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Article

The Q510E mutation in Shp2 perturbs heart valve development by increasing cell migration.

Journal of applied physiology (Bethesda, Md. : 1985) - 1 Jan 2015

Edwards Michelle A, Crombie Kathryn, Schramm Christine, Krenz Maike

Abstract excerpt

Tightly regulated cellular signaling is critical for correct heart valve development, but how and why signaling is dysregulated in congenital heart disease is not very well known. We focused on protein tyrosine phosphatase Shp2, because mutations in this signaling modulator frequently cause valve malformations associated with Noonan syndrome or Noonan syndrome with multiple lentigines (NSML). To model...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Focal Adhesion Protein-Tyrosine Kinases

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Identifiers

PMID: 25359717
DOI: 10.1152/japplphysiol.00008.2014
PMCID: PMC4281644

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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