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Article

Mice null for sox18 are viable and display a mild coat defect.

Molecular and cellular biology - 1 Dec 2000

Pennisi D, Bowles J, Nagy A, Muscat G, Koopman P

Abstract excerpt

We have previously shown that Sox18 is expressed in developing vascular endothelium and hair follicles during mouse embryogenesis and that point mutations in Sox18 are the underlying cause of cardiovascular and hair follicle defects in ragged (Ra) mice. Here we describe the analysis of Sox18(-/-) mice produced by gene targeting. Despite the profound defects seen in Ra mice, Sox18(-/-) mice have no obvious...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

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Identifiers

PMID: 11094083
DOI: 10.1128/MCB.20.24.9331-9336.2000
PMCID: PMC102189

Genes

SOX18
SOX7

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.

Related research

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Mice null for sox18 are viable and display a mild coat defect.PMID 11094083Read ↗

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Essential Role for ADAM19 in Cardiovascular MorphogenesisSemantic proximity Read ↗

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The Sox17CreERT2 knock-in mouse line displays spatiotemporal activation of Cre recombinase in distinct Sox17 lineage progenitors.Semantic proximity Read ↗

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Mutations in the transcription factor gene SOX18 underlie recessive and dominant forms of hypotrichosis-lymphedema-telangiectasia.Semantic proximity Read ↗

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