| 產(chǎn)品編號(hào) | bs-17067R |
| 英文名稱(chēng) | Kir2.1 Rabbit pAb |
| 中文名稱(chēng) | 鉀離子通道Kir2.1抗體 |
| 別 名 | Cardiac inward rectifier potassium channel; HHBIRK 1; HHBIRK1; HHIRK1; HIRK 1; hIRK1; Inward rectifier K; inwardly rectifying subfamily J member 2; IRK 1; IRK2_HUMAN; IRK1; KCNJ2; KIR2.1; LQT7; Potassium channel; Potassium channel inwardly rectifying subf |
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Specific References (5) | bs-17067R has been referenced in 5 publications.
[IF=5.9] Zhao, Jing, et al. "Chronic obstructive sleep apnea causes atrial remodeling in canines: mechanisms and implications." Basic Research in Cardiology 109.5 (2014): 1-13. WB ; Dog.
[IF=3.499] Zhan C et al. Rotenone and 3-bromopyruvate toxicity impacts electrical and structural cardiac remodeling in rats. Toxicol Lett. 2019 Oct 1. pii: S0378-4274(19)30295-4. WB&IHC-P ; Rat.
[IF=1.396] Fang W et al. Lipopolysaccharides increase Kir2. 1 expression in lung endothelial cells. Int J Clin Exp Pathol 2018;11(6):2959-2967 WB ; Mouse.
[IF=1.396] Fang W et al. Lipopolysaccharides increase Kir2.1 expression in lung endothelial cells. Int J Clin Exp Pathol. 2018 Jun 1;11(6):2959-2967. eCollection 2018. WB&ICF ; Mouse.
[IF=1.339] Li W et al. MiR-1/133 attenuates cardiomyocyte apoptosis and electrical remodeling in mice with viral myocarditis. Cardiol J. 2019 Apr 17. WB ; Mouse.
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| 研究領(lǐng)域 | 細(xì)胞生物 神經(jīng)生物學(xué) 通道蛋白 |
| 抗體來(lái)源 | Rabbit |
| 克隆類(lèi)型 | Polyclonal |
| 交叉反應(yīng) | Mouse,Rat (predicted: Human,Rabbit,Pig,Sheep,Cow,Chicken,Dog,Horse) |
| 產(chǎn)品應(yīng)用 | WB=1:500-2000,Flow-Cyt=1μg/Test
not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. |
| 理論分子量 | 48 kDa |
| 檢測(cè)分子量 | |
| 細(xì)胞定位 | 細(xì)胞膜 |
| 性 狀 | Liquid |
| 濃 度 | 1mg/ml |
| 免 疫 原 | KLH conjugated synthetic peptide derived from human Kir2.1: 31-130/427 |
| 亞 型 | IgG |
| 純化方法 | affinity purified by Protein A |
| 緩 沖 液 | 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol. |
| 保存條件 | Shipped at 4℃. Store at -20℃ for one year. Avoid repeated freeze/thaw cycles. |
| 注意事項(xiàng) | This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
| PubMed | PubMed |
| 產(chǎn)品介紹 |
Potassium channels are present in most mammalian cells, where they participate in a wide range of physiologic responses. The protein encoded by this gene is an integral membrane protein and inward-rectifier type potassium channel. The encoded protein, which has a greater tendency to allow potassium to flow into a cell rather than out of a cell, probably participates in establishing action potential waveform and excitability of neuronal and muscle tissues. Mutations in this gene have been associated with Andersen syndrome, which is characterized by periodic paralysis, cardiac arrhythmias, and dysmorphic features. [provided by RefSeq, Jul 2008] Function: Probably participates in establishing action potential waveform and excitability of neuronal and muscle tissues. 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 or cesium. Subcellular Location: Membrane. Tissue Specificity: Heart, brain, placenta, lung, skeletal muscle, and kidney. Diffusely distributed throughout the brain. DISEASE: Defects in KCNJ2 are the cause of long QT syndrome type 7 (LQT7) [MIM:170390]; also called Andersen syndrome or Andersen cardiodysrhythmic periodic paralysis. Long QT syndromes are heart disorders characterized by a prolonged QT interval on the ECG and polymorphic ventricular arrhythmias. They cause syncope and sudden death in response to excercise or emotional stress. LQT7 manifests itself as a clinical triad consisting of potassium-sensitive periodic paralysis, ventricular ectopy and dysmorphic features. Defects in KCNJ2 are the cause of short QT syndrome type 3 (SQT3) [MIM:609622]. Short QT syndromes are heart disorders characterized by idiopathic persistently and uniformly short QT interval on ECG in the absence of structural heart disease in affected individuals. They cause syncope and sudden death. SQT3 has a unique ECG phenotype characterized by asymmetrical T waves. Similarity: Belongs to the inward rectifier-type potassium channel (TC 1.A.2.1) family. KCNJ2 subfamily. SWISS: P63252 Gene ID: 3759 Database links: Entrez Gene: 3759 Human Entrez Gene: 16518 Mouse Omim: 600681 Human SwissProt: P63252 Human SwissProt: P35561 Mouse Unigene: 1547 Human Unigene: 4951 Mouse Unigene: 44415 Rat |
| 產(chǎn)品圖片 |
Sample: heart (Mouse) Lysate at 40 ug
Primary: Anti-Kir2.1(bs-17067R) at 1/300 dilution
Secondary: IRDye800CW Goat Anti-Rabbit IgG at 1/20000 dilution
Predicted band size: 48 kD
Observed band size: 48 kD
Sample:
Bone (Mouse) Lysate at 40 ug
Primary: Anti-Kir2.1 (Bs- 17067R) at 1/300 dilution
Secondary: IRDye800CW Goat Anti-Rabbit IgG at 1/20000 dilution
Predicted band size: 48 kD
Observed band size: 48 kD
Sample:
Muscle (Mouse) Lysate at 40 ug
Primary: Anti-Kir2.1 (Bs- 17067R) at 1/300 dilution
Secondary: IRDye800CW Goat Anti-Rabbit IgG at 1/20000 dilution
Predicted band size: 48 kD
Observed band size: 48 kD
Blank control(blue): RSC96(fixed with 2% paraformaldehyde (10 min)). Primary Antibody:Rabbit Anti- Kir2.1 antibody(bs-17067R), Dilution: 0.2μg in 100 μL 1X PBS containing 0.5% BSA; Isotype Control Antibody: Rabbit IgG(orange) ,used under the same conditions ); Secondary Antibody: Goat anti-rabbit IgG-PE(white blue), Dilution: 1:200 in 1 X PBS containing 0.5% BSA.
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