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

Tbx1 regulates extracellular matrix-cell interactions in the second heart field

20 Mar 2019

Abstract excerpt

Tbx1, the major candidate gene for DiGeorge or 22q11.2 deletion syndrome, is required for efficient incorporation of cardiac progenitors of the second heart field (SHF) into the heart. However, the mechanisms by which TBX1 regulates this process are still unclear. Here, we have used two independent models, mouse embryos and cultured cells, to define the role of TBX1 in establishing morphological and dynamic...

Read the complete abstract on PubMed

Topics

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

Share to Cardiac Fibrosis and Remodeling
Share to Cell Adhesion Molecules Research
Share to Congenital heart defects research

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 31180501
DOI: 10.1093/hmg/ddz058

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Tbx1 regulates extracellular matrix-cell interactions in the second heart fieldPMID 31180501Read ↗

<i>Tbx1</i> regulates extracellular matrix-cell interactions in the second heart fieldSemantic proximity Read ↗

A fate map of Tbx1 expressing cells reveals heterogeneity in the second cardiac fieldSemantic proximity Read ↗

Tbx1 has a dual role in the morphogenesis of the cardiac outflow tract.Semantic proximity Read ↗

The del22q11.2 Candidate Gene <i>Tbx1</i> Controls Regional Outflow Tract Identity and Coronary Artery PatterningSemantic proximity Read ↗

Loss of Wnt5a disrupts second heart field cell deployment and may contribute to OFT malformations in DiGeorge syndromeSemantic proximity Read ↗

<i>Tbx1</i> Regulates Proliferation and Differentiation of Multipotent Heart ProgenitorsSemantic proximity Read ↗

DiGeorge Syndrome Gene tbx1 Functions through wnt11r to Regulate Heart Looping and DifferentiationSemantic proximity Read ↗

Tbx5-hedgehog molecular networks are essential in the second heart field for atrial septation.Semantic proximity Read ↗

Partial rescue of the Tbx1 mutant heart phenotype by Fgf8: genetic evidence of impaired tissue response to Fgf8.Semantic proximity Read ↗

The mesodermal source of fibronectin is required for heart morphogenesis and cardiac outflow tract elongation by regulating cell shape, polarity, and mechanotransduction in the second heart fieldSemantic proximity Read ↗

TBX1 regulates epithelial polarity and dynamic basal filopodia in the second heart fieldSemantic proximity Read ↗

Reduced dosage of β-catenin provides significant rescue of cardiac outflow tract anomalies in a Tbx1 conditional null mouse model of 22q11.2 deletion syndromeSemantic proximity Read ↗

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