ArticleNeurobiology of learning and memory2016
CaMKII regulates proteasome phosphorylation and activity and promotes memory destabilization following retrieval.
Article in Neurobiology of learning and memory, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.
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Who cites it
65 citing papers in PubMed, 1 synthesis or guideline pooled it, 114 citations in OpenAlex.
- Different temporal windows for CB1 receptor involvement in contextual fear memory destabilisation in the amygdala and hippocampus.PloS one · 2019Pooled it
- Temporal- and sex-specific changes in proteasome-dependent and independent polyubiquitination in the amygdala during fear memory formation.Learning & memory (Cold Spring Harbor, N.Y.) · 2026Article
- The Janus face of CaMKII: from memory consolidation to neurotoxic switch in Alzheimer's disease.Archives of toxicology · 2025Review
- Investigating the neuronal role of the proteasomal ATPase subunit gene PSMC5 in neurodevelopmental proteasomopathies.Nature communications · 2025Article
- Degradation of CaMKII is stimulated by its active conformation.The Journal of biological chemistry · 2025Article
- Not the same as it ever was: A review of memory modification, updating, and distortion in humans and rodents.Neuroscience and biobehavioral reviews · 2025Review
- Windows of change: Revisiting temporal and molecular dynamics of memory reconsolidation and persistence.Neuroscience and biobehavioral reviews · 2025Review
- How Fear Memory is Updated: From Reconsolidation to Extinction?Neuroscience bulletin · 2025Review
- Activation of the 26S Proteasome to Reduce Proteotoxic Stress and Improve the Efficacy of PROTACs.ACS pharmacology & translational science · 2025Review
- CaMKII modulates memory destabilization by regulating the interaction of theta and gamma oscillations.Frontiers in cellular neuroscience · 2025Article
- Altered socio-affective communication and amygdala development in mice with protocadherin10-deficient interneurons.Open biology · 2024Article
- The ubiquitin-proteasome system and learning-dependent synaptic plasticity - A 10 year update.Neuroscience and biobehavioral reviews · 2023Review
- Muscarinic receptor activation overrides boundary conditions on memory updating in a calcium/calmodulin-dependent manner.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023Article
- Memory retrieval, reconsolidation, and extinction: Exploring the boundary conditions of post-conditioning cue exposure.Frontiers in synaptic neuroscience · 2023Review
- The role of hippocampal CaMKII in resilience to trauma-related psychopathology.Neurobiology of stress · 2022Article
- Trauma and Remembering: From Neuronal Circuits to Molecules.Life (Basel, Switzerland) · 2022Review
- Sex differences in training-induced activity of the ubiquitin proteasome system in the dorsal hippocampus and medial prefrontal cortex of male and female mice.Learning & memory (Cold Spring Harbor, N.Y.) · 2022Article
- The epigenetic role of proteasome subunit RPT6 during memory formation in female rats.Learning & memory (Cold Spring Harbor, N.Y.) · 2022Article
- Prelimbic proBDNF Facilitates Retrieval-Dependent Fear Memory Destabilization by Regulation of Synaptic and Neural Functions in Juvenile Rats.Molecular neurobiology · 2022Article
- Physiological Overview of the Potential Link between the UPS and CaAntioxidants (Basel, Switzerland) · 2022Review
5 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Numerous studies have suggested that memories "destabilize" and require de novo protein synthesis in order to reconsolidate following retrieval, but very little is known about how this destabilization process is regulated. Recently, ubiquitin-proteasome mediated protein degradation has been identified as a critical regulator of memory trace destabilization following retrieval, though the specific mechanisms controlling retrieval-induced changes in ubiquitin-proteasome activity remain equivocal. Here, we found that proteasome activity is increased in the amygdala in a CaMKII-dependent manner following the retrieval of a contextual fear memory. We show that in vitro inhibition of CaMKII reversed retrieval-induced increases in proteasome activity. Additionally, in vivo pharmacological blockade of CaMKII abolished increases in proteolytic activity and activity related regulatory phosphorylation in the amygdala following retrieval, suggesting that CaMKII was "upstream" of protein degradation during the memory reconsolidation process. Consistent with this, while inhibiting CaMKII in the amygdala did not impair memory following retrieval, it completely attenuated the memory impairments that resulted from post-retrieval protein synthesis blockade. Collectively, these results suggest that CaMKII controls the initiation of the memory reconsolidation process through regulation of the proteasome.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.