ArticleScience advances2021
CaMKII holoenzyme mechanisms that govern the LTP versus LTD decision.
Article in Science advances, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
45 citing papers in PubMed, 70 citations in OpenAlex.
- Neuroligins and Neuropathic Pain: Insights into Synaptic Plasticity and Pain Transmission.Biology · 2026Review
- Synaptic Plasticity as a Function of the Temporal Derivative.bioRxiv : the preprint server for biology · 2026Article
- Depressive and Anxiety Symptoms in Women with Polycystic Ovary Syndrome: A Meta-Analysis.Journal of clinical medicine · 2026Review
- CaMKII as a Multimodal Signalling Hub in Neural Connectivity and Vulnerability.Molecular neurobiology · 2026Review
- Convergence and divergence of molecular mechanisms in Hebbian and homeostatic plasticity.Frontiers in synaptic neuroscience · 2026Review
- Widely Used CaMKII Regulatory Segment Mutations Cause Tight Actinin Binding and Dendritic Spine Enlargement in Unstimulated Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- The CaMKII D135N mutation blocks kinase activity and reduces GluN2B binding.bioRxiv : the preprint server for biology · 2025Article
- Long-term potentiation and long-term depression are both impaired afterBiomedical physics & engineering express · 2025Article
- Aβ impairs the LTP-related movement of endogenous CaMKII but not of exogenous GFP-CaMKII.Molecular biology of the cell · 2025Article
- The neuroprotective γ-hydroxybutyrate analog 3-hydroxycyclopent-1-enecarboxylic acid does not directly affect CaMKIIα autophosphorylation at T286 or binding to GluN2B.Molecular pharmacology · 2025Article
- Oxygen/glucose-deprivation causes long-term impairment of synaptic CaMKII movement.bioRxiv : the preprint server for biology · 2025Article
- MicroRNAs modulate CaMKIIα/SIRT1 signaling pathway as a biomarker of cognitive ability in adolescents.Brain, behavior, & immunity - health · 2025Article
- Release your inhibitions: The cell biology of GABAergic postsynaptic plasticity.Current opinion in neurobiology · 2025Review
- A synapse-specific refractory period for plasticity at individual dendritic spines.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- LTP expression mediated by autonomous activity of GluN2B-bound CaMKII.Cell reports · 2024Article
- Induction of LTP mechanisms in dually innervated dendritic spines.Scientific reports · 2024Article
- A synapse-specific refractory period for plasticity at individual dendritic spines.bioRxiv : the preprint server for biology · 2024Article
- TRPM2 and CaMKII Signaling Drives Excessive GABAergic Synaptic Inhibition Following Ischemia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Studying CaMKII: Tools and standards.Cell reports · 2024Review
- A biochemical description of postsynaptic plasticity-with timescales ranging from milliseconds to seconds.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Higher brain functions are thought to require synaptic frequency decoding that can lead to long-term potentiation (LTP) or depression (LTD). We show that the LTP versus LTD decision is determined by complex cross-regulation of T286 and T305/306 autophosphorylation within the 12meric CaMKII holoenzyme, which enabled molecular computation of stimulus frequency, amplitude, and duration. Both LTP and LTD require T286 phosphorylation, but T305/306 phosphorylation selectively promoted LTD. In response to excitatory LTP versus LTD stimuli, the differential T305/306 phosphorylation directed CaMKII movement to either excitatory or inhibitory synapses, thereby coordinating plasticity at both synapse types. Fast T305/306 phosphorylation required prior T286 phosphorylation and then curbed CaMKII activity by two mechanisms: (i) a cis-subunit reaction reduced both Ca
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What OpenQuestion holds
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.