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Article

SPECC1L deficiency results in increased adherens junction stability and reduced cranial neural crest cell delamination.

Scientific reports - 20 Jan 2016

Wilson Nathan R, Olm-Shipman Adam J, Acevedo Diana S, Palaniyandi Kanagaraj, Hall Everett G, Kosa Edina, Stumpff Kelly M, Smith Guerin J, Pitstick Lenore, Liao Eric C, Bjork Bryan C, Czirok Andras, Saadi Irfan

Abstract excerpt

Cranial neural crest cells (CNCCs) delaminate from embryonic neural folds and migrate to pharyngeal arches, which give rise to most mid-facial structures. CNCC dysfunction plays a prominent role in the etiology of orofacial clefts, a frequent birth malformation. Heterozygous mutations in SPECC1L have been identified in patients with atypical and syndromic clefts. Here, we report that in SPECC1L-knockdown cultured...

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Identifiers

PMID: 26787558
DOI: 10.1038/srep17735
PMCID: PMC4726231

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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.

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SPECC1L deficiency results in increased adherens junction stability and reduced cranial neural crest cell delamination.PMID 26787558Read ↗

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<i>Cse1l</i> Regulates Neural Crest Cell Survival and is Critical for Craniofacial and Cardiac DevelopmentSemantic proximity Read ↗

In-frame deletion of SPECC1L microtubule binding domain results in embryonic tissue movement and fusion defectsSemantic proximity Read ↗

Disruption of the nectin-afadin complex recapitulates features of the human cleft lip/palate syndrome CLPED1.Semantic proximity Read ↗

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