Your browser doesn't support javascript.
loading
Mutations of PTPN23 in developmental and epileptic encephalopathy.
Sowada, Nadine; Hashem, Mais Omar; Yilmaz, Rüstem; Hamad, Muddathir; Kakar, Naseebullah; Thiele, Holger; Arold, Stefan T; Bode, Harald; Alkuraya, Fowzan S; Borck, Guntram.
Afiliação
  • Sowada N; Institute of Human Genetics, University of Ulm, Albert-Einstein-Allee 11, 89081, Ulm, Germany.
  • Hashem MO; Department of Genetics, King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia.
  • Yilmaz R; Institute of Human Genetics, University of Ulm, Albert-Einstein-Allee 11, 89081, Ulm, Germany.
  • Hamad M; Department of Pediatrics, King Khalid University Hospital, Riyadh, Saudi Arabia.
  • Kakar N; Institute of Human Genetics, University of Ulm, Albert-Einstein-Allee 11, 89081, Ulm, Germany.
  • Thiele H; Department of Biotechnology, BUITEMS, Quetta, Pakistan.
  • Arold ST; Cologne Center for Genomics, University of Cologne, Cologne, Germany.
  • Bode H; Division of Biological and Environmental Sciences and Engineering (BESE), Computational Bioscience Research Center (CBRC), King Abdullah University of Science and Technology (KAUST), Thuwal, Saudi Arabia.
  • Alkuraya FS; Division of Pediatric Neurology, Children's Hospital, University of Ulm, Ulm, Germany.
  • Borck G; Department of Genetics, King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia.
Hum Genet ; 136(11-12): 1455-1461, 2017 11.
Article em En | MEDLINE | ID: mdl-29090338
Developmental and epileptic encephalopathies (DEE) are a heterogeneous group of neurodevelopmental disorders with poor prognosis. Recent discoveries have greatly expanded the repertoire of genes that are mutated in epileptic encephalopathies and DEE, often in a de novo fashion, but in many patients, the disease remains molecularly uncharacterized. Here, we describe a new form of DEE in patients with likely deleterious biallelic variants in PTPN23. The phenotype is characterized by early onset drug-resistant epilepsy, severe and global developmental delay, microcephaly, and sometimes premature death. PTPN23 encodes a tyrosine phosphatase with strong brain expression, and its knockout in mouse is embryonically lethal. Structural modeling supports a deleterious effect of the identified alleles. Our data suggest that PTPN23 mutations cause a rare severe form of autosomal-recessive DEE in humans, a finding that requires confirmation.
Assuntos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Espasmos Infantis / Deficiências do Desenvolvimento / Proteínas Tirosina Fosfatases não Receptoras / Mutação Tipo de estudo: Prognostic_studies Limite: Adult / Female / Humans / Male / Newborn Idioma: En Revista: Hum Genet Ano de publicação: 2017 Tipo de documento: Article País de afiliação: Alemanha

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Espasmos Infantis / Deficiências do Desenvolvimento / Proteínas Tirosina Fosfatases não Receptoras / Mutação Tipo de estudo: Prognostic_studies Limite: Adult / Female / Humans / Male / Newborn Idioma: En Revista: Hum Genet Ano de publicação: 2017 Tipo de documento: Article País de afiliação: Alemanha