CHIP represses myocardin-induced smooth muscle cell differentiation via ubiquitin-mediated proteasomal degradation. - Wikidata - wikimedia - TriplyDB

CHIP represses myocardin-induced smooth muscle cell differentiation via ubiquitin-mediated proteasomal degradation.

CHIP represses myocardin-induced smooth muscle cell differentiation via ubiquitin-mediated proteasomal degradation.

http://www.wikidata.org/entity/Q37156982

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The ubiquitin-proteasome system and cardiovascular disease A Decade of Boon or Burden: What Has the CHIP Ever Done for Cellular Protein Quality Control Mechanism Implicated in Neurodegeneration and Aging?The E3 Ligase CHIP Mediates p21 Degradation to Maintain Radioresistance.On to the road to degradation: atherosclerosis and the proteasome Sent to destroy: the ubiquitin proteasome system regulates cell signaling and protein quality control in cardiovascular development and disease.Modulation of myocardin function by the ubiquitin E3 ligase UBR5.Co-activation of nuclear factor-κB and myocardin/serum response factor conveys the hypertrophy signal of high insulin levels in cardiac myoblasts.Bortezomib, a proteasome inhibitor, attenuates angiotensin II-induced hypertension and aortic remodeling in rats.Carboxyl terminus of HSC70-interacting protein (CHIP) down-regulates NF-κB-inducing kinase (NIK) and suppresses NIK-induced liver injury Dysfunction of the ubiquitin-proteasome system in atherosclerotic cardiovascular disease Receptor for Advanced Glycation End-Products Signaling Interferes with the Vascular Smooth Muscle Cell Contractile Phenotype and Function STAT3 Protein Regulates Vascular Smooth Muscle Cell Phenotypic Switch by Interaction with Myocardin.Requirement of miR-9-dependent regulation of Myocd in PASMCs phenotypic modulation and proliferation induced by hepatopulmonary syndrome rat serum Inhibition of Proteasome Activity by Low-dose Bortezomib Attenuates Angiotensin II-induced Abdominal Aortic Aneurysm in Apo E(-/-) Mice.Protection against doxorubicin-induced myocardial dysfunction in mice by cardiac-specific expression of carboxyl terminus of hsp70-interacting protein C terminus of Hsc70-interacting protein promotes smooth muscle cell proliferation and survival through ubiquitin-mediated degradation of FoxO1.Mechanical regulation of the proangiogenic factor CCN1/CYR61 gene requires the combined activities of MRTF-A and CREB-binding protein histone acetyltransferase.Signaling mechanisms that regulate smooth muscle cell differentiation.Physiological and pathological role of the ubiquitin-proteasome system in the vascular smooth muscle cell.The role of ubiquitin ligases in cardiac disease.Myocardin in biology and disease.Protein kinase Cα inhibits myocardin-induced cardiomyocyte hypertrophy through the promotion of myocardin phosphorylation.Potential Role of Glycogen Synthase Kinase-3β in Regulation of Myocardin Activity in Human Vascular Smooth Muscle Cells.Phosphorylation acts positively and negatively to regulate MRTF-A subcellular localisation and activity.Opposite roles of myocardin and atrogin-1 in L6 myoblast differentiation.β-catenin and Smad3 regulate the activity and stability of myocardin-related transcription factor during epithelial-myofibroblast transition.Ubiquitin ligase CHIP induces TRAF2 proteasomal degradation and NF-κB inactivation to regulate breast cancer cell invasion.GSK3 as a Sensor Determining Cell Fate in the Brain.Nuclear import mechanism for myocardin family members and their correlation with vascular smooth muscle cell phenotype.How do your contacts (or their absence) shape your fate?Targeting the ubiquitin-proteasome system for cancer treatment: discovering novel inhibitors from nature and drug repurposing.Atrogin-1 Increases Smooth Muscle Contractility Through Myocardin Degradation.Anisomycin prevents OGD-induced necroptosis by regulating the E3 ligase CHIP.

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CHIP represses myocardin-induced smooth muscle cell differentiation via ubiquitin-mediated proteasomal degradation.

http://www.wikidata.org/entity/Q37156982

description

article científic

@ca

article scientifique

@fr

articolo scientifico

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artigo científico

@pt

bilimsel makale

@tr

scientific article published on 23 February 2009

@en

vedecký článok

@sk

vetenskaplig artikel

@sv

videnskabelig artikel

@da

vědecký článek

@cs

name

CHIP represses myocardin-induc ...... iated proteasomal degradation.

@en

CHIP represses myocardin-induc ...... iated proteasomal degradation.

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type

label

CHIP represses myocardin-induc ...... iated proteasomal degradation.

@en

CHIP represses myocardin-induc ...... iated proteasomal degradation.

@nl

prefLabel

CHIP represses myocardin-induc ...... iated proteasomal degradation.

@en

CHIP represses myocardin-induc ...... iated proteasomal degradation.

@nl

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Molecular and Cellular Biology

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CHIP represses myocardin-induc ...... iated proteasomal degradation.

@en

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Cam Patterson

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

Dongfeng Gu

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

Hua Zhang

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

Huihua Li

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

Mingpeng She

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

Ping Xie

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

Yongna Fan

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

Yuan Zhang

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

P2860

Identification of CHIP, a novel tetratricopeptide repeat-containing protein that interacts with heat shock proteins and negatively regulates chaperone functions.

The co-chaperone CHIP regulates protein triage decisions mediated by heat-shock proteins

Serum response factor and myocardin mediate arterial hypercontractility and cerebral blood flow dysregulation in Alzheimer's phenotype.

Phenotypic modulation of smooth muscle cells through interaction of Foxo4 and myocardin

The cochaperone HspBP1 inhibits the CHIP ubiquitin ligase and stimulates the maturation of the cystic fibrosis transmembrane conductance regulator

The SCFbeta-TRCP-ubiquitin ligase complex associates specifically with phosphorylated destruction motifs in IkappaBalpha and beta-catenin and stimulates IkappaBalpha ubiquitination in vitro

Akt and CHIP coregulate tau degradation through coordinated interactions

Myocardin is a master regulator of smooth muscle gene expression

SCF(beta-TRCP) and phosphorylation dependent ubiquitinationof I kappa B alpha catalyzed by Ubc3 and Ubc4

CHIP-Hsc70 complex ubiquitinates phosphorylated tau and enhances cell survival

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2398-2408

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scholarly article

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10.1128/MCB.01737-08

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9

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29

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2009-02-23T00:00:00Z

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19237536

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2668377

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