ArticlePloS one2020
The CaMKII K42M and K42R mutations are equivalent in suppressing kinase activity and targeting.
Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Multicolor Quantum Dot Tracking Uncovers Phenotypic Rescue of DAT A559V Aberrant Diffusion Upon D2R Antagonism.ACS chemical neuroscience · 2026Article
- Studying CaMKII: Tools and standards.Cell reports · 2024Review
- Real-time single-molecule imaging of CaMKII-calmodulin interactions.Biophysical journal · 2024Article
- Activity-Dependent Stabilization of Nascent Dendritic Spines Requires Nonenzymatic CaMKIIα Function.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Article
- Distinct synaptic pools of DAPK1 differentially regulate activity-dependent synaptic CaMKII accumulation.iScience · 2023Article
- Short-term CaMKII inhibition with tatCN19o does not erase pre-formed memory and is neuroprotective in non-rodents.bioRxiv : the preprint server for biology · 2023Article
- Aβ-induced synaptic impairments require CaMKII activity that is stimulated by indirect signaling events.iScience · 2022Article
- Article
- Young DAPK1 knockout mice have altered presynaptic function.Journal of neurophysiology · 2021Article
- CaMKII binding to GluN2B at S1303 has no role in acute or inflammatory pain.Brain research · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
CaMKII is an important mediator of forms of synaptic plasticity that are thought to underly learning and memory. The CaMKII mutants K42M and K42R have been used interchangeably as research tools, although some reported phenotypic differences suggest that they may differ in the extent to which they impair ATP binding. Here, we directly compared the two mutations at the high ATP concentrations that exist within cells (~4 mM). We found that both mutations equally blocked GluA1 phosphorylation in vitro and GluN2B binding within cells. Both mutations also reduced but did not completely abolish CaMKII T286 autophosphorylation in vitro or CaMKII movement to excitatory synapses in neurons. Thus, despite previously suggested differences, both mutations appear to interfere with ATP binding to the same extent.
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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.