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Evidence for pathogenicity of variant ATM Val1729Leu in a family with ataxia telangiectasia

Ataxia telangiectasia is a rare autosomal recessive multisystem disorder caused by mutations in the gene of ATM serine/threonine kinase. It is characterized by neurodegeneration, leading to severe ataxia, immunodeficiency, increased cancer susceptibility, and telangiectasia. Here, we discovered a co...

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Autores principales: Shalash, Ali S., Rösler, Thomas W., Salama, Mohamed, Pendziwiat, Manuela, Müller, Stefanie H., Hopfner, Franziska, Höglinger, Günter U., Kuhlenbäumer, Gregor
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8119284/
https://www.ncbi.nlm.nih.gov/pubmed/33779842
http://dx.doi.org/10.1007/s10048-021-00639-4
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author Shalash, Ali S.
Rösler, Thomas W.
Salama, Mohamed
Pendziwiat, Manuela
Müller, Stefanie H.
Hopfner, Franziska
Höglinger, Günter U.
Kuhlenbäumer, Gregor
author_facet Shalash, Ali S.
Rösler, Thomas W.
Salama, Mohamed
Pendziwiat, Manuela
Müller, Stefanie H.
Hopfner, Franziska
Höglinger, Günter U.
Kuhlenbäumer, Gregor
author_sort Shalash, Ali S.
collection PubMed
description Ataxia telangiectasia is a rare autosomal recessive multisystem disorder caused by mutations in the gene of ATM serine/threonine kinase. It is characterized by neurodegeneration, leading to severe ataxia, immunodeficiency, increased cancer susceptibility, and telangiectasia. Here, we discovered a co-segregation of two ATM gene variants with ataxia telangiectasia in an Egyptian family. While one of these variants (NM_000051.4(ATM_i001):p.(Val128*)) has previously been reported as pathogenic, the other one (NM_000051.4(ATM_i001):p.(Val1729Leu)) is regarded as a variant of uncertain significance. Our findings in this family provide additional evidence for causality of the second variant and argue that its status should be changed to pathogenic.
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spelling pubmed-81192842021-05-18 Evidence for pathogenicity of variant ATM Val1729Leu in a family with ataxia telangiectasia Shalash, Ali S. Rösler, Thomas W. Salama, Mohamed Pendziwiat, Manuela Müller, Stefanie H. Hopfner, Franziska Höglinger, Günter U. Kuhlenbäumer, Gregor Neurogenetics Short Communication Ataxia telangiectasia is a rare autosomal recessive multisystem disorder caused by mutations in the gene of ATM serine/threonine kinase. It is characterized by neurodegeneration, leading to severe ataxia, immunodeficiency, increased cancer susceptibility, and telangiectasia. Here, we discovered a co-segregation of two ATM gene variants with ataxia telangiectasia in an Egyptian family. While one of these variants (NM_000051.4(ATM_i001):p.(Val128*)) has previously been reported as pathogenic, the other one (NM_000051.4(ATM_i001):p.(Val1729Leu)) is regarded as a variant of uncertain significance. Our findings in this family provide additional evidence for causality of the second variant and argue that its status should be changed to pathogenic. Springer Berlin Heidelberg 2021-03-29 2021 /pmc/articles/PMC8119284/ /pubmed/33779842 http://dx.doi.org/10.1007/s10048-021-00639-4 Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Short Communication
Shalash, Ali S.
Rösler, Thomas W.
Salama, Mohamed
Pendziwiat, Manuela
Müller, Stefanie H.
Hopfner, Franziska
Höglinger, Günter U.
Kuhlenbäumer, Gregor
Evidence for pathogenicity of variant ATM Val1729Leu in a family with ataxia telangiectasia
title Evidence for pathogenicity of variant ATM Val1729Leu in a family with ataxia telangiectasia
title_full Evidence for pathogenicity of variant ATM Val1729Leu in a family with ataxia telangiectasia
title_fullStr Evidence for pathogenicity of variant ATM Val1729Leu in a family with ataxia telangiectasia
title_full_unstemmed Evidence for pathogenicity of variant ATM Val1729Leu in a family with ataxia telangiectasia
title_short Evidence for pathogenicity of variant ATM Val1729Leu in a family with ataxia telangiectasia
title_sort evidence for pathogenicity of variant atm val1729leu in a family with ataxia telangiectasia
topic Short Communication
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8119284/
https://www.ncbi.nlm.nih.gov/pubmed/33779842
http://dx.doi.org/10.1007/s10048-021-00639-4
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