, and not so friendly, roles of Rac1 in islet β-cell function: lessons learnt from pharmacological and molecular biological approaches Neutralizing interleukin-1beta (IL-1beta) induces beta-cell survival by maintaining PDX1 protein nuclear localization.Glutathione peroxidase-1 in health and disease: from molecular mechanisms to therapeutic opportunities Type 2 diabetes and the aging pancreatic beta cell.Preserving Mafa expression in diabetic islet β-cells improves glycemic control in vivo Gliclazide does not fully prevent 2-deoxy-D-ribose-induced oxidative damage because it does not restore glutathione content in a pancreatic β-cell line.NOX2 deficiency protects against streptozotocin-induced beta-cell destruction and development of diabetes in mice.MafA and MafB regulate genes critical to beta-cells in a unique temporal manner Dual Opposing Roles of Metallothionein Overexpression in C57BL/6J Mouse Pancreatic β-Cells.High-fat diet induced insulin resistance in pregnant rats through pancreatic pax6 signaling pathway.Antioxidants Complement the Requirement for Protein Chaperone Function to Maintain β-Cell Function and Glucose Homeostasis.Hnf1α (MODY3) regulates β-cell-enriched MafA transcription factor expression.Understanding selenoprotein function and regulation through the use of rodent models.Anti-hyperglycemic activity of selenium nanoparticles in streptozotocin-induced diabetic rats Mitochondrial hormesis in pancreatic β cells: does uncoupling protein 2 play a role?Effect of aging on islet beta-cell function and its mechanisms in Wistar rats.Beta cell nuclear musculoaponeurotic fibrosarcoma oncogene family A (MafA) is deficient in type 2 diabetes.Thyroid hormone promotes postnatal rat pancreatic β-cell development and glucose-responsive insulin secretion through MAFA.Altered Plasma Profile of Antioxidant Proteins as an Early Correlate of Pancreatic β Cell Dysfunction.Preventing p38 MAPK-mediated MafA degradation ameliorates β-cell dysfunction under oxidative stress.Inactivation of specific β cell transcription factors in type 2 diabetes.Ebselen treatment prevents islet apoptosis, maintains intranuclear Pdx-1 and MafA levels, and preserves β-cell mass and function in ZDF rats The Role of Oxidative Stress and Hypoxia in Pancreatic Beta-Cell Dysfunction in Diabetes Mellitus.MafA and MafB activity in pancreatic β cells.Nutrition-/diet-induced changes in gene expression in pancreatic β-cells.Role of K(ATP) channels in β-cell resistance to oxidative stress.Involvement of oxidative stress in suppression of insulin biosynthesis under diabetic conditions.

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beta-Cell-specific overexpression of glutathione peroxidase preserves intranuclear MafA and reverses diabetes in db/db mice.

http://www.wikidata.org/entity/Q37418222

description

article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 09 October 2009

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vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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name

beta-Cell-specific overexpress ...... verses diabetes in db/db mice.

@en

beta-Cell-specific overexpress ...... verses diabetes in db/db mice.

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type

label

beta-Cell-specific overexpress ...... verses diabetes in db/db mice.

@en

beta-Cell-specific overexpress ...... verses diabetes in db/db mice.

@nl

prefLabel

beta-Cell-specific overexpress ...... verses diabetes in db/db mice.

@en

beta-Cell-specific overexpress ...... verses diabetes in db/db mice.

@nl

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beta-Cell-specific overexpress ...... verses diabetes in db/db mice.

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Elizabeth A Oseid

http://www.w3.org/2001/XMLSchema#string

Jamie S Harmon

http://www.w3.org/2001/XMLSchema#string

Marika Bogdani

http://www.w3.org/2001/XMLSchema#string

Marleen Berghmans

http://www.w3.org/2001/XMLSchema#string

R Paul Robertson

http://www.w3.org/2001/XMLSchema#string

Renée C Leboeuf

http://www.w3.org/2001/XMLSchema#string

Sabrina S M Mak

http://www.w3.org/2001/XMLSchema#string

Susan D Parazzoli

http://www.w3.org/2001/XMLSchema#string

P2860

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

Reactive oxygen species, antioxidants, and the mammalian thioredoxin system

A role for glutathione peroxidase in protecting pancreatic beta cells against oxidative stress in a model of glucose toxicity.

The glutathione peroxidases.

Oxidative stress-mediated, post-translational loss of MafA protein as a contributing mechanism to loss of insulin gene expression in glucotoxic beta cells.

The mechanisms of alloxan- and streptozotocin-induced diabetes.

Development of insulin resistance and obesity in mice overexpressing cellular glutathione peroxidase.

Preservation of insulin mRNA levels and insulin secretion in HIT cells by avoidance of chronic exposure to high glucose concentrations.

Prevention of glucose toxicity in HIT-T15 cells and Zucker diabetic fatty rats by antioxidants.

Transgenic copper/zinc superoxide dismutase modulates susceptibility to type I diabetes.

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4855-4862

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scholarly article

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10.1210/EN.2009-0708

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11

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150

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2009-10-09T00:00:00Z

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19819955

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2775976

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