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Mouse Anti-KCNT2 Recombinant Antibody (CBXS-2346) (CBMAB-S5105-CQ)

This product is a mouse antibody that recognizes KCNT2. The antibody CBXS-2346 can be used for immunoassay techniques such as: IHC, WB.
See all KCNT2 antibodies

Summary

Host Animal
Mouse
Specificity
Mouse, Rat
Clone
CBXS-2346
Antibody Isotype
IgG1
Application
IHC, WB

Basic Information

Immunogen
Fusion protein aa 564-624 of mouse Slo2.1 (Slick; XP_920840)
Specificity
Mouse, Rat
Antibody Isotype
IgG1
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Buffer
PBS, pH 7.4, 50% glycerol
Preservative
0.09% sodium azide
Concentration
1 mg/mL
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
potassium channel, subfamily T, member 2
Introduction
Outward rectifying potassium channel. Produces rapidly activating outward rectifier K(+) currents. Activated by high intracellular sodium and chloride levels. Channel activity is inhibited by ATP and by inhalation anesthetics, such as isoflurane (By similarity). Inhibited upon stimulation of G-protein coupled receptors, such as CHRM1 and GRIA1.
Entrez Gene ID
Mouse240776
Rat304827
UniProt ID
MouseD3Z649
RatQ6UVM4
Alternative Names
E330038N15Rik; Slick
Function
Outward rectifying potassium channel. Produces rapidly activating outward rectifier K(+) currents. Activated by high intracellular sodium and chloride levels (PubMed:14684870, PubMed:16687497, PubMed:29069600).
Channel activity is inhibited by ATP and by inhalation anesthetics, such as isoflurane (PubMed:16687497) (By similarity).
Inhibited upon stimulation of G-protein coupled receptors, such as CHRM1 and GRM1 (PubMed:16687497).
Biological Process
Potassium ion export across plasma membraneManual Assertion Based On ExperimentIMP:UniProtKB
Cellular Location
Cell membrane
Involvement in disease
Developmental and epileptic encephalopathy 57 (DEE57):
A form of epileptic encephalopathy, a heterogeneous group of severe early-onset epilepsies characterized by refractory seizures, neurodevelopmental impairment, and poor prognosis. Development is normal prior to seizure onset, after which cognitive and motor delays become apparent. DEE57 is an autosomal dominant condition.
Topology
Cytoplasmic: 1-63
Helical: 64-84
Extracellular: 85-101
Helical: 102-122
Cytoplasmic: 123-137
Helical: 138-158
Extracellular: 159-164
Helical: 165-185
Cytoplasmic: 186-198
Helical: 199-219
Extracellular: 220-228
Pore-forming: 229-249
Extracellular: 250-256
Helical: 257-277
Cytoplasmic: 278-1135
PTM
Phosphorylated by protein kinase C. Phosphorylation of the C-terminal domain inhibits channel activity.

Cioclu, M. C., Mosca, I., Ambrosino, P., Puzo, D., Bayat, A., Wortmann, S. B., ... & Taglialatela, M. (2023). KCNT2‐related disorders: phenotypes, functional and pharmacological properties. Annals of Neurology.

Gong, P., Jiao, X., Yu, D., & Yang, Z. (2021). Case Report: Causative De novo Variants of KCNT2 for Developmental and Epileptic Encephalopathy. Frontiers in Genetics, 12, 649556.

Jackson, A., Banka, S., Stewart, H., Genomics England Research Consortium, Robinson, H., Lovell, S., & Clayton‐Smith, J. (2021). Recurrent KCNT2 missense variants affecting p. Arg190 result in a recognizable phenotype. American Journal of Medical Genetics Part A, 185(10), 3083-3091.

Mao, X., Bruneau, N., Gao, Q., Becq, H., Jia, Z., Xi, H., ... & Aniksztejn, L. (2020). The epilepsy of infancy with migrating focal seizures: identification of de novo mutations of the KCNT2 gene that exert inhibitory effects on the corresponding heteromeric KNa1. 1/KNa1. 2 potassium channel. Frontiers in Cellular Neuroscience, 14, 1.

Yu, L., Li, H., Li, Z., Jia, J., Wu, Z., Wang, M., ... & Gao, G. (2020). RETRACTED ARTICLE: Long Non-Coding RNA HAND2-AS1 Inhibits Growth and Migration of Gastric Cancer Cells Through Regulating the miR-590-3p/KCNT2 Axis. OncoTargets and therapy, 3187-3196.

Alagoz, M., Kherad, N., Bozkurt, S., & Yuksel, A. (2020). New mutations in KCNT2 gene causing early infantile epileptic encephalopathy type 57: Case study and literature review. Acta Biochimica Polonica, 67(3), 431-434.

Inuzuka, L. M., Macedo-Souza, L. I., Della-Ripa, B., Monteiro, F. P., Ramos, L., Kitajima, J. P., ... & Kok, F. (2020). Additional observation of a de novo pathogenic variant in KCNT2 leading to epileptic encephalopathy with clinical features of frontal lobe epilepsy. Brain and Development, 42(9), 691-695.

Manocchio, L. (2018). Genetic, pathophysiological, and pharmacological implications of KCNT1 and KCNT2 potassium channels in neurodevelopmental disorders and epileptic encephalopathies.

Ambrosino, P., Soldovieri, M. V., Bast, T., Turnpenny, P. D., Uhrig, S., Biskup, S., ... & Lemke, J. R. (2018). De novo gain‐of‐function variants in KCNT2 as a novel cause of developmental and epileptic encephalopathy. Annals of neurology, 83(6), 1198-1204.

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For research use only. Not intended for any clinical use.

Custom Antibody Labeling

We also offer labeled antibodies developed using our catalog antibody products and nonfluorescent conjugates (HRP, AP, Biotin, etc.) or fluorescent conjugates (Alexa Fluor, FITC, TRITC, Rhodamine, Texas Red, R-PE, APC, Qdot Probes, Pacific Dyes, etc.).

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