Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

The actin depolymerizing factor destrin serves as a negative feedback inhibitor of smooth muscle cell differentiation.

American journal of physiology. Heart and circulatory physiology - 1 Nov 2021

Liao Kuo An, Rangarajan Krsna V, Bai Xue, Taylor Joan M, Mack Christopher P

Abstract excerpt

We have previously shown that several components of the RhoA signaling pathway control smooth muscle cell (SMC) phenotype by altering serum response factor (SRF)-dependent gene expression. Because our genome-wide analyses of chromatin structure and transcription factor binding suggested that the actin depolymerizing factor, destrin (DSTN), was regulated in a SMC-selective fashion, the goals of the current study...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Carotid Artery Injuries
Share to Chemokine CXCL12

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Feedback, Physiological

Share to Muscle, Smooth, Vascular

Share to Myocytes, Smooth Muscle

Share to Rats, Wistar

Share to Receptors, Notch

Share to rhoA GTP-Binding Protein

Source

Open in PubMed Open full text

Identifiers

PMID: 34559579
DOI: 10.1152/ajpheart.00142.2021
PMCID: PMC8616609

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

The actin depolymerizing factor destrin serves as a negative feedback inhibitor of smooth muscle cell differentiation.PMID 34559579Read ↗

Inhibition of Diaphanous Formin Signaling In Vivo Impairs Cardiovascular Development and Alters Smooth Muscle Cell Phenotype.Semantic proximity Read ↗

DeltaEF1 mediates TGF-beta signaling in vascular smooth muscle cell differentiation.Semantic proximity Read ↗

Coronary Disease-Associated Gene TCF21 Inhibits Smooth Muscle Cell Differentiation by Blocking the Myocardin-Serum Response Factor Pathway.Semantic proximity Read ↗

Smooth muscle cell-specific transcription is regulated by nuclear localization of the myocardin-related transcription factors.Semantic proximity Read ↗

Redistribution of the chromatin remodeler Brg1 directs smooth muscle–derived adventitial progenitor–to–myofibroblast differentiation and vascular fibrosisSemantic proximity Read ↗

Myocardin-related transcription factor B is required for normal mouse vascular development and smooth muscle gene expression.Semantic proximity Read ↗

Smooth muscle cells and myofibroblasts use distinct transcriptional mechanisms for smooth muscle alpha-actin expression.Semantic proximity Read ↗

SMYD2 Regulates Vascular Smooth Muscle Cell Phenotypic Switching and Intimal Hyperplasia via Interaction with MyocardinSemantic proximity Read ↗

Myocardin Enhances Smad3-Mediated Transforming Growth Factor-β <sub>1</sub> Signaling in a CArG Box-Independent MannerSemantic proximity Read ↗

The mechanism of stem cell differentiation into smooth muscle cellsSemantic proximity Read ↗

Myocardin-dependent Activation of the CArG Box-rich Smooth Muscle γ-Actin GeneSemantic proximity Read ↗

Myocardin: a component of a molecular switch for smooth muscle differentiation.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.