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

Transient early embryonic expression of Nkx2-5 mutations linked to congenital heart defects in human causes heart defects in Xenopus laevis.

Developmental dynamics : an official publication of the American Association of Anatomists - 1 Sept 2007

Bartlett Heather L, Sutherland Lillian, Kolker Sandra J, Welp Chelsea, Tajchman Urszula, Desmarais Vera, Weeks Daniel L

Abstract excerpt

Nkx2-5 is a homeobox containing transcription factor that is conserved and expressed in organisms that form hearts. Fruit flies lacking the gene (tinman) fail to form a dorsal vessel, mice that are homozygous null for Nkx2-5 form small, deformed hearts, and several human cardiac defects have been...

Read the complete abstract on PubMed

Topics

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

Share to Heart Defects, Congenital
Share to Homeobox Protein Nkx-2.5

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Homeodomain Proteins

Share to Microscopy, Video

Share to Myocardial Contraction

Share to Point Mutation

Share to Xenopus laevis

Share to Xenopus Proteins

Source

Open in PubMed Open full text

Identifiers

PMID: 17685485
DOI: 10.1002/dvdy.21244
PMCID: PMC2078326

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026. Prepared record publication-17685485-2026-09-02.2. Manifest publication-graph-cohort-2026-09-02.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Transient early embryonic expression of Nkx2-5 mutations linked to congenital heart defects in human causes heart defects in Xenopus laevis.PMID 17685485Read ↗

Developmental paradigms in heart disease: insights from tinman.Semantic proximity Read ↗

Nkx2.5 and Nkx2.6, homologs of Drosophila tinman, are required for development of the pharynx.Semantic proximity Read ↗

Congenital heart disease caused by mutations in the transcription factor NKX2-5.Semantic proximity Read ↗

A novel conditional mouse model for Nkx2-5 reveals transcriptional regulation of cardiac ion channels.Semantic proximity Read ↗

Mutations in the cardiac transcription factor NKX2.5 affect diverse cardiac developmental pathways.Semantic proximity Read ↗

Tinman function is essential for vertebrate heart development: elimination of cardiac differentiation by dominant inhibitory mutants of the tinman-related genes, XNkx2-3 and XNkx2-5.Semantic proximity Read ↗

Two novel frameshift mutations in <i>NKX2.5</i> result in novel features including visceral inversus and sinus venosus type ASDSemantic proximity Read ↗

Point mutations in murine Nkx2-5 phenocopy human congenital heart disease and induce pathogenic Wnt signaling.Semantic proximity Read ↗

Genetics of Congenital Heart Defects: The NKX2-5 Gene, a Key PlayerSemantic proximity Read ↗

Nkx2.7 and Nkx2.5 function redundantly and are required for cardiac morphogenesis of zebrafish embryos.Semantic proximity Read ↗

Expression of Nkx2.5 in wild type, cardiac mutant, and thyroxine-induced metamorphosed hearts of the Mexican axolotl.Semantic proximity Read ↗

Nkx genes are essential for maintenance of ventricular identity.Semantic proximity Read ↗

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