Tubulin hyperacetylation is adaptive in cardiac proteotoxicity by promoting autophagy. - Wikidata - wikimedia - TriplyDB

Tubulin hyperacetylation is adaptive in cardiac proteotoxicity by promoting autophagy.

Tubulin hyperacetylation is adaptive in cardiac proteotoxicity by promoting autophagy.

http://www.wikidata.org/entity/Q34661083

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Histone Deacetylases Exert Class-Specific Roles in Conditioning the Brain and Heart Against Acute Ischemic Injury Emerging strategies to effectively target autophagy in cancer Functional genetic variants within the SIRT2 gene promoter in acute myocardial infarction.Early transcriptional alteration of histone deacetylases in a murine model of doxorubicin-induced cardiomyopathy.Tubulin acetylation: responsible enzymes, biological functions and human diseases.Non-sirtuin histone deacetylases in the control of cardiac aging Autophagy in Ischemic Livers: A Critical Role of Sirtuin 1/Mitofusin 2 Axis in Autophagy Induction.Proteotoxicity and cardiac dysfunction.Tubulin acetylation accompanies autophagy development induced by different abiotic stimuli in Arabidopsis thaliana.Keeping up the balance: role of HDACs in cardiac proteostasis and therapeutic implications for atrial fibrillation.Chronic heart failure: Ca(2+), catabolism, and catastrophic cell death.Methodological approaches and insights on protein aggregation in biological systems.Research progress of hydroxychloroquine and autophagy inhibitors on cancer.HDAC6: A Novel Histone Deacetylase Implicated in Pulmonary Arterial Hypertension.The Effects of Guizhi Gancao Decoction on Pressure Overload-Induced Heart Failure and Posttranslational Modifications of Tubulin in Mice.Posttranslational modifications of α-tubulin in alzheimer disease.The role of αB-crystallin in skeletal and cardiac muscle tissues.HDAC Inhibition Improves the Sarcoendoplasmic Reticulum Ca2+-ATPase Activity in Cardiac Myocytes.Food Bioactive HDAC Inhibitors in the Epigenetic Regulation of Heart Failure Histone deacetylase 6 in cancer The Crosstalk between Acetylation and Phosphorylation: Emerging New Roles for HDAC Inhibitors in the Heart

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P2860

Tubulin hyperacetylation is adaptive in cardiac proteotoxicity by promoting autophagy.

http://www.wikidata.org/entity/Q34661083

description

2014 nî lūn-bûn

@nan

2014 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած

@hyw

2014 թվականի նոյեմբերին հրատարակված գիտական հոդված

@hy

2014年の論文

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2014年論文

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2014年論文

@zh-hant

2014年論文

@zh-hk

2014年論文

@zh-mo

2014年論文

@zh-tw

2014年论文

@wuu

name

Tubulin hyperacetylation is adaptive in cardiac proteotoxicity by promoting autophagy.

@ast

Tubulin hyperacetylation is adaptive in cardiac proteotoxicity by promoting autophagy.

@en

Tubulin hyperacetylation is adaptive in cardiac proteotoxicity by promoting autophagy.

@nl

type

label

Tubulin hyperacetylation is adaptive in cardiac proteotoxicity by promoting autophagy.

@ast

Tubulin hyperacetylation is adaptive in cardiac proteotoxicity by promoting autophagy.

@en

Tubulin hyperacetylation is adaptive in cardiac proteotoxicity by promoting autophagy.

@nl

prefLabel

Tubulin hyperacetylation is adaptive in cardiac proteotoxicity by promoting autophagy.

@ast

Tubulin hyperacetylation is adaptive in cardiac proteotoxicity by promoting autophagy.

@en

Tubulin hyperacetylation is adaptive in cardiac proteotoxicity by promoting autophagy.

@nl

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PNAS.1415589111

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Proceedings of the National Academy of Sciences of the United States of America

P1476

Tubulin hyperacetylation is adaptive in cardiac proteotoxicity by promoting autophagy.

@en

P2093

Bradley S Ferguson

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Hanna Osinska

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

Jeanne James

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

Jeffrey Robbins

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Md Shenuarin Bhuiyan

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Patrick M McLendon

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Timothy A McKinsey

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P2860

The deacetylase HDAC6 regulates aggresome formation and cell viability in response to misfolded protein stress

A missense mutation in the alphaB-crystallin chaperone gene causes a desmin-related myopathy

HDAC6 and microtubules are required for autophagic degradation of aggregated huntingtin

Exercise-induced BCL2-regulated autophagy is required for muscle glucose homeostasis

Histone deacetylase (HDAC) inhibitors attenuate cardiac hypertrophy by suppressing autophagy

The many roles of histone deacetylases in development and physiology: implications for disease and therapy

Mammalian heart renewal by pre-existing cardiomyocytes

Histone deacetylase inhibition reduces myocardial ischemia-reperfusion injury in mice

The HDAC inhibitor 4b ameliorates the disease phenotype and transcriptional abnormalities in Huntington's disease transgenic mice.

Histone deacetylase 6 plays a role as a distinct regulator of diverse cellular processes

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10.1073/PNAS.1415589111

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Bradley S. Ferguson

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2014-11-17T00:00:00Z

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