CAMDI interacts with the human memory-associated protein KIBRA and regulates AMPAR cell surface expression and cognition.
Animals
Cell Line, Tumor
Cell Membrane
/ metabolism
Cognition
Endocytosis
Humans
Intracellular Signaling Peptides and Proteins
/ metabolism
Long-Term Potentiation
Memory
Mice, Knockout
Nerve Tissue Proteins
/ metabolism
Phosphoproteins
/ metabolism
Protein Binding
Receptors, AMPA
/ metabolism
Spatial Memory
rab GTP-Binding Proteins
/ metabolism
Journal
PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081
Informations de publication
Date de publication:
2019
2019
Historique:
received:
08
05
2019
accepted:
25
10
2019
entrez:
16
11
2019
pubmed:
16
11
2019
medline:
24
3
2020
Statut:
epublish
Résumé
Little is known about the molecular mechanisms of cognitive deficits in psychiatric disorders. CAMDI is a psychiatric disorder-related factor, the deficiency of which in mice results in delayed neuronal migration and psychiatrically abnormal behaviors. Here, we found that CAMDI-deficient mice exhibited impaired recognition memory and spatial reference memory. Knockdown of CAMDI in hippocampal neurons increased the amount of internalized alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptor (AMPAR) and attenuated the chemical long-term potentiation (LTP)-dependent cell surface expression of AMPAR. KIBRA was identified as a novel CAMDI-binding protein that retains AMPAR in the cytosol after internalization. KIBRA inhibited CAMDI-dependent Rab11 activation, thereby attenuating AMPAR cell surface expression. These results suggest that CAMDI regulates AMPAR cell surface expression during LTP. CAMDI dysfunction may partly explain the mechanism underlying cognitive deficits in psychiatric diseases.
Identifiants
pubmed: 31730661
doi: 10.1371/journal.pone.0224967
pii: PONE-D-19-13012
pmc: PMC6857912
doi:
Substances chimiques
CCDC141 protein, mouse
0
Intracellular Signaling Peptides and Proteins
0
Nerve Tissue Proteins
0
Phosphoproteins
0
Receptors, AMPA
0
Wwc1 protein, mouse
0
rab11 protein
EC 3.6.1.-
rab GTP-Binding Proteins
EC 3.6.5.2
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e0224967Déclaration de conflit d'intérêts
The authors have declared that no competing interests exist.
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