Anti-KCNT1 polyclonal antibody (DPABH-06296)

Rabbit anti-Human KCNT1 (C-terminal) polyclonal antibody for IHC-P


Host Species
Antibody Isotype
Species Reactivity
Mouse, Rat, Human
Synthetic peptide derived from the C terminus of Human KCNT1.


Application Notes
IHC-P: 5 μg/ml.
*Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own experiment using appropriate negative and positive controls.


Alternative Names
KCNT1; potassium channel, subfamily T, member 1; potassium channel subfamily T member 1; KCa4.1; KIAA1422; SLACK
Entrez Gene ID
UniProt ID

Product Background

Gene summary
KCNT1 (Potassium Sodium-Activated Channel Subfamily T Member 1) is a Protein Coding gene. Diseases associated with KCNT1 include epilepsy, nocturnal frontal lobe, 5 and epileptic encephalopathy, early infantile, 14. Among its related pathways are Hepatic ABC Transporters and Sweet Taste Signaling. GO annotations related to this gene include voltage-gated potassium channel activity and calcium-activated potassium channel activity. An important paralog of this gene is KCNU1. 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.
Antigen Description
Outwardly rectifying potassium channel subunit that may co-assemble with other Slo-type channel subunits. Activated by high intracellular sodium or chloride levels. Activated upon stimulation of G-protein coupled receptors, such as CHRM1 and GRIA1. May be regulated by calcium in the absence of sodium ions (in vitro). Epilepsy, nocturnal frontal lobe, 5 (ENFL5) [MIM:615005]: An autosomal dominant focal epilepsy syndrome characterized by childhood onset of clusters of motor seizures during sleep. Some patients may develop behavioral or psychiatric manifestations and/or intellectual disability. The phenotype is more severe than observed in other genetic forms of nocturnal frontal lobe epilepsy. Note=The disease is caused by mutations affecting the gene represented in this entry. Epileptic encephalopathy, early infantile, 14 (EIEE14) [MIM:614959]: A rare epileptic encephalopathy of infancy that combines pharmacoresistant seizures with developmental delay. This severe neurologic disorder is characterized by onset in the first 6 months of life of refractory focal seizures and arrest of psychomotor development. Ictal EEG shows discharges that arise randomly from various areas of both hemispheres and migrate from one brain region to another. Potassium channel subfamily T, member 1, also known as KCNT1 is a human gene that encodes the KCa4. 1 protein. KCa4. 1 is a member of the calcium-activated potassium channel protein family 0The function about KCNT1 antigen include calcium-activated potassium channel activity; ion channel activity; nucleotide binding; voltage-gated potassium channel activity.


Have you cited DPABH-06296 in a publication? Let us know and earn a reward for your research.

Custom Antibody Labeling

We offer labeled antibodies using our catalogue antibody products and a broad range of intensely fluorescent dyes and labels including HRP, biotin, ALP, Alexa Fluor® dyes, DyLight® Fluor dyes, R-phycoerythrin (R-PE), at scales from less than 100 μg up to 1 g of IgG antibody. Learn More

Customer Reviews

Write a review, share your experiences with others and get rewarded !
Product Name Cat. No. Applications Host Species Datasheet Price Add to Basket


Impaired motor skill learning and altered seizure susceptibility in mice with loss or gain of function of the Kcnt1 gene encoding Slack (K(Na)1.1) Na+-activated K+ channels


Authors: Quraishi, Imran H.; Mercier, Michael R.; McClure, Heather; Couture, Rachael L.; Schwartz, Michael L.; Lukowski, Robert; Ruth, Peter; Kaczmarek, Leonard K.

Gain-of-function mutations in KCNT1, the gene encoding Slack (K(Na)1.1) channels, result in epilepsy of infancy with migrating focal seizures (EIMFS) and several other forms of epilepsy associated with severe intellectual disability. We have generated a mouse model of this condition by replacing the wild type gene with one encoding Kcnt1(R455H), a cytoplasmic C-terminal mutation homologous to a human R474H variant that results in EIMFS. We compared behavior patterns and seizure activity in these mice with those of wild type mice and Kcnt1(-/-) mice. Complete loss of Kcnt1 produced deficits in open field behavior and motor skill learning. Although their thresholds for electrically and chemically induced seizures were similar to those of wild type animals, Kcnt1(-/-) mice were significantly protected from death after maximum electroshock-induced seizures. In contrast, homozygous Kcnt1(R455H/R455H) mice were embryonic lethal. Video-EEG monitoring of heterozygous Kcnt1(+/R455H) animals revealed persistent interictal spikes, spontaneous seizures and a substantially decreased threshold for pentylenetetrazole-induced seizures. Surprisingly, Kcnt1(+/R455H) mice were not impaired in tasks of exploratory behavior or procedural motor learning. These findings provide an animal model for EIMFS and suggest that Slack channels are required for the development of procedural learning and of pathways that link cortical seizures to other regions required for animal survival.

De Novo 15q13.3 Microdeletion With Cryptogenic West Syndrome


Authors: Lacaze, Elodie; Gruchy, Nicolas; Penniello-Valette, Marie-Jose; Plessis, Ghislaine; Richard, Nicolas; Decamp, Mathieu; Mittre, Herve; Leporrier, Nathalie; Andrieux, Joris; Kottler, Marie-Laure; Gerard, Marion

West syndrome is a well-recognized form of epilepsy, defined by a triad of infantile spasms, hypsarrhythmia and developmental arrest. West syndrome is heterogenous, caused by mutations of genes ARX, STXBP1, KCNT1 among others; 16p13.11 and 17q21.31 microdeletions are less frequent, usually associated with intellectual disability and facial dysmorphism. So-called idiopathic West syndrome is of better prognostic, without prior intellectual deficiency and usually responsive to anti-epileptic treatment. We report on a boy falling within the scope of idiopathic West syndrome, with no dysmorphic features and normal development before the beginning of West syndrome, with a good resolution after treatment, bearing a de novo 15q13.3 microdeletion. Six genes are located in the deleted region, including CHRNA7, which encodes a subunit of a nicotinic acetylcholine receptor, and is frequently associated with epilepsy. Exploration of the 15q13.3 region should be proposed in idiopathic West syndrome. (c) 2013 Wiley Periodicals, Inc.

Online Inquiry

Phone: *
E-mail Address: *
Technology Interest:
Type of Organization:
Service & Products Interested: *
Project Description:

Related Products

Related Resources

Ordering Information

Payment methods we support:
Invoice / Purchase Order
Credit card

Inquiry Basket