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Na(+)-activated potassium channel; may be involved in regulating the firing properties of neurons. Zusätzlich bieten wir Ihnen Potassium Channel, Subfamily T, Member 1 Proteine (4) und viele weitere Produktgruppen zu diesem Protein an.
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Mammalian Monoclonal KCNT1 Primary Antibody für ISt, IHC - ABIN1304961
Lu, Bausch, Kallenborn-Gerhardt, Stoetzer, Debruin, Ruth, Geisslinger, Leffler, Lukowski, Schmidtko: Slack channels expressed in sensory neurons control neuropathic pain in mice. in The Journal of neuroscience : the official journal of the Society for Neuroscience 2015
Show all 7 Pubmed References
Case report describing 3 infants with malignant migrating partial seizures with KCNT1 mutations accompanied by massive systemic to pulmonary collateral arteries.
Stimulation of Slack K(+) channels alters mass at the plasma membrane by triggering dissociation of Phactr-1.
In the present study, we evaluated two other potential mechanisms for stabilization of Slo2 channels in a closed state: (1) dewetting and collapse of the inner pore (hydrophobic gating) and (2) constriction of the inner pore by tight criss-crossing of the cytoplasmic ends of the S6 alpha-helical segments.
two de novo, heterozygous KCNT1 mutations were identified in two unrelated malignant migrating partial seizures probands. Both mutations induced a marked leftward shift in homomeric channel activation gating.
Better understanding of the mechanisms underlying KCNT1-related disease will produce further improvements in treatment of the associated severe seizure disorders.
We demonstrate that KCNT1 mutations are highly pleiotropic and are associated with phenotypes other than nocturnal frontal lobe epilepsy and malignant migrating focal seizures of infancy.
This study demonstrate that KCNT1 mutations are strongly associated with early-onset epileptic encephalopathy.
Five de novo mutations were identified in four genes (SCNN1A (zeige SCNN1A Antikörper), KCNJ16 (zeige KCNJ16 Antikörper), KCNB2 (zeige KCNB2 Antikörper), and KCNT1) in three Brugada syndrome patients (20%)
Nine different mutations of the KCNT1 (Slack) Na(+)-activated K(+) channel (zeige KCNC4 Antikörper) give rise to three distinct forms of epilepsy.
Slick (zeige KCNT2 Antikörper) channels, in contrast to the similar Slack channels, are the only high-conductance K+ channels strongly sensitive to small changes in cell volume.
The highest Slack channel expression was detected in the olfactory bulb, lateral septal nuclei, basal ganglia, and distinct areas of the midbrain, brainstem, and cerebellar cortex.
The authors find that knockout of Slo2.2, but not Slo2.1, results in enhanced itch and pain responses.
Results provide evidence for a role for endogenous Slack channels in higher brain functions, i.e., learning and memory, cognitive flexibility, locomotoric and the ability to initially respond to novel situations and environments
Global ablation of Slack led to increased hypersensitivity in models of neuropathic pain. Neuropathic pain behaviors were also exaggerated after ablation of Slack selectively in sensory neurons.
partly colocalized with PSD-95 (zeige DLG4 Antikörper) in mouse neocortical neurons
This is the first demonstration of an epithelial cell membrane, Na+-activated, large-conductance K+ channel (zeige KCNC4 Antikörper) resembling K(Na) channels of excitable cells. The Slo2.2 type, Na+- and Cl--activated K+ channel (zeige KCNC4 Antikörper) is located in the ascending limb of the kidney.
Slick (zeige KCNT2 Antikörper) and Slack are expressed at high levels auditory brainstem. Activation of these KNa channels allows temporal accuracy of firing to be increased at high frequencies of stimulation.
Potassium channels represent the most complex class of voltage-gated ion channels from both functional and structural standpoints. Their diverse functions include regulating neurotransmitter release, heart rate, insulin secretion, neuronal excitability, epithelial electrolyte transport, smooth muscle contraction, and cell volume. This gene encodes a sodium-activated potassium channel subunit which is thought to function in ion conductance and developmental signaling pathways. Mutations in this gene cause the early-onset epileptic disorders, malignant migrating partial seizures of infancy and autosomal dominant nocturnal frontal lobe epilepsy. Alternative splicing results in multiple transcript variants.
potassium channel, subfamily T, member 1
, potassium channel subfamily T member 1-like
, potassium channel subfamily T member 1
, sodium-activated potassium channel
, potassium channel subunit (Slack)
, sequence like a calcium-activated potassium channel subunit
, potassium channel subunit