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

A defect in a novel ADAMTS family member is the cause of the belted white-spotting mutation.

Development (Cambridge, England) - 1 Oct 2003

Rao Cherie, Foernzler Dorothee, Loftus Stacie K, Liu Shanming, McPherson John D, Jungers Katherine A, Apte Suneel S, Pavan William J, Beier David R

Abstract excerpt

Several features of the pigment defect in belted (bt) mutant mice suggest that it occurs as a result of a defect in melanocyte development that is unique from those described for other classical white-spotting mutations. We report here that bt mice carry mutations in Adamts20, a novel member of t...

Read the complete abstract on PubMed

Topics

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

Share to ADAM Proteins
Share to ADAMTS Proteins
Share to Embryo, Mammalian

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to In Situ Hybridization

Share to Melanocytes

Share to Metalloendopeptidases

Share to Pigmentation

Source

Identifiers

PMID: 12925592
DOI: 10.1242/dev.00668

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 1 Sept 2026. Prepared record publication-12925592-2026-09-01.1. Manifest publication-graph-cohort-2026-09-01.1.

Source receipt: PubMed via Helena Literature Corpus, retrieved 1 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

A defect in a novel ADAMTS family member is the cause of the belted white-spotting mutation.PMID 12925592Read ↗

The secreted metalloprotease ADAMTS20 is required for melanoblast survival.Semantic proximity Read ↗

Adamts9 is widely expressed during mouse embryo development.Semantic proximity Read ↗

Mutations in fibulin-1 and collagen IV suppress the short healthspan of mig-17/ADAMTS mutants in Caenorhabditis elegans.Semantic proximity Read ↗

Cooperation of two ADAMTS metalloproteases in closure of the mouse palate identifies a requirement for versican proteolysis in regulating palatal mesenchyme proliferation.Semantic proximity Read ↗

C. elegans ADAMTS ADT-2 regulates body size by modulating TGFβ signaling and cuticle collagen organization.Semantic proximity Read ↗

The secreted AdamTS-A metalloprotease is required for collective cell migration.Semantic proximity Read ↗

Genetic interactions among ADAMTS metalloproteases and basement membrane molecules in cell migration in Caenorhabditis elegans.Semantic proximity Read ↗

A new Adamts9 conditional mouse allele identifies its non-redundant role in interdigital web regression.Semantic proximity Read ↗

ADAMTS9 and ADAMTS20 are differentially affected by loss of B3GLCT in mouse model of Peters plus syndromeSemantic proximity Read ↗

Spotlight on spotted mice: a review of white spotting mouse mutants and associated human pigmentation disorders.Semantic proximity Read ↗

Melanocyte development in the mouse tail epidermis requires the Adamts9 metalloproteinase.Semantic proximity Read ↗

Identification and Characterization of ADAMTS-20 Defines a Novel Subfamily of Metalloproteinases-Disintegrins with Multiple Thrombospondin-1 Repeats and a Unique GON DomainSemantic proximity Read ↗

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