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

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

Molecular and cellular biology - 1 Jul 2001

Tanaka M, Schinke M, Liao H S, Yamasaki N, Izumo S

Abstract excerpt

Nkx2.5 and Nkx2.6 are murine homologs of Drosophila tinman. Their genes are expressed in the ventral region of the pharynx at early stages of embryogenesis. However, no abnormalities in the pharynges of embryos with mutations in either Nkx2.5 or Nkx2.6 have been reported. To examine the function of Nkx2.5 and Nkx2.6 in the formation of the pharynx, we generated and analyzed Nkx2.5 and Nkx2.6 double-mutant mice....

Read the complete abstract on PubMed

Topics

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

Share to Heart
Share to Embryonic and Fetal Development
Share to Endoderm

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Genes, Homeobox

Share to Homeobox Protein Nkx-2.5

Share to In Situ Nick-End Labeling

Share to Pharynx

Share to Xenopus Proteins

Source

Open in PubMed Open full text

Identifiers

PMID: 11390666
DOI: 10.1128/MCB.21.13.4391-4398.2001
PMCID: PMC87098

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Nkx2.5 and Nkx2.6, homologs of Drosophila tinman, are required for development of the pharynx.PMID 11390666Read ↗

Phenotypic characterization of the murine Nkx2.6 homeobox gene by gene targeting.Semantic proximity Read ↗

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

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

tinman, a Drosophila homeobox gene required for heart and visceral mesoderm specification, may be represented by a family of genes in vertebrates: XNkx-2.3, a second vertebrate homologue of tinman.Semantic proximity Read ↗

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

Developmental paradigms in heart disease: insights from tinman.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 ↗

Nkx genes are essential for maintenance of ventricular identity.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 ↗

A systematic analysis of Tinman function reveals Eya and JAK-STAT signaling as essential regulators of muscle development.Semantic proximity Read ↗

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

Cooperative interaction of Nkx2.5 and Mef2c transcription factors during heart development.Semantic proximity Read ↗

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