Deletion of RBMX RGG/RG motif in Shashi-XLID syndrome leads to aberrant p53 activation and neuronal differentiation defects-Reference-Cited by-同舟云学术

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Deletion of RBMX RGG/RG motif in Shashi-XLID syndrome leads to aberrant p53 activation and neuronal differentiation defects

Published:2021-07 Issue:2 Volume:36 Page:109337
ISSN:2211-1247
Container-title:Cell Reports
language:en
Short-container-title:Cell Reports

Author:

Cai Ting,Cinkornpumin Jessica K.,Yu Zhenbao,Villarreal Oscar D.,Pastor William A.,Richard Stéphane

Funder

Canadian Institutes of Health Research

Fonds de Recherche du Québec - Santé

Publisher

Elsevier BV

Subject

General Biochemistry, Genetics and Molecular Biology

Reference72 articles.

1. Metabotropic glutamate receptor 5 responses dictate differentiation of neural progenitors to NMDA-responsive cells in fragile X syndrome;Achuta;Dev. Neurobiol.,2017

2. A genome-wide homologous recombination screen identifies the RNA-binding protein RBMX as a component of the DNA-damage response;Adamson;Nat. Cell Biol.,2012

3. Neuronal medium that supports basic synaptic functions and activity of human neurons in vitro;Bardy;Proc. Natl. Acad. Sci. USA,2015

4. Genomic and proteomic resolution of heterochromatin and its restriction of alternate fate genes;Becker;Mol. Cell,2017

5. Protein arginine methylation in mammals: Who, what, and why;Bedford;Mol. Cell,2009

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