Equivalent missense variant in the FOXP2 and FOXP1 transcription factors causes distinct neurodevelopmental disorders-Reference-Cited by-同舟云学术

Equivalent missense variant in the FOXP2 and FOXP1 transcription factors causes distinct neurodevelopmental disorders

Published:2017-08-14 Issue:11 Volume:38 Page:1542-1554
ISSN:1059-7794
Container-title:Human Mutation
language:en
Short-container-title:Human Mutation

Author:

Sollis Elliot¹^ORCID,Deriziotis Pelagia¹^ORCID,Saitsu Hirotomo²^ORCID,Miyake Noriko³^ORCID,Matsumoto Naomichi³^ORCID,Hoffer Mariëtte J.V.⁴^ORCID,Ruivenkamp Claudia A.L.⁴^ORCID,Alders Mariëlle⁵^ORCID,Okamoto Nobuhiko⁶^ORCID,Bijlsma Emilia K.⁴,Plomp Astrid S.⁵,Fisher Simon E.¹⁷^ORCID

Affiliation:

1. Language and Genetics Department Max Planck Institute for Psycholinguistics Nijmegen The Netherlands

2. Department of Biochemistry Hamamatsu University School of Medicine Hamamatsu Japan

3. Department of Human Genetics Yokohama City University Graduate School of Medicine Yokohama Japan

4. Department of Clinical Genetics Leiden University Medical Center Leiden The Netherlands

5. Department of Clinical Genetics Academic Medical Center Amsterdam The Netherlands

6. Department of Medical Genetics Osaka Medical Center and Research Institute for Maternal and Child Health Osaka Japan

7. Donders Institute for Brain Cognition and Behaviour Nijmegen The Netherlands

Funder

Max-Planck-Gesellschaft

Japan Agency for Medical Research and Development

Publisher

Wiley

Subject

Genetics (clinical),Genetics

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1002/humu.23303

Reference54 articles.

1. A method and server for predicting damaging missense mutations

2. FoxP1 orchestration of ASD-relevant signaling pathways in the striatum

3. Brain-specific Foxp1 deletion impairs neuronal development and causes autistic-like behaviour

4. A Novel Missense Mutation in Human TTF-2 (FKHL15) Gene Associated with Congenital Hypothyroidism But Not Athyreosis

5. Whole-exome sequencing in the molecular diagnosis of individuals with congenital anomalies of the kidney and urinary tract and identification of a new causative gene

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