Recombinant Human ATP-sensitive inward rectifier potassium channel 10(KCNJ10)

Code CSB-CF012048HUb0
Size
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  • (Tris-Glycine gel) Discontinuous SDS-PAGE (reduced) with 5% enrichment gel and 15% separation gel.
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Product Details

Purity Greater than 85% as determined by SDS-PAGE.
Target Names KCNJ10
Uniprot No. P78508
Research Area Neuroscience
Species Homo sapiens (Human)
Source in vitro E.coli expression system
Expression Region 1-379aa
Target Protein Sequence MTSVAKVYYSQTTQTESRPLMGPGIRRRRVLTKDGRSNVRMEHIADKRFLYLKDLWTTFIDMQWRYKLLLFSATFAGTWFLFGVVWYLVAVAHGDLLELDPPANHTPCVVQVHTLTGAFLFSLESQTTIGYGFRYISEECPLAIVLLIAQLVLTTILEIFITGTFLAKIARPKKRAETIRFSQHAVVASHNGKPCLMIRVANMRKSLLIGCQVTGKLLQTHQTKEGENIRLNQVNVTFQVDTASDSPFLILPLTFYHVVDETSPLKDLPLRSGEGDFELVLILSGTVESTSATCQVRTSYLPEEILWGYEFTPAISLSASGKYIADFSLFDQVVKVASPSGLRDSTVRYGDPEKLKLEESLREQAEKEGSALSVRISNV
Note: The complete sequence including tag sequence, target protein sequence and linker sequence could be provided upon request.
Mol. Weight 48.6 kDa
Protein Length Full Length
Tag Info N-terminal 10xHis-tagged
Form Liquid or Lyophilized powder
Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand.
Buffer If the delivery form is liquid, the default storage buffer is Tris/PBS-based buffer, 5%-50% glycerol. If the delivery form is lyophilized powder, the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, pH 8.0.
Reconstitution We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20℃/-80℃. Our default final concentration of glycerol is 50%. Customers could use it as reference.
Troubleshooting
and FAQs
Protein FAQs
Storage Condition Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
Shelf Life The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
Lead Time Delivery time may differ from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
Notes Repeated freezing and thawing is not recommended. Store working aliquots at 4℃ for up to one week.
Datasheet & COA Please contact us to get it.

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Target Background

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.
Gene References into Functions
  1. 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
  2. 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
  3. rs17375748, rs1130183, rs12133079 and rs1186688 associated with sudden infant death syndrome PMID: 28520217
  4. kcnj10 plays a role in K(+) recycling across the basolateral membrane in corresponding nephron segments and in generating negative membrane potential--{REVIEW} PMID: 27122539
  5. Previous research had shown that Kir4.1 protein autoantibodies were specific for multiple sclerosis but they found that they weren't. PMID: 27074083
  6. This study identifies potential SNPs of KCNJ10 gene that may contribute to seizure susceptibility and anti-epileptic drug resistance. PMID: 25874548
  7. 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
  8. 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
  9. This study showed that rs2486253, but not rs61822012, polymorphism of KCNJ10 gene was associated with childhood idiopathic generalized epilepsy. PMID: 25008907
  10. we confirmed the presence of anti-Kir4.1 antibodies in multiple sclerosis patients, but at a much lower prevalence than previously reported. PMID: 24756568
  11. KCNJ10 SNP is not associated with nonsyndromic enlargement of vestibular aqueduct in Chinese patients. PMID: 25372295
  12. 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
  13. 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
  14. 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
  15. Mislocalization of the Kir4.1 channels contributes to renal salt wasting. PMID: 24561201
  16. KCNJ10rs1130183 did not contribute to risk of seizure susceptibility. PMID: 24378235
  17. Study confirms that EAST syndrome can be caused by many different mutations in KCNJ10 that significantly reduce K+ conductance. PMID: 21849804
  18. Ordered disorder of the astrocytic dystrophin-associated protein complex in the norm and pathology. PMID: 24014171
  19. 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
  20. the modulation of tyrosine phosphorylation of KCNJ10 should play a role in regulating membrane transport function in DCT1. PMID: 23873931
  21. We found no evidence for a significant association between mutations of KCNJ10 and FOXI1 with SLC26A4 in Pendred syndrome/enlarged vestibular aqueducts. PMID: 23965030
  22. 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
  23. Oligodendrocyte precursor cells establish themselves progressively through postnatal upregulation of Kir4.1 potassium channels. PMID: 23392672
  24. 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
  25. This study demonistrated that Loss of perivascular Kir4.1 potassium channels in the sclerotic hippocampus of patients with mesial temporal lobe epilepsy. PMID: 22878665
  26. No KCNJ10 mutations were present in bilateral deafness patients with inner ear malformation. PMID: 22412181
  27. Downregulation of Kir4.1 channels aggravates the visual impairment caused by the initial photoreceptor degeneration. PMID: 22055109
  28. 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
  29. extracellular volume recordings indicate that compromised K(+) spatial buffering in brain underlies the epilepsy phenotype associated with human KCNJ10 mutations PMID: 21748805
  30. 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
  31. 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
  32. 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
  33. CaR decreases cell surface expression of Kir4.1 channels via a mechanism that involves Galpha(q) and caveolin. PMID: 21084311
  34. 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
  35. 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
  36. SLC26A4, FOXI1 and KCNJ10 are not major determinants in unilateral deafness and enlarged vestibular aqueduct PMID: 20621367
  37. When expressed in CHO and HEK293 cells, the KCNJ10 mutations R65P, G77R, and R175Q caused a marked impairment of channel function PMID: 20651251
  38. Variations in the AQP4 and the KCNJ10/KCNJ9 region are likely to be associated with temporal lobe epilepsy. PMID: 19864112
  39. molecular analysis on chromosome 1q as a candidate gene for Type 2 diabetes in Pima Indians PMID: 12401729
  40. Arg271Cys missense variation in KCNJ10 (or a nearby variation) is related to general seizure susceptibility in humans. PMID: 15120748
  41. Our results support previous evidence that the common KCNJ10 Arg271Cys missense variation influences seizure susceptibility of common IGE syndromes. PMID: 15725393
  42. Calcium-sensing receptor interacts directly with Kir4.1 and Kir4.2 and can decrease their currents. PMID: 17122384
  43. 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
  44. 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
  45. 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
  46. 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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Involvement in disease Seizures, sensorineural deafness, ataxia, mental retardation, and electrolyte imbalance (SESAMES)
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
Tissue Specificity Expressed in kidney (at protein level).
Database Links

HGNC: 6256

OMIM: 602208

KEGG: hsa:3766

STRING: 9606.ENSP00000357068

UniGene: Hs.408960

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