Chop deletion reduces oxidative stress, improves beta cell function, and promotes cell survival in multiple mouse models of diabetes. - Wikidata - wikimedia - TriplyDB

Chop deletion reduces oxidative stress, improves beta cell function, and promotes cell survival in multiple mouse models of diabetes.

Chop deletion reduces oxidative stress, improves beta cell function, and promotes cell survival in multiple mouse models of diabetes.

http://www.wikidata.org/entity/Q36861224

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Endoplasmic reticulum stress and the inflammatory basis of metabolic disease Atf4 regulates obesity, glucose homeostasis, and energy expenditure Adaptive preconditioning in neurological diseases – therapeutic insights from proteostatic perturbations The balance of powers: Redox regulation of fibrogenic pathways in kidney injury Endoplasmic reticulum stress and Nox-mediated reactive oxygen species signaling in the peripheral vasculature: potential role in hypertension Neuronal endoplasmic reticulum stress in axon injury and neurodegeneration Endoplasmic reticulum stress and type 2 diabetes Endoplasmic reticulum stress in the β-cell pathogenesis of type 2 diabetes Lost in translation: endoplasmic reticulum stress and the decline of β-cell health in diabetes mellitus Guards and culprits in the endoplasmic reticulum: glucolipotoxicity and β-cell failure in type II diabetes Xenobiotic perturbation of ER stress and the unfolded protein response Stress responses from the endoplasmic reticulum in cancer Lack of Wdr13 gene in mice leads to enhanced pancreatic beta cell proliferation, hyperinsulinemia and mild obesity RNase L controls terminal adipocyte differentiation, lipids storage and insulin sensitivity via CHOP10 mRNA regulation Chaperones ameliorate beta cell dysfunction associated with human islet amyloid polypeptide overexpression The genetic architecture of the genome-wide transcriptional response to ER stress in the mouse JNK1 protects against glucolipotoxicity-mediated beta-cell apoptosis Ubiquitin fold modifier 1 (UFM1) and its target UFBP1 protect pancreatic beta cells from ER stress-induced apoptosis Role of ERO1-alpha-mediated stimulation of inositol 1,4,5-triphosphate receptor activity in endoplasmic reticulum stress-induced apoptosis 12/15-Lipoxygenase signaling in the endoplasmic reticulum stress response.The unfolded protein response in immunity and inflammation Integrating the mechanisms of apoptosis induced by endoplasmic reticulum stress Inhibition of deoxyhypusine synthase enhances islet {beta} cell function and survival in the setting of endoplasmic reticulum stress and type 2 diabetes Peroxisome proliferator-activated receptor gamma activation restores islet function in diabetic mice through reduction of endoplasmic reticulum stress and maintenance of euchromatin structure.Sleep, plasticity and the pathophysiology of neurodevelopmental disorders: the potential roles of protein synthesis and other cellular processes.DDIT3/CHOP and the sarcoma fusion oncoprotein FUS-DDIT3/TLS-CHOP bind cyclin-dependent kinase 2.An islet in distress: β cell failure in type 2 diabetes.Aging and sleep deprivation induce the unfolded protein response in the pancreas: implications for metabolism.Targeting MUC1-C is synergistic with bortezomib in downregulating TIGAR and inducing ROS-mediated myeloma cell death.β-Cell failure in type 2 diabetes.Paraoxonase 2 protein is spatially expressed in the human placenta and selectively reduced in labour Lack of TXNIP protects against mitochondria-mediated apoptosis but not against fatty acid-induced ER stress-mediated beta-cell death.A point mutation in Sec61alpha1 leads to diabetes and hepatosteatosis in mice.Inactivation of C/ebp homologous protein-driven immune-metabolic interactions exacerbate obesity and adipose tissue leukocytosis.Myostatin augments muscle-specific ring finger protein-1 expression through an NF-kB independent mechanism in SMAD3 null muscle.Linking ER Stress to Autophagy: Potential Implications for Cancer Therapy.Glial cell-line derived neurotrophic factor protects human islets from nutrient deprivation and endoplasmic reticulum stress induced apoptosis.Glucose induces pancreatic islet cell apoptosis that requires the BH3-only proteins Bim and Puma and multi-BH domain protein Bax.Insulin gene mutations resulting in early-onset diabetes: marked differences in clinical presentation, metabolic status, and pathogenic effect through endoplasmic reticulum retention.Induction of ER stress in macrophages of tuberculosis granulomas.

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P2860

Chop deletion reduces oxidative stress, improves beta cell function, and promotes cell survival in multiple mouse models of diabetes.

http://www.wikidata.org/entity/Q36861224

description

2008 nî lūn-bûn

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2008年の論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年论文

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2008年论文

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2008年论文

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name

Chop deletion reduces oxidativ ...... iple mouse models of diabetes.

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Chop deletion reduces oxidativ ...... iple mouse models of diabetes.

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Chop deletion reduces oxidativ ...... iple mouse models of diabetes.

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Journal of Clinical Investigation

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Chop deletion reduces oxidativ ...... iple mouse models of diabetes.

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P2093

Benbo Song

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

Donalyn Scheuner

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Randal J Kaufman

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Subramaniam Pennathur

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P2860

Mammalian transcription factor ATF6 is synthesized as a transmembrane protein and activated by proteolysis in response to endoplasmic reticulum stress

Growth arrest and DNA damage-inducible protein GADD34 assembles a novel signaling complex containing protein phosphatase 1 and inhibitor 1.

XBP1 mRNA is induced by ATF6 and spliced by IRE1 in response to ER stress to produce a highly active transcription factor

Oxidative protein folding in eukaryotes: mechanisms and consequences

Signal integration in the endoplasmic reticulum unfolded protein response

EIF2AK3, encoding translation initiation factor 2-alpha kinase 3, is mutated in patients with Wolcott-Rallison syndrome

Translational control is required for the unfolded protein response and in vivo glucose homeostasis

Method for the isolation of intact islets of Langerhans from the rat pancreas

Control of mRNA translation preserves endoplasmic reticulum function in beta cells and maintains glucose homeostasis

Cotranslocational degradation protects the stressed endoplasmic reticulum from protein overload

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10.1172/JCI34587

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2528909

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