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PKMζ-KIBRA interactions, molecular turnover, and memory.

Changchi Hsieh1, David A Cano2, Panayiotis Tsokas1,3,4

  • 1Department of Physiology and Pharmacology, The Robert F. Furchgott Center for Neural and Behavioral Science, State University of New York Downstate Health Sciences University; Brooklyn, New York 11203, USA.

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|January 16, 2026
PubMed
Summary
This summary is machine-generated.

Persistent KIBRA-PKMζ oligomers maintain long-term memory by overcoming molecular turnover. New structures reveal how inhibitors disrupt these essential molecular interactions for memory persistence.

Keywords:
PKM-zetaPKMzetaWWC1long-term potentiation (LTP)

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Structural Biology

Background:

  • Persistent interaction between KIBRA and PKMζ is vital for synaptic plasticity and memory.
  • Molecular turnover challenges the stability of long-term memory.
  • Oligomeric structures are hypothesized to overcome molecular degradation.

Purpose of the Study:

  • To elucidate the structural basis of KIBRA-PKMζ interactions.
  • To investigate the mechanism by which KIBRA-PKMζ oligomers maintain long-term memory.
  • To analyze the action of KIBRA-PKMζ interaction inhibitors.

Main Methods:

  • Utilized AlphaFold 3 for structural prediction of KIBRA-PKMζ complexes.
  • Employed KIBRA-PKMζ inhibitors (K-ZAP and ζ-stat) to study memory disruption.
  • Assessed the impact of inhibitors on established spatial memory.

Main Results:

  • Predicted structures of KIBRA-PKMζ heterodimers and heterohexamers.
  • Identified distinct inhibition mechanisms for K-ZAP (heterodimer formation) and ζ-stat (oligomerization).
  • Demonstrated that ζ-stat disrupts 1-month-old spatial memory, similar to K-ZAP.

Conclusions:

  • Continual formation of KIBRA-PKMζ oligomers is a key mechanism for long-term memory persistence.
  • Structural insights explain how inhibitors impair memory maintenance.
  • Oligomerization is crucial for overcoming molecular turnover in memory consolidation.