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WH0003766M1

Sigma-Aldrich

Monoclonal Anti-KCNJ10 antibody produced in mouse

clone 1C11, purified immunoglobulin, buffered aqueous solution

Sinónimos:

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

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100 μG
417,00 €

417,00 €


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100 μG
417,00 €

About This Item

Número MDL:
Código UNSPSC:
12352203
NACRES:
NA.41

417,00 €


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origen biológico

mouse

Nivel de calidad

conjugado

unconjugated

forma del anticuerpo

purified immunoglobulin

tipo de anticuerpo

primary antibodies

clon

1C11, monoclonal

Formulario

buffered aqueous solution

reactividad de especies

human

técnicas

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

isotipo

IgG2aκ

Nº de acceso GenBank

Nº de acceso UniProt

Condiciones de envío

dry ice

temp. de almacenamiento

−20°C

modificación del objetivo postraduccional

unmodified

Información sobre el gen

human ... KCNJ10(3766)

Descripción general

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)

Inmunógeno

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

Aplicación

Monoclonal Anti-KCNJ10 antibody has been used in immunohistochemistry.

Acciones bioquímicas o fisiológicas

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).

Forma física

Solution in phosphate buffered saline, pH 7.4

Información legal

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

Cláusula de descargo de responsabilidad

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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Código de clase de almacenamiento

10 - Combustible liquids

Punto de inflamabilidad (°F)

Not applicable

Punto de inflamabilidad (°C)

Not applicable

Equipo de protección personal

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


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Visite la Librería de documentos

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)
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)
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)

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