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
In one paragraphArticle 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.
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0citing papers in PubMed
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1 · What the graph read from itWhat it found
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2 · The registryThe trial behind it
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3 · Its place in the literatureWho cites it
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4 · The recordCorrections and comments
5 · Who and what moneyAuthors 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
$4.9MCaMKII 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 ischemia: mechanisms and therapeutic interventionR01NS118786 · NINDS · UNIVERSITY OF COLORADO DENVER · PI BAYER, K. ULRICH, HERSON, PACO S · 2021 to 2025
$1.9MAPP as a mediator of amyloid beta effects on CaMKII synaptic functionsF31AG084197 · NIA · UNIVERSITY OF COLORADO DENVER · PI LARSEN, MATTHEW E · 2023 to 2025
$115kNIA NIH HHS F31 AG084197NIA NIH HHS R01 AG067713NINDS NIH HHS R01 NS081248NINDS NIH HHS R01 NS118786
6 · The paper itselfAbstract
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
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