Evidence map›Paper›PMID 42218098›Full record

ArticleMolecular pharmacology

The CaMKII D135N mutation blocks kinase activity and reduces GluN2B binding.

Matthew E Larsen, C Madison Barker, Raul Satoshi Vargas, Steven J Coultrap, K Ulrich Bayer

Abstract read
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In one paragraph

Article in Molecular pharmacology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors.

Matthew E LarsenDepartment of Pharmacology, University of Colorado Anschutz Medical Campus, Aurora, Colorado; Program in Neuroscience, University of Colorado Anschutz Medical Campus, Aurora, Colorado.
C Madison BarkerDepartment of Pharmacology, University of Colorado Anschutz Medical Campus, Aurora, Colorado.
Raul Satoshi VargasDepartment of Pharmacology, University of Colorado Anschutz Medical Campus, Aurora, Colorado.
Steven J CoultrapDepartment of Pharmacology, University of Colorado Anschutz Medical Campus, Aurora, Colorado.
K Ulrich BayerDepartment of Pharmacology, University of Colorado Anschutz Medical Campus, Aurora, Colorado; Program in Neuroscience, University of Colorado Anschutz Medical Campus, Aurora, Colorado. Electronic address: ulli.bayer@cuanschutz.edu.

Funding

CaMKII substrate-selection in opposing forms of synaptic plasticityR01NS081248 · NINDS · UNIVERSITY OF COLORADO DENVER · PI K. Ulrich Bayer · 2013 to 2026
$4.9M
CaMKII nitrosylation in the age-related decline of synaptic plasticityR01AG067713 · NIA · UNIVERSITY OF COLORADO DENVER · PI BAYER, K. ULRICH · 2020 to 2024
$2.7M
CaMKII in global cerebral ischemia: mechanisms and therapeutic interventionR01NS118786 · NINDS · UNIVERSITY OF COLORADO DENVER · PI BAYER, K. ULRICH, HERSON, PACO S · 2021 to 2025
$1.9M
APP as a mediator of amyloid beta effects on CaMKII synaptic functionsF31AG084197 · NIA · UNIVERSITY OF COLORADO DENVER · PI LARSEN, MATTHEW E · 2023 to 2025
$115k
NIA NIH HHS F31 AG084197NIA NIH HHS R01 AG067713NINDS NIH HHS R01 NS081248NINDS NIH HHS R01 NS118786
6 · The paper itself

Abstract

Three recent studies claimed that induction of long-term potentiation of synaptic strength requires structural rather than enzymatic functions of the Ca

Indexed as

Calcium-Calmodulin-Dependent Protein Kinase Type 2MutationReceptors, N-Methyl-D-AspartateAnimalsHumansLong-Term PotentiationPhosphorylationProtein BindingCalcium-Calmodulin-Dependent Protein Kinase Type 2NR2B NMDA receptorReceptors, N-Methyl-D-AspartateCaMKIID135NGluN2BNMDAR

Identifiers

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.