Homer1a regulates Shank3 expression and underlies behavioral vulnerability to stress in a model of Phelan-McDermid syndrome.
Animals
Chromosome Deletion
Chromosome Disorders
/ metabolism
Chromosomes, Human, Pair 22
/ metabolism
Disease Models, Animal
Gene Expression
/ genetics
Gene Expression Regulation
/ genetics
Homer Scaffolding Proteins
/ metabolism
Male
Mice
Mice, Inbred C57BL
Mice, Transgenic
Microfilament Proteins
/ genetics
Nerve Tissue Proteins
/ genetics
Phenotype
Pyramidal Cells
/ metabolism
Stress, Psychological
/ metabolism
Homer1a
NMDAR
Phelan-McDermid syndrome
Shank3
autism
social behavior
stress
synapse
Journal
Cell reports
ISSN: 2211-1247
Titre abrégé: Cell Rep
Pays: United States
ID NLM: 101573691
Informations de publication
Date de publication:
16 11 2021
16 11 2021
Historique:
received:
08
06
2021
revised:
13
09
2021
accepted:
26
10
2021
entrez:
17
11
2021
pubmed:
18
11
2021
medline:
15
2
2022
Statut:
ppublish
Résumé
Mutations of SHANK3 cause Phelan-McDermid syndrome (PMS), and these individuals can exhibit sensitivity to stress, resulting in behavioral deterioration. Here, we examine the interaction of stress with genotype using a mouse model with face validity to PMS. In Shank3
Identifiants
pubmed: 34788607
pii: S2211-1247(21)01496-0
doi: 10.1016/j.celrep.2021.110014
pii:
doi:
Substances chimiques
HOMER1 protein, human
0
Homer Scaffolding Proteins
0
Microfilament Proteins
0
Nerve Tissue Proteins
0
SHANK3 protein, human
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
110014Subventions
Organisme : NINDS NIH HHS
ID : R35 NS097966
Pays : United States
Informations de copyright
Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of interests The authors declare no competing interests.