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Na(+)-activated potassium channel; may be involved in regulating the firing properties of neurons. Additionally we are shipping Potassium Channel, Subfamily T, Member 1 Proteins (4) and many more products for this protein.
Showing 10 out of 56 products:
Human Monoclonal KCNT1 Primary Antibody for ICC, IF - ABIN863116
Yuan, Santi, Wei, Wang, Pollak, Nonet, Kaczmarek, Crowder, Salkoff: The sodium-activated potassium channel is encoded by a member of the Slo gene family. in Neuron 2003
Show all 2 references for ABIN863116
Human Polyclonal KCNT1 Primary Antibody for IHC, ELISA - ABIN1535188
Humphray, Oliver, Hunt, Plumb, Loveland, Howe, Andrews, Searle, Hunt, Scott, Jones, Ainscough, Almeida, Ambrose, Ashwell, Babbage, Babbage, Bagguley, Bailey, Banerjee, Barker, Barlow, Bates, Beasley et al.: DNA sequence and analysis of human chromosome 9. ... in Nature 2004
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 (show SCNN1A Antibodies), KCNJ16 (show KCNJ16 Antibodies), KCNB2 (show KCNB2 Antibodies), and KCNT1) in three Brugada syndrome patients (20%)
Nine different mutations of the KCNT1 (Slack) Na(+)-activated K(+) channel (show KCNC4 Antibodies) give rise to three distinct forms of epilepsy.
Slick (show KCNT2 Antibodies) channels, in contrast to the similar Slack channels, are the only high-conductance K+ channels strongly sensitive to small changes in cell volume.
Genetic studies reveal two novel genes for Ohtahara Syndrome: KCNT1 and PIGQ (show PIGQ Antibodies).
Novel variations in KCNT1 do not allow prediction of functional phenotypes that might explain, at least in part, the symptoms of malignant migrating partial seizures of infancy (MMPSI).
This gene-wide tagging study revealed no association between KCNT1 17 common variations and susceptibility of GGEs or AEDs (anti-epileptic drugs) efficacy of genetic generalized epilepsies in Chinese population.
This study demonistrated that KCNT1 mutations implicated in epilepsy cause a marked increase in function
this study performed analysis of KCNT1 in two unrelated patients with malignant migrating partial seizures in infancy.Because the G-to-A transition was located at CG dinucleotide sequences as previously reported for KCNT1 mutations, the recurrent occurrence of de novo KCNT1 mutations indicated the hot spots of these locations.
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 (show DLG4 Antibodies) in mouse neocortical neurons
This is the first demonstration of an epithelial cell membrane, Na+-activated, large-conductance K+ channel (show KCNC4 Antibodies) resembling K(Na) channels of excitable cells. The Slo2.2 type, Na+- and Cl--activated K+ channel (show KCNC4 Antibodies) is located in the ascending limb of the kidney.
Slick (show KCNT2 Antibodies) 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