Recombinant Human Atp-Sensitive Inward Rectifier Potassium Channel 10 (KCNJ10) Protein (His-SUMO)

Name: Recombinant Human Atp-Sensitive Inward Rectifier Potassium Channel 10 (KCNJ10) Protein (His-SUMO)
Brand: Beta LifeScience
SKU: BLC-10211P
Availability: InStock

Greater than 90% as determined by SDS-PAGE.

Based on the SEQUEST from database of E.coli host and target protein, the LC-MS/MS Analysis result of this product could indicate that this peptide derived from E.coli-expressed Homo sapiens (Human) KCNJ10.

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Product Overview

Description	Recombinant Human Atp-Sensitive Inward Rectifier Potassium Channel 10 (KCNJ10) Protein (His-SUMO) is produced by our E.coli expression system. This is a cytoplasmic protein.
Purity	Greater than 90% as determined by SDS-PAGE.
Uniprotkb	P78508
Target Symbol	KCNJ10
Synonyms	KCNJ10; ATP-sensitive inward rectifier potassium channel 10; ATP-dependent inwardly rectifying potassium channel Kir4.1; Inward rectifier K(+ channel Kir1.2; Potassium channel, inwardly rectifying subfamily J member 10
Species	Homo sapiens (Human)
Expression System	E.coli
Tag	N-6His-SUMO
Target Protein Sequence	FLAKIARPKKRAETIRFSQHAVVASHNGKPCLMIRVANMRKSLLIGCQVTGKLLQTHQTKEGENIRLNQVNVTFQVDTASDSPFLILPLTFYHVVDETSPLKDLPLRSGEGDFELVLILSGTVESTSATCQVRTSYLPEEILWGYEFTPAISLSASGKYIADFSLFDQVVKVASPSGLRDSTVRYGDPEKLKLEESLREQAEKEGSALSVRISNV
Expression Range	165-379aa
Protein Length	Cytoplasmic Domain
Mol. Weight	39.8kDa
Research Area	Transport
Form	Liquid or Lyophilized powder
Buffer	Liquid form: default storage buffer is Tris/PBS-based buffer, 5%-50% glycerol. Lyophilized powder form: the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, pH 8.0.
Reconstitution	Briefly centrifuged the vial prior to opening to bring the contents to the bottom. Reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL. It is recommended to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20°C/-80°C. The default final concentration of glycerol is 50%.
Storage	1. Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. 2. Avoid repeated freeze-thaw cycles. 3. Store working aliquots at 4°C for up to one week. 4. In general, protein in liquid form is stable for up to 6 months at -20°C/-80°C. Protein in lyophilized powder form is stable for up to 12 months at -20°C/-80°C.
Notes	Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.

Target Details

Target Function	May be responsible for potassium buffering action of glial cells in the brain. Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it. Their voltage dependence is regulated by the concentration of extracellular potassium; as external potassium is raised, the voltage range of the channel opening shifts to more positive voltages. The inward rectification is mainly due to the blockage of outward current by internal magnesium. Can be blocked by extracellular barium and cesium. In the kidney, together with KCNJ16, mediates basolateral K(+) recycling in distal tubules; this process is critical for Na(+) reabsorption at the tubules.
Subcellular Location	Membrane; Multi-pass membrane protein. Basolateral cell membrane.
Protein Families	Inward rectifier-type potassium channel (TC 1.A.2.1) family, KCNJ10 subfamily
Database References	HGNC: 6256 OMIM: 602208 KEGG: hsa:3766 STRING: 9606.ENSP00000357068 UniGene: Hs.408960
Associated Diseases	Seizures, sensorineural deafness, ataxia, mental retardation, and electrolyte imbalance (SESAMES)
Tissue Specificity	Expressed in kidney (at protein level).

Gene Functions References

results show that a glia-neuron interaction at the perisomatic space of LHb is involved in setting the neuronal firing mode in models of a major psychiatric disease. Kir4.1 in the LHb might have potential as a target for treating clinical depression. PMID: 29446379
A novel mutation in the KCNJ10 and previously characterized mutation in KCNT1 were identified in boy with seizures and neurodevelopmental delay. KCNJ10 L218F mutation associated with disease resulted in reduced Kir current. PMID: 28747464
rs17375748, rs1130183, rs12133079 and rs1186688 associated with sudden infant death syndrome PMID: 28520217
kcnj10 plays a role in K(+) recycling across the basolateral membrane in corresponding nephron segments and in generating negative membrane potential--{REVIEW} PMID: 27122539
Previous research had shown that Kir4.1 protein autoantibodies were specific for multiple sclerosis but they found that they weren't. PMID: 27074083
This study identifies potential SNPs of KCNJ10 gene that may contribute to seizure susceptibility and anti-epileptic drug resistance. PMID: 25874548
disruption of cav-1 decreases basolateral K(+) channel activity and depolarizes the cell membrane potential in the DCT1 at least in part by suppressing the stimulatory effect of c-Src on Kcnj10 PMID: 25848073
anti-KIR4.1 antibody levels differed in multiple sclerosis patients during relapse and remission; as such, they may represent a marker of disease exacerbation PMID: 25392324
This study showed that rs2486253, but not rs61822012, polymorphism of KCNJ10 gene was associated with childhood idiopathic generalized epilepsy. PMID: 25008907
we confirmed the presence of anti-Kir4.1 antibodies in multiple sclerosis patients, but at a much lower prevalence than previously reported. PMID: 24756568
KCNJ10 SNP is not associated with nonsyndromic enlargement of vestibular aqueduct in Chinese patients. PMID: 25372295
No KIR4.1-specific antigen is detected in serum or cerebrospinal fluid of multiple sclerosis (MS) patients; the target antigen of MS remains elusive. PMID: 25008548
This study observed a decrease of astroglial KIR4.1 but not glial fibrillary acidic protein 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. PMID: 24777949
study provides an explanation for the pathophysiology of the p.A167V KCNJ10 mutation, which had not been considered pathogenic on its own; findings provide evidence for functional cooperation of KCNJ10 and KCNJ16; in vitro ascertainment of KCNJ10 function may necessitate co-expression with KCNJ16 PMID: 24193250
Mislocalization of the Kir4.1 channels contributes to renal salt wasting. PMID: 24561201
KCNJ10rs1130183 did not contribute to risk of seizure susceptibility. PMID: 24378235
Study confirms that EAST syndrome can be caused by many different mutations in KCNJ10 that significantly reduce K+ conductance. PMID: 21849804
Ordered disorder of the astrocytic dystrophin-associated protein complex in the norm and pathology. PMID: 24014171
Serum antibodies to KIR4.1 are found in the majority of children with acquired demylinating disease but not in children with other diseases or in healthy controls. PMID: 24415573
the modulation of tyrosine phosphorylation of KCNJ10 should play a role in regulating membrane transport function in DCT1. PMID: 23873931
We found no evidence for a significant association between mutations of KCNJ10 and FOXI1 with SLC26A4 in Pendred syndrome/enlarged vestibular aqueducts. PMID: 23965030
The results of this study indicated that alterations in expression of Kir4.1 occurring in epilepsy-associated lesions are possibly influenced by the local inflammatory environment and in particular by the inflammatory cytokine IL-1beta. PMID: 23270518
Oligodendrocyte precursor cells establish themselves progressively through postnatal upregulation of Kir4.1 potassium channels. PMID: 23392672
The subcellular co-localisation of K(ir)4.1 and AQP4 in the supporting cells of the cochlea described in this study resembles that of the astroglia of the central nervous system and the glial Mueller cells in the retina. PMID: 22802001
This study demonistrated that Loss of perivascular Kir4.1 potassium channels in the sclerotic hippocampus of patients with mesial temporal lobe epilepsy. PMID: 22878665
No KCNJ10 mutations were present in bilateral deafness patients with inner ear malformation. PMID: 22412181
Downregulation of Kir4.1 channels aggravates the visual impairment caused by the initial photoreceptor degeneration. PMID: 22055109
Gain-of-function defects in Kir4.1 causes dysfunction in astrocytic-dependent potassium buffering and contributes to autism/epilepsy phenotype by altering neuronal excitability and synaptic function. PMID: 21458570
extracellular volume recordings indicate that compromised K(+) spatial buffering in brain underlies the epilepsy phenotype associated with human KCNJ10 mutations PMID: 21748805
Role of KCNJ10 function in the physiology of proximal and possibly also the distal retina. Impact of KCNJ10 mutations on the electroretinogram in four unrelated patients with EAST syndrome. PMID: 21300747
Mutations in the K+ channel gene KCNJ10 (Kir4.1) cause the autosomal recessive EAST syndrome which is characterized by epilepsy, ataxia, sensorineural deafness, and a salt-wasting tubulopathy. PMID: 21221631
This study suggests that the SNPs within the kcnj10 genes we examined do not play a major role in schizophrenia in the Han Chinese population. PMID: 20933057
CaR decreases cell surface expression of Kir4.1 channels via a mechanism that involves Galpha(q) and caveolin. PMID: 21084311
Perturbed pH gating may underlie the loss of channel function for the disease-associated mutant Kir4.1 channels and may have important physiologic consequences. [review] PMID: 21088294
The Kir4.1 channel transgene plays a role in setting the membrane potential of glial cells and in maintaining potassium permeability in glial-conditioned Kir4.1 knock-out mice. PMID: 21106816
SLC26A4, FOXI1 and KCNJ10 are not major determinants in unilateral deafness and enlarged vestibular aqueduct PMID: 20621367
When expressed in CHO and HEK293 cells, the KCNJ10 mutations R65P, G77R, and R175Q caused a marked impairment of channel function PMID: 20651251
Variations in the AQP4 and the KCNJ10/KCNJ9 region are likely to be associated with temporal lobe epilepsy. PMID: 19864112
molecular analysis on chromosome 1q as a candidate gene for Type 2 diabetes in Pima Indians PMID: 12401729
Arg271Cys missense variation in KCNJ10 (or a nearby variation) is related to general seizure susceptibility in humans. PMID: 15120748
Our results support previous evidence that the common KCNJ10 Arg271Cys missense variation influences seizure susceptibility of common IGE syndromes. PMID: 15725393
Calcium-sensing receptor interacts directly with Kir4.1 and Kir4.2 and can decrease their currents. PMID: 17122384
The results showed that the expression of Kir 4.1 mRNA and protein, as well as the Kir 4.1 immunoreactivity score (IRS), increased markedly with increasing pathologic grade. PMID: 18191638
identifY previously unidentified KCNJ10 missense or nonsense mutations on both alleles in all subjects affected by a unique human syndrome, and establish the essential role of basolateral K(+) channels in renal electrolyte homeostasis. PMID: 19289823
Mutations in KCNJ10 cause a specific disorder. Our findings indicate that KCNJ10 plays a major role in renal salt handling and possibly also in blood-pressure maintenance and its regulation. PMID: 19420365
mutations in the inwardly rectifying K(+) channel gene KCNJ10 are associated with nonsyndromic hearing loss in carriers of SLC26A4 mutations with an EVA/PS phenotype. PMID: 19426954

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