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

Name: Mouse Anti-KCNT2 Recombinant Antibody (CBXS-2346)
SKU: CBMAB-S5105-CQ
Rating: 5 (1 reviews)

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Datasheet

SDS

Request for COA

Datasheet Target References Q & As Review & reward Protocols Associated Products

Basic Information

Host Animal

Mouse

Clone

CBXS-2346

Application

IHC, WB

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.

More Infomation

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

Mouse	240776
Rat	304827

UniProt ID

Mouse	D3Z649
Rat	Q6UVM4

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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Please try the standard protocols which include: protocols, troubleshooting and guide.

Enzyme-linked Immunosorbent Assay (ELISA)
Flow Cytometry
Immunofluorescence (IF)
Immunohistochemistry (IHC)
Immunoprecipitation (IP)
Western Blot (WB)
Enzyme-Linked Immunospot (ELISpot)
Proteogenomics
Other Protocols

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

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