Inability to switch from ARID1A-BAF to ARID1B-BAF impairs exit from pluripotency and commitment towards neural crest formation in ARID1B-related neurodevelopmental disorders.
Journal
Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555
Informations de publication
Date de publication:
09 11 2021
09 11 2021
Historique:
received:
08
04
2021
accepted:
21
10
2021
entrez:
10
11
2021
pubmed:
11
11
2021
medline:
28
12
2021
Statut:
epublish
Résumé
Subunit switches in the BAF chromatin remodeler are essential during development. ARID1B and its paralog ARID1A encode for mutually exclusive BAF subunits. De novo ARID1B haploinsufficient mutations cause neurodevelopmental disorders, including Coffin-Siris syndrome, which is characterized by neurological and craniofacial features. Here, we leveraged ARID1B
Identifiants
pubmed: 34753942
doi: 10.1038/s41467-021-26810-x
pii: 10.1038/s41467-021-26810-x
pmc: PMC8578637
doi:
Substances chimiques
ARID1A protein, human
0
ARID1B protein, human
0
Chromatin
0
DNA-Binding Proteins
0
NANOG protein, human
0
Nanog Homeobox Protein
0
SOX2 protein, human
0
SOXB1 Transcription Factors
0
Transcription Factors
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
6469Subventions
Organisme : NCI NIH HHS
ID : R01 CA257251
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL127895
Pays : United States
Organisme : NCI NIH HHS
ID : T32 CA009171
Pays : United States
Informations de copyright
© 2021. The Author(s).
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