Recombinant Rat ATP-sensitive inward rectifier potassium channel 10 (Kcnj10)-VLPs

中文名稱：

Recombinant Rat ATP-sensitive inward rectifier potassium channel 10 (Kcnj10)-VLPs
貨號：

CSB-MP012048RA
說明書：

MSDS Datasheet
規格：
其他：

產品詳情
產品評價
相關產品
靶點詳情

產品詳情

基因名：

Kcnj10
Uniprot No.：

P49655
別名：

(ATP-sensitive inward rectifier potassium channel KAB-2)(BIR10)(Brain-specific inwardly rectifying K(+) channel 1)(BIRK1)(Inward rectifier K(+) channel Kir4.1)(Potassium channel, inwardly rectifying subfamily J member 10)
種屬：

Rattus norvegicus (Rat)
蛋白長度：

Full Length
來源：

Mammalian cell
表達區域：

1-379aa
氨基酸序列

MTSVAKVYYSQTTQTESRPLVAPGIRRRRVLTKDGRSNVRMEHIADKRFLYLKDLWTTFIDMQWRYKLLLFSATFAGTWFLFGVVWYLVAVAHGDLLELGPPANHTPCVVQVHTLTGAFLFSLESQTTIGYGFRYISEECPLAIVLLIAQLVLTTILEIFITGTFLAKIARPKKRAETIRFSQHAVVAYHNGKLCLMIRVANMRKSLLIGCQVTGKLLQTHQTKEGENIRLNQVNVTFQVDTASDSPFLILPLTFYHVVDETSPLKDLPLRSGEGDFELVLILSGTVESTSATCQVRTSYLPEEILWGYEFTPAISLSASGKYVADFSLFDQVVKVASPGGLRDSTVRYGDPEKLKLEESLREQAEKEGSALSVRISNV
Note: The complete sequence may include tag sequence, target protein sequence, linker sequence and extra sequence that is translated with the protein sequence for the purpose(s) of secretion, stability, solubility, etc.
If the exact amino acid sequence of this recombinant protein is critical to your application, please explicitly request the full and complete sequence of this protein before ordering.
蛋白標簽：

C-terminal 10xHis-tagged
If you have specified tag type, please tell us and we will check if it's possible to develop.
產品提供形式：

Lyophilized powder Warning: in_array() expects parameter 2 to be array, null given in /www/web/cusabio_cn/public_html/caches/caches_template/default/content/show_product_protein.php on line 662
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.
緩沖液：

Lyophilized from PBS, 6% Trehalose, pH 7.4.
復溶：

We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein indeionized sterile water to a concentration of 0.1-1.0 mg/mL.Aliquot for long-term storage at -80℃. Solubilize for 60 minutes at room temperature with occasional gentle mixing. Avoid vigorous shaking or vortexing.
儲存條件：

Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
保質期：

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.
貨期：

Delivery time may differ from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
注意事項：

The VLPs are expressed from human 293 cells (HEK293).Mix the sample gently by repeatedly pipetting it up and down. Do not vortex. Repeated freezing and thawing is not recommended.Store the protein at -20℃/-80℃ upon receiving it, and ensure to avoid repeated freezing and thawing, otherwise, it will affect the protein activity. The immunization strategy should be optimized (antigen dose, regimen and adjuvant).
Datasheet & COA：

Please contact us to get it.

產品評價

靶點詳情

功能：

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.
基因功能參考文獻：
1. H3K9me2 and G9a are sensitive to epileptic seizure activity during the acute phase of epilepsy and can affect the transcriptional regulation of the Kcnj10 (Kir4.1) channel. PMID: 29115470
2. studies suggest that AGE-modification of laminin is detrimental to Kir4.1 channels. By studying the role of AGEs in Kir4.1 channels we have identified a novel mechanism of Muller cell dysfunction and its subsequent involvement in Diabetic retinopathy. PMID: 29474462
3. IL-1beta promotes the proliferation of cultured astrocytes by influencing the expression of Kir4.1. PMID: 28395711
4. Kir4.1 channels possess a diurnal rhythm, and this rhythm is dampened with diabetes, thereby suggesting that the increase in TNF-alpha is detrimental to normal Kir4.1 rhythm and expression. PMID: 28460049
5. This study demonstrated changes in Kir4.1 expression in an animal model of PTS in the acute and chronic stages of the condition. PMID: 26768400
6. This study demonstrated that Kir4.1 developmental expression both in the cortex and hippocampus and support the glial role of Kir4.1 in K(+) spatial buffering. PMID: 26427731
7. data suggest that G83V, L166Q, and Q212R residues play a pivotal role in controlling Kir4.1 channel function. PMID: 26867573
8. Data suggest that lipopolysaccharide (LPS)-induced downregulation of inwardly rectifying K(+) channel Kir4.1 mRNA in cultured astrocytes might be related with the inflammatory cytokine IL-1beta. PMID: 26927380
9. Over-activation of NMDA receptors is a primary cause of the reduction of Kir4.1 expression in CNS disorders associated with increased exposure to glutamate. PMID: 25451797
10. Ependymal cells and tanycytes differentially operate Kir4.1 and AQP4 actively to control the property of fluids at local areas in the brain. PMID: 25380566
11. This study demonistrated that the epigenetic regulation of Kir4.1, a glial-specific K+ channel, known to be essential for normal CNS development. PMID: 24415225
12. The present results suggest that reduced activity of astrocytic Kir4.1 channels in the amygdala is involved in limbic hyperexcitability in NERs. PMID: 23603404
13. Decreased expression of Kir4.1 is observed in the brainstem and cortex from rats in an amyotrophic lateral sclerosis model. PMID: 22987392
14. An uncoupling expression of AQP4 and Kir4.1 on astrocytic end feet is partly responsible for mediation of cytotoxic edema following subarachnoid hemorrhage. PMID: 22420318
15. Kir4.1 channels in satellite glial cells are suppressed during trigeminal inflammatory pain. PMID: 21680091
16. Pigment epithelium-derived factor acts as an antioxidative agent against the decrease in Kir4.1 expression in retinal Muller cells in diabetic conditions. PMID: 22266516
17. down-regulation of Kir4.1 may mediate distinct aspects of Glutamine-induced astrocytic dysfunction in hepatic encephalopathy. PMID: 21538466
18. Astrocytes in the CA1 region of the hippocampus are progressively depolarized following cerebral ischemia coinciding with decreased potassium channel Kir4.1 protein expression in glial cells. PMID: 20833221
19. Heteromeric Kir4.1-Kir5.1 channels confer pH sensitivity to retrotrapezoid nucleus astrocytes. PMID: 20926613
20. Data show that all Kir4.1 mutations compromised channel function, but the underlying mechanisms were different. PMID: 20807765
21. CaR decreases cell surface expression of Kir4.1 channels via a mechanism that involves Galpha(q) and caveolin. PMID: 21084311
22. These results indicate the differential loss of KIR4.1 channel function among SeSAME syndrome mutations. PMID: 20678478
23. In adult rats, Kir4.1 expression is reduced by nearly 80% following crush spinal cord injury. PMID: 20375134
24. data suggest the signals on the COOH terminus of Kir4.1 potassium channel determine the intracellular localization of Kir5.1 potassium channel/Kir4.1 heteromer in distal tubules PMID: 15292049
25. Results demonstrate that variations (T262S and R271C) in the gene encoding Kir4.1 do not produce any observable changes in channel function or in predicted channel structure. PMID: 15936844
26. disruption of the carboxyl-terminal PDZ-binding motif induced mostly clustered distribution but did not reduce whole-cell channel activity PMID: 16033858
27. Kir4.1 channels are primarily responsible for significant hyperpolarization of cortical astrocytes and are likely to play a major role in potassium buffering. Significant inhibition of glutamate clearance in astrocytes with knock-down of Kir4.1 occurs. PMID: 17091490
28. Modulation of the Kcnj10 channel by multiple neuotransmitters via Galphaq-coupled receptors is reported. PMID: 17559083
29. Regional differences in astrocytic expression of Kir4.1 channels result in marked changes in potassium clearance rates in these two regions of the spinal cord. PMID: 17581847
30. While confirming similar properties of glial Kir and recombinant Kir4.1, the results also suggest mechanisms underlying K+ buffering in glial cells. PMID: 18293411
31. These results demonstrate that the phosphorylation-dependent scaffolding of the basolateral K(+) channels by MAGI-1a-long participates in the renal regulation of the fluid and electrolyte homeostasis. PMID: 18303016
32. Silencing Kir4.1 in the trigeminal ganglion using RNA interference (RNAi) results in a reversible change in nociceptive threshold and nociceptive-related behavior. PMID: 18417695
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亞細胞定位：

Membrane; Multi-pass membrane protein. Basolateral cell membrane.
蛋白家族：

Inward rectifier-type potassium channel (TC 1.A.2.1) family, KCNJ10 subfamily
組織特異性：

Predominantly expressed in the brain, including in glial cells of the cerebellum and forebrain. Expressed at lower levels in the kidney, and other peripheral tissues.
數據庫鏈接：

KEGG: rno:29718

STRING: 10116.ENSRNOP00000010146

UniGene: Rn.10196