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Article

Crkl deficiency disrupts Fgf8 signaling in a mouse model of 22q11 deletion syndromes.

Developmental cell - 1 Jan 2006

Moon Anne M, Guris Deborah L, Seo Ji-heui, Li Leiming, Hammond Jennetta, Talbot Amy, Imamoto Akira

Abstract excerpt

Deletions on chromosome 22q11.21 disrupt pharyngeal and cardiac development and cause DiGeorge and related human syndromes. CRKL (CRK-Like) lies within 22q11.21, and Crkl-/- mice have phenotypic features of 22q11 deletion (del22q11) syndromes. While human FGF8 does not localize to 22q11, deficiency of Fgf8 also generates many features of del22q11 syndrome in mice. Since Fgf8 signals via receptor-type tyrosine...

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Source

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Identifiers

PMID: 16399079
DOI: 10.1016/j.devcel.2005.12.003
PMCID: PMC1780033

Genes

CRK
CRKL
FGF8

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

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