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Article

Toward pathogenesis of Apert cleft palate: FGF, FGFR, and TGF beta genes are differentially expressed in sequential stages of human palatal shelf fusion.

The Cleft palate-craniofacial journal : official publication of the American Cleft Palate-Craniofacial Association - 1 May 2002

Britto Jonathan A, Evans Robert D, Hayward Richard D, Jones Barry M

Abstract excerpt

OBJECTIVE: Critical cellular events at the palatal medial edge epithelium (MEE) occur in unperturbed mammalian palatogenesis, the molecular control of which involves a number of growth factors including transforming growth factor beta 3 (TGF beta 3). Apert syndrome is a monogenic human disorder in which cleft palate has been significantly correlated to the fibroblast growth factor receptor (FGFR) 2-Ser252Trp...

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Source

Identifiers

PMID: 12019011
DOI: 10.1597/1545-1569_2002_039_0332_tpoacp_2.0.co_2

Genes

FGFR2
STAT1
FGF2
FGF4
FGF7
FGFR1
FGFR3

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

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Toward pathogenesis of Apert cleft palate: FGF, FGFR, and TGF beta genes are differentially expressed in sequential stages of human palatal shelf fusion.PMID 12019011Read ↗

From shape to cells: mouse models reveal mechanisms altering palate development in Apert syndrome.Semantic proximity Read ↗

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Negative autoregulation of fibroblast growth factor receptor 2 expression characterizing cranial development in cases of Apert (P253R mutation) and Pfeiffer (C278F mutation) syndromes and suggesting a basis for differences in their cranial phenotypes.Semantic proximity Read ↗

From genotype to phenotype: the differential expression of FGF, FGFR, and TGFbeta genes characterizes human cranioskeletal development and reflects clinical presentation in FGFR syndromes.Semantic proximity Read ↗

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