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A mutational hotspot in AMOTL1 defines a new syndrome of orofacial clefting, cardiac anomalies, and tall stature
Journal article   Open access   Peer reviewed

A mutational hotspot in AMOTL1 defines a new syndrome of orofacial clefting, cardiac anomalies, and tall stature

Alanna Strong, Soumya Rao, Sandra von Hardenberg, Dong Li, Liza L Cox, Paul C Lee, Li Q Zhang, Waheed Awotoye, Tamir Diamond, Jessica Gold, …
American journal of medical genetics. Part A, Vol.191(5), pp.1227-1239
05/2023
DOI: 10.1002/ajmg.a.63130
PMCID: PMC10081944
PMID: 36751037
url
https://pmc.ncbi.nlm.nih.gov/articles/PMC10081944/pdf/nihms-1867303.pdfView
Open Access

Abstract

AMOTL1 encodes angiomotin-like protein 1, an actin-binding protein that regulates cell polarity, adhesion, and migration. The role of AMOTL1 in human disease is equivocal. We report a large cohort of individuals harboring heterozygous AMOTL1 variants and define a core phenotype of orofacial clefting, congenital heart disease, tall stature, auricular anomalies, and gastrointestinal manifestations in individuals with variants in AMOTL1 affecting amino acids 157-161, a functionally undefined but highly conserved region. Three individuals with AMOTL1 variants outside this region are also described who had variable presentations with orofacial clefting and multi-organ disease. Our case cohort suggests that heterozygous missense variants in AMOTL1, most commonly affecting amino acid residues 157-161, define a new orofacial clefting syndrome, and indicates an important functional role for this undefined region.
Congenital Heart Disease cleft lip YAP cleft palate genome sequencing exome sequencing

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