5' CArG degeneracy in smooth muscle alpha-actin is required for injury-induced gene suppression in vivo. - Wikidata - awgldk - TriplyDB

5' CArG degeneracy in smooth muscle alpha-actin is required for injury-induced gene suppression in vivo.

5' CArG degeneracy in smooth muscle alpha-actin is required for injury-induced gene suppression in vivo.

http://www.wikidata.org/entity/Q30435837

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Myocardin is sufficient for a smooth muscle-like contractile phenotype Hairy-related transcription factors inhibit Notch-induced smooth muscle alpha-actin expression by interfering with Notch intracellular domain/CBF-1 complex interaction with the CBF-1-binding site PIAS1 activates the expression of smooth muscle cell differentiation marker genes by interacting with serum response factor and class I basic helix-loop-helix proteins.Kruppel-like factor 4, Elk-1, and histone deacetylases cooperatively suppress smooth muscle cell differentiation markers in response to oxidized phospholipids.Bone morphogenetic protein-induced MSX1 and MSX2 inhibit myocardin-dependent smooth muscle gene transcription Cooperative binding of KLF4, pELK-1, and HDAC2 to a G/C repressor element in the SM22α promoter mediates transcriptional silencing during SMC phenotypic switching in vivo.Yap1 protein regulates vascular smooth muscle cell phenotypic switch by interaction with myocardin.Genome-wide microarray analyses identify the protein C receptor as a novel calcineurin/nuclear factor of activated T cells-dependent gene in vascular smooth muscle cell phenotypic modulation.Chromatin immunoprecipitation (ChIP): revisiting the efficacy of sample preparation, sonication, quantification of sheared DNA, and analysis via PCR.Smooth and cardiac muscle-selective knock-out of Kruppel-like factor 4 causes postnatal death and growth retardation.The smooth muscle cell-restricted KCNMB1 ion channel subunit is a direct transcriptional target of serum response factor and myocardin.Sp1-dependent activation of KLF4 is required for PDGF-BB-induced phenotypic modulation of smooth muscle.PDGF-DD, a novel mediator of smooth muscle cell phenotypic modulation, is upregulated in endothelial cells exposed to atherosclerosis-prone flow patterns Control of SRF binding to CArG box chromatin regulates smooth muscle gene expression in vivo.Local delivery of the KCa3.1 blocker, TRAM-34, prevents acute angioplasty-induced coronary smooth muscle phenotypic modulation and limits stenosis.Multiple repressor pathways contribute to phenotypic switching of vascular smooth muscle cells.Atherosclerosis-prone hemodynamics differentially regulates endothelial and smooth muscle cell phenotypes and promotes pro-inflammatory priming.Intronic CArG box regulates cysteine-rich protein 2 expression in the adult but not in developing vasculature.Modulation of myocardin function by the ubiquitin E3 ligase UBR5.Sm22α transcription occurs at the early onset of the cardiovascular system and the intron 1 is dispensable for its transcription in smooth muscle cells during mouse development.Myocardin-related transcription factor-a controls myofibroblast activation and fibrosis in response to myocardial infarction.Molecular regulation of contractile smooth muscle cell phenotype: implications for vascular tissue engineering.Development of viral vectors for use in cardiovascular gene therapy.Transforming growth factor-beta1 (TGF-beta1) utilizes distinct pathways for the transcriptional activation of microRNA 143/145 in human coronary artery smooth muscle cells.Myocardin regulates vascular smooth muscle cell inflammatory activation and disease Myocardin-related transcription factor-A complexes activate type I collagen expression in lung fibroblasts.Transforming growth factor-β1-induced transcript 1 protein, a novel marker for smooth muscle contractile phenotype, is regulated by serum response factor/myocardin protein Defining smooth muscle cells and smooth muscle injury.Characterization of zebrafish intestinal smooth muscle development using a novel sm22α-b promoter.Maintenance of radiation-induced intestinal fibrosis: cellular and molecular features CHIP represses myocardin-induced smooth muscle cell differentiation via ubiquitin-mediated proteasomal degradation.Smooth muscle phenotypic plasticity in mechanical obstruction of the small intestine.Set7 mediated interactions regulate transcriptional networks in embryonic stem cells.Signaling mechanisms that regulate smooth muscle cell differentiation.Vascular smooth muscle cell differentiation-2010.Extracellular matrix synthesis in vascular disease: hypertension, and atherosclerosis.Myocardin in biology and disease.Potential Role of Glycogen Synthase Kinase-3β in Regulation of Myocardin Activity in Human Vascular Smooth Muscle Cells.Phenotypic transition of corpus cavernosum smooth muscle cells subjected to hypoxia.Differentiated Smooth Muscle Cells Generate a Subpopulation of Resident Vascular Progenitor Cells in the Adventitia Regulated by Klf4.

P2860

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P2860

5' CArG degeneracy in smooth muscle alpha-actin is required for injury-induced gene suppression in vivo.

http://www.wikidata.org/entity/Q30435837

description

2005 nî lūn-bûn

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2005 թուականի Փետրուարին հրատարակուած գիտական յօդուած

@hyw

2005 թվականի փետրվարին հրատարակված գիտական հոդված

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2005年の論文

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2005年論文

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2005年論文

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2005年論文

@zh-hk

2005年論文

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2005年論文

@zh-tw

2005年论文

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name

5' CArG degeneracy in smooth m ...... uced gene suppression in vivo.

@ast

5' CArG degeneracy in smooth m ...... uced gene suppression in vivo.

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type

label

5' CArG degeneracy in smooth m ...... uced gene suppression in vivo.

@ast

5' CArG degeneracy in smooth m ...... uced gene suppression in vivo.

@en

prefLabel

5' CArG degeneracy in smooth m ...... uced gene suppression in vivo.

@ast

5' CArG degeneracy in smooth m ...... uced gene suppression in vivo.

@en

P1433

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P1433

Journal of Clinical Investigation

P1476

5' CArG degeneracy in smooth m ...... uced gene suppression in vivo.

@en

P2093

Brian R Wamhoff

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

Gary K Owens

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

Jennifer A Hendrix

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

Oliver G McDonald

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Tadashi Yoshida

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P2860

Myocardin is a critical serum response factor cofactor in the transcriptional program regulating smooth muscle cell differentiation.

Megakaryoblastic leukemia factor-1 transduces cytoskeletal signals and induces smooth muscle cell differentiation from undifferentiated embryonic stem cells

Potentiation of serum response factor activity by a family of myocardin-related transcription factors.

Human and Drosophila homeodomain proteins that enhance the DNA-binding activity of serum response factor

Megakaryoblastic leukemia 1, a potent transcriptional coactivator for serum response factor (SRF), is required for serum induction of SRF target genes

Transitions in histone acetylation reveal boundaries of three separately regulated neighboring loci

Myocardin: a component of a molecular switch for smooth muscle differentiation

Activation of cardiac gene expression by myocardin, a transcriptional cofactor for serum response factor

MAPKAP kinase 2 phosphorylates serum response factor in vitro and in vivo

Actin dynamics control SRF activity by regulation of its coactivator MAL

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418-427

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scholarly article

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10.1172/JCI22648

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2

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115

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2005-02-01T00:00:00Z

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15690088

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546420

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