ArticlebioRxiv : the preprint server for biology2025
CaMKII monomers are sufficient for GluN2B binding, co-condensation, and synaptic potentiation.
Carolyn Nicole Brown, C Madison Barker, Carley N Miller, Jason Aoto, Steven J Coultrap, K Ulrich Bayer
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In one paragraphArticle in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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4 · The recordCorrections and comments
5 · Who and what moneyAuthors and funding
6 authors.
Carolyn Nicole BrownDepartment of Pharmacology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.
C Madison BarkerDepartment of Pharmacology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.
Carley N MillerDepartment of Pharmacology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.
Jason AotoDepartment of Pharmacology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.
Steven J CoultrapDepartment of Pharmacology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.
K Ulrich BayerDepartment of Pharmacology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.ORCID 0000-0003-0893-2200 Funding
Medical Scientist Training ProgramT32GM008497 · NIGMS · UNIVERSITY OF COLORADO DENVER · PI WILSON, CARA C. · 1993 to 2022
$15.2MPREDOCTORAL TRAINING PROGRAM IN PHARMACOLOGYT32GM007635 · NIGMS · UNIVERSITY OF COLORADO DENVER · PI DELL'ACQUA, MARK L · 1985 to 2023
$6.1MCaMKII substrate-selection in opposing forms of synaptic plasticityR01NS081248 · NINDS · UNIVERSITY OF COLORADO DENVER · PI K. Ulrich Bayer · 2013 to 2026
$4.9MCaMKII nitrosylation in the age-related decline of synaptic plasticityR01AG067713 · NIA · UNIVERSITY OF COLORADO DENVER · PI BAYER, K. ULRICH · 2020 to 2024
$2.7MCaMKII in global cerebral ischemiaR01NS080851 · NINDS · UNIVERSITY OF COLORADO DENVER · PI BAYER, K. ULRICH, HERSON, PACO S · 2013 to 2017
$2.1MCaMKII in global cerebral ischemia: mechanisms and therapeutic interventionR01NS118786 · NINDS · UNIVERSITY OF COLORADO DENVER · PI BAYER, K. ULRICH, HERSON, PACO S · 2021 to 2025
$1.9MThe identification and interrogation of novel intracellular proteins that underlie the distinct nanoscopic architecture of Neurexin-1 and Neurexin-3R21MH140328 · NIMH · UNIVERSITY OF COLORADO DENVER · PI AOTO, JASON · 2025 to 2025
$422kImpact of stress on heroin seeking and ventral pallidal synapse functionF30DA057053 · NIDA · UNIVERSITY OF COLORADO DENVER · PI MILLER, CARLEY N · 2022 to 2024
$117kMolecular computation by the CaMKII holoenzymeF31NS129254 · NINDS · UNIVERSITY OF COLORADO DENVER · PI BROWN, CAROLYN NICOLE · 2022 to 2024
$112kNIA NIH HHS R01 AG067713NIDA NIH HHS F30 DA057053NIGMS NIH HHS T32 GM007635NIGMS NIH HHS T32 GM008497NIMH NIH HHS R21 MH140328NINDS NIH HHS F31 NS129254NINDS NIH HHS R01 NS080851NINDS NIH HHS R01 NS081248NINDS NIH HHS R01 NS118786
6 · The paper itselfAbstract
Cognitive functions require synaptic plasticity, specifically long-term potentiation (LTP). LTP is thought to require CaMKII binding to the NMDA-type glutamate receptor subunit GluN2B, but this poses a major conundrum: Truncated CaMKII monomers (without the hub domain that forms 12meric holoenzymes) fail to bind GluN2B, but still potentiate synapses when made constitutively active. We hypothesized that CaMKII monomer binding to GluN2B has just eluded detection. Instead, even though full-length CaMKII monomers (with hub domain mutations) were found to indeed bind and even co-condensate with GluN2B, truncated monomers were not. Nonetheless, truncated monomers still potentiated synapses, even in neurons with GluN2B mutations that ablate CaMKII binding. However, potentiation occurred only with monomers that were made Ca
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PMID40631338
PMCPMC12236485
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