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Article

Therapeutic effect of nanogel-based delivery of soluble FGFR2 with S252W mutation on craniosynostosis.

PloS one - 1 Jan 2014

Yokota Masako, Kobayashi Yukiho, Morita Jumpei, Suzuki Hiroyuki, Hashimoto Yoshihide, Sasaki Yoshihiro, Akiyoshi Kazunari, Moriyama Keiji

Abstract excerpt

Apert syndrome is an autosomal dominantly inherited disorder caused by missense mutations in fibroblast growth factor receptor 2 (FGFR2). Surgical procedures are frequently required to reduce morphological and functional defects in patients with Apert syndrome; therefore, the development of noninvasive procedures to treat Apert syndrome is critical. Here we aimed to clarify the etiological mechanisms of...

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Share to Acrocephalosyndactylia
Share to Calcification, Physiologic

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

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Identifiers

PMID: 25003957
DOI: 10.1371/journal.pone.0101693
PMCID: PMC4086955

Genes

FGFR2

Variants

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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Therapeutic effect of nanogel-based delivery of soluble FGFR2 with S252W mutation on craniosynostosis.PMID 25003957Read ↗

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Insights and future directions of potential genetic therapy for Apert syndrome: A systematic review.Semantic proximity Read ↗

A Ser252Trp mutation in fibroblast growth factor receptor 2 (FGFR2) mimicking human Apert syndrome reveals an essential role for FGF signaling in the regulation of endochondral bone formation.Semantic proximity Read ↗

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