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KCNJ10 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. Additionally we are shipping KCNJ10 Kits (11) and KCNJ10 Proteins (6) and many more products for this protein.
Showing 10 out of 72 products:
Rat (Rattus) Polyclonal KCNJ10 Primary Antibody for IHC, WB - ABIN350384
Li, Head, Timpe: Identification of an inward rectifier potassium channel gene expressed in mouse cortical astrocytes. in Glia 2001
Show all 5 references for ABIN350384
Human Monoclonal KCNJ10 Primary Antibody for ELISA, WB - ABIN393249
Reichold, Zdebik, Lieberer, Rapedius, Schmidt, Bandulik, Sterner, Tegtmeier, Penton, Baukrowitz, Hulton, Witzgall, Ben-Zeev, Howie, Kleta, Bockenhauer, Warth: KCNJ10 gene mutations causing EAST syndrome (epilepsy, ataxia, sensorineural deafness, and tubulopathy) disrupt channel function. in Proceedings of the National Academy of Sciences of the United States of America 2010
Show all 5 references for ABIN393249
Human Polyclonal KCNJ10 Primary Antibody for IHC, IHC (p) - ABIN4328477
Locher, de Groot, van Iperen, Huisman, Frijns, Chuva de Sousa Lopes: Development of the stria vascularis and potassium regulation in the human fetal cochlea: Insights into hereditary sensorineural hearing loss. in Developmental neurobiology 2015
Human Monoclonal KCNJ10 Primary Antibody for ELISA, WB - ABIN561584
Singh, Wangemann: Free radical stress-mediated loss of Kcnj10 protein expression in stria vascularis contributes to deafness in Pendred syndrome mouse model. in American journal of physiology. Renal physiology 2008
Ordered disorder of the astrocytic dystrophin (show DMD Antibodies)-associated protein complex in the norm and pathology.
disruption of cav-1 (show CAV1 Antibodies) decreases basolateral K(+) channel (show KCNC4 Antibodies) activity and depolarizes the cell membrane potential in the DCT1 (show SLC11A2 Antibodies) at least in part by suppressing the stimulatory effect of c-Src (show SRC Antibodies) on Kcnj10
Data suggest that astroglial Kir4.1 channels are crucially involved in extracellular potassium homeostasis regulating theta rhythmic activity.
thyroglobulin (show TG Antibodies) trafficking might be modulated by Kir4.1/5.1.
Kcnj10 plays a role in Muller glia maturation during retinal development probably through ionic channel activities.
Kir (show GEM Antibodies).4.1 is expressed in the basolateral membrane of cortical thick ascending limb (cTAL) and that the disruption of Kir (show GEM Antibodies).4.1 has no significant effect on the membrane potential of the cTAL limb and Na-K-Cl cotransporter (show SLC12A1 Antibodies) 2 (show SLC12A5 Antibodies) expression
Kcnj10 is a main potassium channel (show KCNAB2 Antibodies) expressed in corneal epithelial cells.
Kcnj10 is a main contributor to the basolateral K conductance in the early distal convoluted tubule (DCT1 (show SLC11A2 Antibodies)) and determines the expression of the apical Na-Cl cotransporter (NCC (show SLC12A3 Antibodies)) in the DCT (show DCT Antibodies).
TBI affects expression of Kir4.1 and GLT-1 (show SLC1A2 Antibodies) genes in age- and time dependent manner and it may lead to accumulations of more K(+) and glutamate (show GRIN1 Antibodies) early in the synapse of old mice as compared to adult
the modulation of tyrosine phosphorylation of KCNJ10 should play a role in regulating membrane transport function in DCT1 (show SLC11A2 Antibodies).
Previous research had shown that Kir4.1 protein autoantibodies were specific for multiple sclerosis but they found that they weren't.
This study identifies potential SNPs of KCNJ10 gene that may contribute to seizure susceptibility and anti-epileptic drug resistance.
anti-KIR4.1 antibody levels differed in multiple sclerosis patients during relapse and remission; as such, they may represent a marker of disease exacerbation
This study showed that rs2486253, but not rs61822012, polymorphism of KCNJ10 gene was associated with childhood idiopathic generalized epilepsy.
we confirmed the presence of anti-Kir4.1 antibodies in multiple sclerosis patients, but at a much lower prevalence than previously reported.
KCNJ10 SNP is not associated with nonsyndromic enlargement of vestibular aqueduct in Chinese patients.
No KIR4.1-specific antigen is detected in serum or cerebrospinal fluid of multiple sclerosis (MS) patients; the target antigen of MS remains elusive.
This study observed a decrease of astroglial KIR4.1 but not glial fibrillary acidic protein (show GFAP Antibodies) IR. In chronic inactive and remyelinating MS lesions, KIR4.1 IR was restored on astrocytes and found in a subset of presumably new myelinating oligodendrocytes.
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.
potassium inwardly-rectifying channel, subfamily J, member 10
, ATP-sensitive inward rectifier potassium channel 10
, potassium inwardly-rectifying channel J10
, inward rectifier K(+) channel Kir4.1
, potassium channel, inwardly rectifying subfamily J member 10
, ATP-dependent inwardly rectifying potassium channel Kir4.1
, glial ATP-dependent inwardly rectifying potassium channel KIR4.1
, inward rectifier K(+) channel Kir1.2
, inward rectifier K+ channel KIR1.2
, ATP-sensitive inward rectifier potassium channel KAB-2
, brain-specific inwardly rectifying K(+) channel 1