Monoclonal Anti-KCNJ10 antibody produced in mouse

clone 1C11, purified immunoglobulin, buffered aqueous solution

Anti-BIRK10, Anti-KIR4.1, Anti-KIR1.2, Anti-KCNJ13PEN, Anti-potassium inwardly-rectifying channel, subfamily J, member 10
MDL number:

Quality Level

biological source


antibody form

purified immunoglobulin

antibody product type

primary antibodies


1C11, monoclonal


buffered aqueous solution

species reactivity



indirect ELISA: suitable
western blot: 1-5 μg/mL





GenBank® accession no.

UniProt accession no.

shipped in

dry ice

storage temp.


Gene Information

human ... KCNJ10(3766)

General description

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)
Kir4.1/KCNJ10 (potassium voltage-gated channel subfamily J member 10) is an inwardly rectifying potassium (K+) channel. This gene is expressed in the brain, inner ear and kidney. KCNJ10 gene is mapped to human chromosome 1q23.


KCNJ10 (NP_002232, 276 a.a. ~ 379 a.a) partial recombinant protein with GST tag. MW of the GST tag alone is 26 KDa.



Monoclonal Anti-KCNJ10 antibody has been used in immunohistochemistry.

Biochem/physiol Actions

Kir4.1/KCNJ10 (potassium voltage-gated channel subfamily J member 10) helps to regulate the basolateral K+ conductance in the DCT (distal convoluted tubule). It participates in the K+ spatial buffering process, that helps to maintain the resting membrane potential of neurons. Kir4.1 is essential for producing the endocochlear potential of intermediate cells and for retaining high K+ content of the endolymph in ear. In the eye, Kir4.1 plays a vital role in the modulation of the extracellular K+ level and in controlling the healing process of cornea epithelial cells. Mutations in KCNJ10 results in SeSAME (seizures, sensorineural deafness, ataxia, mental retardation and electrolyte imbalance).

Physical form

Solution in phosphate buffered saline, pH 7.4

Legal Information

GenBank is a registered trademark of United States Department of Health and Human Services


Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

Personal Protective Equipment

dust mask type N95 (US),Eyeshields,Gloves


NONH for all modes of transport

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Certificate of Analysis

Certificate of Origin

Differential loss of KIR4.1 immunoreactivity in multiple sclerosis lesions
Schirmer L, et al.
Annals of Neurology, 75(6), 810-828 (2014)
Seizures, sensorineural deafness, ataxia, mental retardation, and electrolyte imbalance (SeSAME syndrome) caused by mutations in KCNJ10
Scholl UI, et al.
Proceedings of the National Academy of Sciences of the USA, 106(14), 5842-5847 (2009)
The expression, regulation, and function of Kir4.1 (Kcnj10) in the mammalian kidney
Su XT and Wang WH
American Journal of Physiology: Renal Physiology, 311(1), F12-F15 (2016)
Rong Zhong et al.
Neuroimmunomodulation, 23(5-6), 295-300 (2017-04-10)
The aim of this study was to explore the frequency of KIR4.1 antibodies in patients with multiple sclerosis (MS) and in control groups using a cell-based assay. A transfected HEK-293A cell line expressing KIR4.1 was established to test for the...
Jaqueline R Silva et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 37(27), 6408-6422 (2017-06-04)
Herpetic neuralgia is the most important symptom of herpes zoster disease, which is caused by

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