CAMDI interacts with the human memory-associated protein KIBRA and regulates AMPAR cell surface expression and cognition.

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  • Additional Information
    • Source:
      Publisher: Public Library of Science Country of Publication: United States NLM ID: 101285081 Publication Model: eCollection Cited Medium: Internet ISSN: 1932-6203 (Electronic) Linking ISSN: 19326203 NLM ISO Abbreviation: PLoS One Subsets: MEDLINE
    • Publication Information:
      Original Publication: San Francisco, CA : Public Library of Science
    • Subject Terms:
      Cognition* ; Memory*; Cell Membrane/*metabolism ; Intracellular Signaling Peptides and Proteins/*metabolism ; Nerve Tissue Proteins/*metabolism ; Phosphoproteins/*metabolism ; Receptors, AMPA/*metabolism; Animals ; Cell Line, Tumor ; Endocytosis ; Humans ; Long-Term Potentiation ; Mice, Knockout ; Protein Binding ; Spatial Memory ; rab GTP-Binding Proteins/metabolism
    • Abstract:
      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.
      Competing Interests: The authors have declared that no competing interests exist.
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    • Accession Number:
      0 (CCDC141 protein, mouse)
      0 (Intracellular Signaling Peptides and Proteins)
      0 (Nerve Tissue Proteins)
      0 (Phosphoproteins)
      0 (Receptors, AMPA)
      0 (Wwc1 protein, mouse)
      EC 3.6.1.- (rab11 protein)
      EC 3.6.5.2 (rab GTP-Binding Proteins)
    • Publication Date:
      Date Created: 20191116 Date Completed: 20200323 Latest Revision: 20200323
    • Publication Date:
      20240104
    • Accession Number:
      PMC6857912
    • Accession Number:
      10.1371/journal.pone.0224967
    • Accession Number:
      31730661