biological source
mouse
Quality Level
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
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 Code
10 - Combustible liquids
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Personal Protective Equipment
dust mask type N95 (US), Eyeshields, Gloves
Regulatory Information
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Differential loss of KIR4.1 immunoreactivity in multiple sclerosis lesions
Schirmer L, et al.
Annals of Neurology, 75(6), 810-828 (2014)
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)
Masato Kinboshi et al.
International journal of molecular sciences, 20(5) (2019-03-01)
The dysfunction of astrocytic inwardly rectifying potassium (Kir) 4.1 channels, which mediate the spatial potassium-buffering function of astrocytes, is known to be involved in the development of epilepsy. Here, we analyzed the Kir4.1 expressional changes in Leucine-Rich Glioma-Inactivated 1 (Lgi1)
Unidirectional photoreceptor-to-Muller glia coupling and unique K+ channel expression in Caiman retina
Zayas-Santiago A, et al.
PLoS ONE, 9(5) (2014)
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