| Literature DB >> 27681385 |
Lijiang Ma1, Yavuz Bayram2, Heather M McLaughlin3, Megan T Cho3, Alyson Krokosky4, Clesson E Turner4, Kristin Lindstrom5, Caleb P Bupp6, Katey Mayberry6, Weiyi Mu7, Joann Bodurtha7, Veronique Weinstein8, Neda Zadeh9, Wendy Alcaraz10, Zöe Powis10, Yunru Shao2, Daryl A Scott2,11, Andrea M Lewis2, Janson J White2, Shalani N Jhangiani2,12, Elif Yilmaz Gulec13, Seema R Lalani2, James R Lupski2,12,14,15, Kyle Retterer3, Rhonda E Schnur3, Ingrid M Wentzensen3, Sherri Bale3, Wendy K Chung16.
Abstract
Intellectual disabilities are genetically heterogeneous and can be associated with congenital anomalies. Using whole-exome sequencing (WES), we identified five different de novo missense variants in the protein phosphatase-1 catalytic subunit beta (PPP1CB) gene in eight unrelated individuals who share an overlapping phenotype of dysmorphic features, macrocephaly, developmental delay or intellectual disability (ID), congenital heart disease, short stature, and skeletal and connective tissue abnormalities. Protein phosphatase-1 (PP1) is a serine/threonine-specific protein phosphatase involved in the dephosphorylation of a variety of proteins. The PPP1CB gene encodes a PP1 subunit that regulates the level of protein phosphorylation. All five altered amino acids we observed are highly conserved among the PP1 subunit family, and all are predicted to disrupt PP1 subunit binding and impair dephosphorylation. Our data suggest that our heterozygous de novo PPP1CB pathogenic variants are associated with syndromic intellectual disability.Entities:
Mesh:
Substances:
Year: 2016 PMID: 27681385 PMCID: PMC5663278 DOI: 10.1007/s00439-016-1731-1
Source DB: PubMed Journal: Hum Genet ISSN: 0340-6717 Impact factor: 4.132