Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

GRIN2B disease-associated mutations disrupt the function of BK channels and NMDA receptor signaling nanodomains.

The Journal of general physiology - 1 Sept 2025

Martínez-Lázaro Rebeca, Minguez-Viñas Teresa, Reyes-Carrión Andrea, Gómez Ricardo, Alvarez de la Rosa Diego, Bartolomé-Martín David, Giraldez Teresa

Abstract excerpt

Large conductance calcium-activated potassium channels (BK channels) are unique in their ability to respond to two distinct physiological stimuli: intracellular Ca2+ and membrane depolarization. In neurons, these channels are activated through a coordinated response to both signals; however, for BK channels to respond to physiological voltage changes, elevated concentrations of intracellular Ca2+ (ranging from 1...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to HEK293 Cells
Share to Large-Conductance Calcium-Activated Potassium Channels

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Mutation

Share to Neurons

Share to Receptors, N-Methyl-D-Aspartate

Share to Signal Transduction

Source

Open in PubMed Open full text

Identifiers

PMID: 40763259
DOI: 10.1085/jgp.202513799
PMCID: PMC12324158

Genes

GRIN2B

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

GRIN2B disease-associated mutations disrupt the function of BK channels and NMDA receptor signaling nanodomains.PMID 40763259Read ↗

GRIN2B disease-associated mutations disrupt the function of BK channels and NMDA receptor signalling nanodomainsSemantic proximity Read ↗

GRIN1 mutation associated with intellectual disability alters NMDA receptor trafficking and function.Semantic proximity Read ↗

GRIN1 variants associated with neurodevelopmental disorders reveal channel gating pathomechanismsSemantic proximity Read ↗

NMDA Receptors in Neurodevelopmental Disorders: Pathophysiology and Disease ModelsSemantic proximity Read ↗

Mutations in GRIN2A and GRIN2B encoding regulatory subunits of NMDA receptors cause variable neurodevelopmental phenotypes.Semantic proximity Read ↗

Disease-Associated Variants in GRIN1, GRIN2A and GRIN2B genes: Insights into NMDA Receptor Structure, Function, and Pathophysiology.Semantic proximity Read ↗

Phenotype of mice carrying an NMDA receptor GluN2B protein-truncating variant associated with intellectual disabilitySemantic proximity Read ↗

Mice carrying a GluN2B protein-truncating variant have altered NMDA receptor subunit composition and their behavior recapitulates patient phenotypes.Semantic proximity Read ↗

Disruption of GRIN2B Impairs Differentiation in Human Neurons.Semantic proximity Read ↗

Common synaptic phenotypes arising from diverse mutations in the human NMDA receptor subunit GluN2A.Semantic proximity Read ↗

Common synaptic phenotypes arising from diverse mutations in the human NMDA receptor subunit GluN2ASemantic proximity Read ↗

Functional Investigation of a GRIN2A Variant Associated with Rolandic Epilepsy.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.