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

Kir6.2-containing ATP-sensitive potassium channels protect cortical neurons from ischemic/anoxic injury in vitro and in vivo.

Neuroscience - 23 Feb 2007

Sun H-S, Feng Z-P, Barber P A, Buchan A M, French R J

Abstract excerpt

ATP-sensitive potassium (K(ATP)) channels are weak inward rectifiers that appear to play an important role in protecting neurons against ischemic damage. Cerebral stroke is a major health issue, and vulnerability to stroke damage is regional within the brain. Thus, we set out to determine whether K(ATP) channels protect cortical neurons against ischemic insults. Experiments were performed using Kir6.2(-/-) K(ATP)...

Read the complete abstract on PubMed

Topics

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

Share to Brain Infarction
Share to Cell Death
Share to Cerebral Cortex

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Cytoprotection

Share to Hypoxia-Ischemia, Brain

Share to Nerve Degeneration

Share to Organ Culture Techniques

Share to Potassium Channels, Inwardly Rectifying

Source

Identifiers

PMID: 17175112
DOI: 10.1016/j.neuroscience.2006.10.043

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Kir6.2-containing ATP-sensitive potassium channels protect cortical neurons from ischemic/anoxic injury in vitro and in vivo.PMID 17175112Read ↗

Protection against hypoxic-ischemic injury in transgenic mice overexpressing Kir6.2 channel pore in forebrain.Semantic proximity Read ↗

Genetic Mutation of GluN2B Protects Brain Cells Against Stroke Damages.Semantic proximity Read ↗

Tyrosine Phosphorylation of the Kv2.1 Channel Contributes to Injury in Brain Ischemia.Semantic proximity Read ↗

Migraine mutations increase stroke vulnerability by facilitating ischemic depolarizations.Semantic proximity Read ↗

Analysis of the protective effects of a neuronal Cav2.1 calcium channel in brain injury.Semantic proximity Read ↗

Spatiotemporally selective ATP events from astrocytes encode injury information and guide sustained microglial responseSemantic proximity Read ↗

Deletion of mitochondrial uncoupling protein-2 increases ischemic brain damage after transient focal ischemia by altering gene expression patterns and enhancing inflammatory cytokines.Semantic proximity Read ↗

Anaesthetic preconditioning : the role of ATP-sensitive K+ channelsSemantic proximity Read ↗

Role of Ca(v) 2.3 (alpha1E ) Ca2+ channel in ischemic neuronal injury.Semantic proximity Read ↗

The loss-of-function disease-mutation G301R in the Na+/K+-ATPase α2 isoform decreases lesion volume and improves functional outcome after acute spinal cord injury in mice.Semantic proximity Read ↗

Elevated synaptic activity preconditions neurons against an in vitro model of ischemia.Semantic proximity Read ↗

Enhanced neuronal death from focal ischemia in AMPA-receptor transgenic mice.Semantic proximity Read ↗

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