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

Edar/Eda interactions regulate enamel knot formation in tooth morphogenesis.

Development (Cambridge, England) - 1 Nov 2000

Tucker A S, Headon D J, Schneider P, Ferguson B M, Overbeek P, Tschopp J, Sharpe P T

Abstract excerpt

tabby and downless mutant mice have apparently identical defects in teeth, hair and sweat glands. Recently, genes responsible for these spontaneous mutations have been identified. downless (Dl) encodes Edar, a novel member of the tumour necrosis factor (TNF) receptor family, containing the charac...

Read the complete abstract on PubMed

Topics

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

Share to Amelogenesis
Share to Ectodysplasins
Share to Edar Receptor

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Embryonic and Fetal Development

Share to Odontogenesis

Share to Organ Culture Techniques

Share to Receptors, Tumor Necrosis Factor

Source

Identifiers

PMID: 11023871
DOI: 10.1242/dev.127.21.4691

Genes

TNF

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026. Prepared record publication-11023871-2026-09-04.2. Manifest publication-graph-cohort-2026-09-04.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 4 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Edar/Eda interactions regulate enamel knot formation in tooth morphogenesis.PMID 11023871Read ↗

Regulation of hair follicle development by the TNF signal ectodysplasin and its receptor Edar.Semantic proximity Read ↗

Gene defect in ectodermal dysplasia implicates a death domain adapter in development.Semantic proximity Read ↗

Traf6 is essential for murine tooth cusp morphogenesis.Semantic proximity Read ↗

Cusp patterning defect in Tabby mouse teeth and its partial rescue by FGF.Semantic proximity Read ↗

Involvement of a novel Tnf receptor homologue in hair follicle induction.Semantic proximity Read ↗

Ectodysplasin-A1 is sufficient to rescue both hair growth and sweat glands in Tabby miceSemantic proximity Read ↗

Signaling and subcellular localization of the TNF receptor Edar.Semantic proximity Read ↗

Edar and Troy signalling pathways act redundantly to regulate initiation of hair follicle developmentSemantic proximity Read ↗

Distinct impacts of Eda and Edar loss of function on the mouse dentition.Semantic proximity Read ↗

Ectodysplasin regulates the lymphotoxin-beta pathway for hair differentiation.Semantic proximity Read ↗

Inducible mEDA-A1 transgene mediates sebaceous gland hyperplasia and differential formation of two types of mouse hair folliclesSemantic proximity Read ↗

The Tabby phenotype is caused by mutation in a mouse homologue of the EDA gene that reveals novel mouse and human exons and encodes a protein (ectodysplasin-A) with collagenous domains.Semantic proximity Read ↗

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