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Mouse Anti-KCNJ10 Recombinant Antibody (1C11) (CBMAB-K0562-LY)

This product is antibody recognizes KCNJ10. The antibody 1C11 immunoassay techniques such as: WB, IP, ELISA.
See all KCNJ10 antibodies
Published Data
Fig.1 Immunohistochemistry of the glial proteins KIR4.1.
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Summary

Host Animal
Mouse
Specificity
Mouse, Rat, Human
Clone
1C11
Antibody Isotype
IgG
Application
WB, IP, ELISA

Basic Information

Specificity
Mouse, Rat, Human
Antibody Isotype
IgG
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
Purity
> 95% Purity determined by SDS-PAGE.
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freezethaw cycles.

Target

Full Name
Potassium Voltage-Gated Channel Subfamily J Member 10
Introduction
This gene encodes a member of the inward rectifier-type potassium channel family, characterized by having a greater tendency to allow potassium to flow into, rather than out of, a cell. The encoded protein may form a heterodimer with another potassium channel protein and may be responsible for the potassium buffering action of glial cells in the brain. Mutations in this gene have been associated with seizure susceptibility of common idiopathic generalized epilepsy syndromes. [provided by RefSeq, Jul 2008]
Entrez Gene ID
Human3766
Mouse16513
Rat29718
UniProt ID
HumanP78508
MouseQ9JM63
RatP49655
Function
May be responsible for potassium buffering action of glial cells in the brain. Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it. Their voltage dependence is regulated by the concentration of extracellular potassium; as external potassium is raised, the voltage range of the channel opening shifts to more positive voltages. The inward rectification is mainly due to the blockage of outward current by internal magnesium. Can be blocked by extracellular barium and cesium (By similarity).
In the kidney, together with KCNJ16, mediates basolateral K(+) recycling in distal tubules; this process is critical for Na(+) reabsorption at the tubules.
Biological Process
Adult walking behaviorIEA:Ensembl
Central nervous system myelinationIEA:Ensembl
Glutamate reuptakeIEA:Ensembl
Non-motile cilium assemblyIEA:Ensembl
Potassium ion homeostasisIEA:Ensembl
Potassium ion import across plasma membraneManual Assertion Based On ExperimentIBA:GO_Central
Potassium ion transportManual Assertion Based On ExperimentTAS:ProtInc
Regulation of ion transmembrane transportManual Assertion Based On ExperimentIBA:GO_Central
Regulation of long-term neuronal synaptic plasticityIEA:Ensembl
Regulation of resting membrane potentialIEA:Ensembl
Visual perceptionIEA:Ensembl
Cellular Location
Membrane; Basolateral cell membrane. In kidney distal convoluted tubules, located in the basolateral membrane where it colocalizes with KCNJ16.
Involvement in disease
Seizures, sensorineural deafness, ataxia, mental retardation, and electrolyte imbalance (SESAMES):
A complex disorder characterized by generalized seizures with onset in infancy, delayed psychomotor development, ataxia, sensorineural hearing loss, hypokalemia, metabolic alkalosis, and hypomagnesemia.
Topology
Cytoplasmic: 1-64
Helical: 65-89
Extracellular: 90-114
Helical: 115-126
Pore-forming: 127-133
Extracellular: 134-142
Helical: 143-164
Cytoplasmic: 165-379

Stee, K., Van Poucke, M., Pumarola, M., Geerinckx, L., Van Soens, I., Bhatti, S. F., ... & Cornelis, I. (2023). Spinocerebellar ataxia in the Bouvier des Ardennes breed is caused by a KCNJ10 missense variant. Journal of Veterinary Internal Medicine, 37(1), 216-222.

Klarov, L. A., Pshennikova, V. G., Romanov, G. P., Cherdonova, A. M., Solovyev, A. V., Teryutin, F. M., ... & Barashkov, N. A. (2022). Analysis of SLC26A4, FOXI1, and KCNJ10 Gene Variants in Patients with Incomplete Partition of the Cochlea and Enlarged Vestibular Aqueduct (EVA) Anomalies. International Journal of Molecular Sciences, 23(23), 15372.

Suzumoto, Y., Columbano, V., Gervasi, L., Giunta, R., Mattina, T., Trimarchi, G., ... & Trepiccione, F. (2021). A case series of adult patients affected by EAST/SeSAME syndrome suggests more severe disease in subjects bearing KCNJ10 truncating mutations. Intractable & Rare Diseases Research, 10(2), 95-101.

Jiang, C., Li, L., Wu, M., Hao, M., & Feng, J. (2021). Association of KCNJ10 variants and the susceptibility to clinical epilepsy. Clinical Neurology and Neurosurgery, 200, 106340.

Zhu, H., Zhang, M., Fu, Y., Long, H., Xiao, W., Feng, L., ... & Zhou, L. (2020). Effects of AQP4 and KCNJ10 gene polymorphisms on drug resistance and seizure susceptibility in Chinese Han patients with focal epilepsy. Neuropsychiatric Disease and Treatment, 119-129.

Penton, D., Vohra, T., Banki, E., Wengi, A., Weigert, M., Forst, A. L., ... & Loffing, J. (2020). Collecting system–specific deletion of Kcnj10 predisposes for thiazide-and low-potassium diet–induced hypokalemia. Kidney international, 97(6), 1208-1218.

Morin, M., Forst, A. L., Pérez-Torre, P., Jiménez-Escrig, A., Barca-Tierno, V., García-Galloway, E., ... & Moreno-Pelayo, M. A. (2020). Novel mutations in the KCNJ10 gene associated to a distinctive ataxia, sensorineural hearing loss and spasticity clinical phenotype. neurogenetics, 21, 135-143.

Mir, A., Chaudhary, M., Alkhaldi, H., Alhazmi, R., Albaradie, R., & Housawi, Y. (2019). Epilepsy in patients with EAST syndrome caused by mutation in the KCNJ10. Brain and Development, 41(8), 706-715.

Zhang, H., Zhu, L., Wang, F., Wang, R., Hong, Y., Chen, Y., ... & Wang, X. (2019). Novel KCNJ10 compound heterozygous mutations causing EAST/SeSAME-like syndrome compromise potassium channel function. Frontiers in Genetics, 10, 912.

Nicita, F., Tasca, G., Nardella, M., Bellacchio, E., Camponeschi, I., Vasco, G., ... & Zanni, G. (2018). Novel homozygous KCNJ10 mutation in a patient with non-syndromic early-onset cerebellar ataxia. The Cerebellum, 17, 499-503.

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

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