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Key Documents

WH0003766M1

Sigma-Aldrich

Monoclonal Anti-KCNJ10 antibody produced in mouse

clone 1C11, purified immunoglobulin, buffered aqueous solution

Synonym(s):

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

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About This Item

MDL number:
UNSPSC Code:
12352203
NACRES:
NA.41

biological source

mouse

conjugate

unconjugated

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

1C11, monoclonal

form

buffered aqueous solution

species reactivity

human

technique(s)

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

isotype

IgG2aκ

GenBank accession no.

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... KCNJ10(3766)

General description

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.
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)

Immunogen

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

Sequence
DFELVLILSGTVESTSATCQVRTSYLPEEILWGYEFTPAISLSASGKYIADFSLFDQVVKVASPSGLRDSTVRYGDPEKLKLEESLREQAEKEGSALSVRISNV

Application

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

Disclaimer

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.

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Storage Class

10 - Combustible liquids

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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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)
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)
Differential loss of KIR4.1 immunoreactivity in multiple sclerosis lesions
Schirmer L, et al.
Annals of Neurology, 75(6), 810-828 (2014)
Unidirectional photoreceptor-to-Muller glia coupling and unique K+ channel expression in Caiman retina
Zayas-Santiago A, et al.
PLoS ONE, 9(5) (2014)
John J Kelly et al.
Journal of cell science, 132(2) (2018-12-19)
Mutations in the genes that encode the gap junction proteins connexin 26 (Cx26, encoded by GJB2) and Cx30 (GJB6) are the leading cause of hereditary hearing loss. That said, the Cx30 p.Ala88Val (A88V) mutant causes Clouston syndrome, but not hearing

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