| Literature DB >> 27426734 |
Carine Le Goff1, Curtis Rogers2, Wilfried Le Goff3, Graziella Pinto4, Damien Bonnet5, Maya Chrabieh6, Olivier Alibeu7, Patrick Nistchke8, Arnold Munnich1, Capucine Picard9, Valérie Cormier-Daire10.
Abstract
Cardiospondylocarpofacial (CSCF) syndrome is characterized by growth retardation, dysmorphic facial features, brachydactyly with carpal-tarsal fusion and extensive posterior cervical vertebral synostosis, cardiac septal defects with valve dysplasia, and deafness with inner ear malformations. Whole-exome sequencing identified heterozygous MAP3K7 mutations in six distinct CSCF-affected individuals from four families and ranging in age from 5 to 37 years. MAP3K7 encodes transforming growth factor β (TGF-β)-activated kinase 1 (TAK1), which is involved in the mitogen-activated protein kinase (MAPK)-p38 signaling pathway. MAPK-p38 signaling was markedly altered when expression of non-canonical TGF-β-driven target genes was impaired. These findings support the loss of transcriptional control of the TGF-β-MAPK-p38 pathway in fibroblasts obtained from affected individuals. Surprisingly, although TAK1 is located at the crossroad of inflammation, immunity, and cancer, this study reports MAP3K7 mutations in a developmental disorder affecting mainly cartilage, bone, and heart.Entities:
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Year: 2016 PMID: 27426734 PMCID: PMC4974068 DOI: 10.1016/j.ajhg.2016.06.005
Source DB: PubMed Journal: Am J Hum Genet ISSN: 0002-9297 Impact factor: 11.025