Gene Ontology annotation through association of InterPro records with GO terms.
Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity.
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot keyword mapping
Combined Automated Annotation using Multiple IEA Methods.
Requirement of Ca2+ and CaMKII for Stat1 Ser-727 phosphorylation in response to IFN-gamma.
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CaMKII directly phosphorylates STAT1 at Ser727 in response to IFN-gamma
"CaMKII can interact directly with Stat1 and phosphorylate Stat1 on S727 in vitro . Inhibition of Ca 2+ flux or CaMKII results in a lack of S727 phosphorylation"
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IFN-gamma induces Ca2+ flux that activates CaMKII
"IFN-γ induced a rapid and sharp increase in [Ca 2+ ] i in a dose-dependent manner"
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Inhibition of CaMKII prevents STAT1 Ser727 phosphorylation and gene activation
"Inhibition of Ca 2+ flux or CaMKII results in a lack of S727 phosphorylation"
Bcl10 is phosphorylated on Ser138 by Ca2+/calmodulin-dependent protein kinase II.
Phosphorylation status of the NR2B subunit of NMDA receptor regulates its interaction with calcium/calmodulin-dependent protein kinase II.
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CaMKII binds to NR2B (GluN2B) subunit of NMDA receptors for synaptic targeting during LTP
"Phosphorylation status of the NR2B subunit of NMDA receptor regulates its interaction with calcium/calmodulin-dependent protein kinase II"
Structure of the CaMKIIdelta/calmodulin complex reveals the molecular mechanism of CaMKII kinase activation.
Quantitative analysis of HSP90-client interactions reveals principles of substrate recognition.
Integrative analysis of kinase networks in TRAIL-induced apoptosis provides a source of potential targets for combination therapy.
An organelle-specific protein landscape identifies novel diseases and molecular mechanisms.
A Novel Human CAMK2A Mutation Disrupts Dendritic Morphology and Synaptic Transmission, and Causes ASD-Related Behaviors.
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De novo E183V mutation in CAMK2A causes autism spectrum disorder
"a de novo Glu183 to Val (E183V) mutation in the CaMKIIα catalytic domain, identified in a proband diagnosed with ASD"
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E183V mutation reduces kinase activity and acts in dominant-negative manner
"decreases both CaMKIIα substrate phosphorylation and regulatory autophosphorylation, and that the mutated kinase acts in a dominant-negative manner"
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E183V decreases spine density and excitatory synaptic transmission
"neuronal expression of CaMKIIα-E183V increases dendritic arborization and decreases both dendritic spine density and excitatory synaptic transmission"
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Mutant mice show ASD-related behavioral phenotypes
"The CaMKIIα-E183V mice also display aberrant behavioral phenotypes, including hyperactivity, social interaction deficits, and increased repetitive behaviors"
Network Analysis of UBE3A/E6AP-Associated Proteins Provides Connections to Several Distinct Cellular Processes.
Extensive rewiring of the EGFR network in colorectal cancer cells expressing transforming levels of KRAS(G13D).
A reference map of the human binary protein interactome.
Kinase Interaction Network Expands Functional and Disease Roles of Human Kinases.
Interactome Mapping Provides a Network of Neurodegenerative Disease Proteins and Uncovers Widespread Protein Aggregation in Affected Brains.
A family of conserved bacterial virulence factors dampens interferon responses by blocking calcium signaling.
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Bacterial virulence factors block Ca2+ signaling to inhibit CaMKII activation and interferon responses
"A family of conserved bacterial virulence factors dampens interferon responses by blocking calcium signaling"
PSAT1 impairs ferroptosis and reduces immunotherapy efficacy via GPX4 hydroxylation.
Deep Research Report on CAMK2A
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CAMK2A is essential for LTP and spatial learning
"Silva et al. in the 1990s generated Camk2a-deficient mice, which revealed that CaMKIIα is essential for hippocampal LTP and spatial learning. These knockout mice could not sustain LTP"
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CAMK2A is a master regulator of synaptic plasticity
"CaMKIIα is a master regulator of synaptic plasticity (GO:0048167) – the ability of synapses to strengthen or weaken over time"
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CAMK2A mutations cause intellectual disability
"Mice lacking CaMKIIα cannot establish normal LTP and exhibit impaired spatial learning, highlighting this gene's role in memory consolidation"
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt.
Automatic Gene Ontology annotation based on Rhea mapping.
Electronic Gene Ontology annotations created by ARBA machine learning models
Activation of Na+/H+ exchanger NHE3 by angiotensin II is mediated by inositol 1,4,5-triphosphate (IP3) receptor-binding protein released with IP3 (IRBIT) and Ca2+/calmodulin-dependent protein kinase II.
Proteomic characterization of the human sperm nucleus.
A mechanism for tunable autoinhibition in the structure of a human Ca2+/calmodulin- dependent kinase II holoenzyme.
De Novo Mutations in Protein Kinase Genes CAMK2A and CAMK2B Cause Intellectual Disability.
Dual proteome-scale networks reveal cell-specific remodeling of the human interactome.
A central chaperone-like role for 14-3-3 proteins in human cells.
Trafficking of GluR1-containing AMPA receptors
Ca2+ influx into the post-synaptic cell
Dissociation of CaM and CAMK2 autophosphorylation
Active calmodulin binds CAMK2
Autophosphorylation and activation of CAMK2
Activation of MAP3K7 in response to WNT
Phosphorylation of HSF1 at Ser230 induces transactivation
RAS GEFs promote RAS nucleotide exchange
Phosphorylation of STAT1 at Ser727