Activating transcription factor 6 protects insulin receptor from ER stress-stimulated desensitization via p42/44 ERK pathway - Wikidata - thesis-toulmin - TriplyDB

Activating transcription factor 6 protects insulin receptor from ER stress-stimulated desensitization via p42/44 ERK pathway

Activating transcription factor 6 protects insulin receptor from ER stress-stimulated desensitization via p42/44 ERK pathway

http://www.wikidata.org/entity/Q28658223

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Inhibitory cross-talk between the AMPK and ERK pathways mediates endoplasmic reticulum stress-induced insulin resistance in skeletal muscle.SP6616 as a new Kv2.1 channel inhibitor efficiently promotes β-cell survival involving both PKC/Erk1/2 and CaM/PI3K/Akt signaling pathways.Calcium signalling and ER stress in insulin resistance and atherosclerosis.Novel approaches to drug discovery for the treatment of type 2 diabetes.Hyperglycemia- and hyperinsulinemia-induced insulin resistance causes alterations in cellular bioenergetics and activation of inflammatory signaling in lymphatic muscle.Hepatocyte DACH1 Is Increased in Obesity via Nuclear Exclusion of HDAC4 and Promotes Hepatic Insulin Resistance

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Activating transcription factor 6 protects insulin receptor from ER stress-stimulated desensitization via p42/44 ERK pathway

http://www.wikidata.org/entity/Q28658223

description

2011 nî lūn-bûn

@nan

2011 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած

@hyw

2011 թվականի սեպտեմբերին հրատարակված գիտական հոդված

@hy

2011年の論文

@ja

2011年論文

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2011年論文

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2011年論文

@zh-hk

2011年論文

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2011年論文

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2011年论文

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name

Activating transcription facto ...... ization via p42/44 ERK pathway

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Activating transcription facto ...... ization via p42/44 ERK pathway

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Activating transcription facto ...... ization via p42/44 ERK pathway

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Activating transcription facto ...... ization via p42/44 ERK pathway

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Activating transcription facto ...... ization via p42/44 ERK pathway

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Acta Pharmacologica Sinica

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Activating transcription facto ...... ization via p42/44 ERK pathway

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Hong Shen

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

Hua-liang Jiang

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

Jing Chen

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Li-li Chen

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Vatcharin Rukachaisirikul

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

Xu Shen

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

Xu Wang

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

Xuan Tang

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

P2860

Identification of the cis-acting endoplasmic reticulum stress response element responsible for transcriptional induction of mammalian glucose-regulated proteins. Involvement of basic leucine zipper transcription factors

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

Coupling of stress in the ER to activation of JNK protein kinases by transmembrane protein kinase IRE1

ER stress induces cleavage of membrane-bound ATF6 by the same proteases that process SREBPs

Insulin signalling and the regulation of glucose and lipid metabolism

ASK1 is essential for endoplasmic reticulum stress-induced neuronal cell death triggered by expanded polyglutamine repeats

Endoplasmic reticulum stress and the inflammatory basis of metabolic disease

IRE1-mediated unconventional mRNA splicing and S2P-mediated ATF6 cleavage merge to regulate XBP1 in signaling the unfolded protein response

Adipose expression of tumor necrosis factor-alpha: direct role in obesity-linked insulin resistance

The c-Jun NH(2)-terminal kinase promotes insulin resistance during association with insulin receptor substrate-1 and phosphorylation of Ser(307)

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scholarly article

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1841150

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10.1038/APS.2011.75

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1046511031

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