| 產(chǎn)品編號 | bs-6760R |
| 英文名稱 | KCNQ1 Rabbit pAb |
| 中文名稱 | 鉀離子通道蛋白家族KCNQ1抗體 |
| 別 名 | KCNQ-1; ATFB1; ATFB3; IKs producing slow voltage-gated potassium channel subunit alpha; IKs producing slow voltage-gated potassium channel subunit alpha KvLQT1; Jervell and Lange-Nielsen syndrome 1; JLNS1; KCNA8; KCNA9; KCNQ1; KCNQ1_HUMAN; kidney and card |
 |
Specific References (2) | bs-6760R has been referenced in 2 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=0] Trotta et al. Inhibition of aldose-reductase-2 by a benzofuroxane derivative bf-5m increases the expression of kcne1, kcnq1 in high glucose cultured H9c2 cardiac cells and sudden cardiac death. (2018) Oncotarget. 9:17257-17269 IF ; Rat.
|
| 研究領(lǐng)域 | 心血管 細胞生物 神經(jīng)生物學 通道蛋白 細胞膜受體 細胞表面分子 |
| 抗體來源 | Rabbit |
| 克隆類型 | Polyclonal |
| 交叉反應(yīng) | (predicted: Human,Mouse,Rat,Cow,Chicken,Dog) |
| 產(chǎn)品應(yīng)用 | WB=1:500-2000,IHC-P=1:100-500,IHC-F=1:100-500,IF=1:100-500,ELISA=1:5000-10000
not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. |
| 理論分子量 | 75 kDa |
| 檢測分子量 | |
| 細胞定位 | 細胞漿 細胞膜 |
| 性 狀 | Liquid |
| 濃 度 | 1mg/ml |
| 免 疫 原 | KLH conjugated synthetic peptide derived from human KCNQ-1: 501-600/676 |
| 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 | 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 |
Probably important in cardiac repolarization. Associates with KCNE1 (MinK) to form the I(Ks) cardiac potassium current. Elicits a rapidly activating, potassium-selective outward current. Muscarinic agonist oxotremorine-M strongly suppresses KCNQ1/KCNE1 current in CHO cells in which cloned KCNQ1/KCNE1 channels were coexpressed with M1 muscarinic receptors. May associate also with KCNE3 (MiRP2) to form the potassium channel that is important for cyclic AMP-stimulated intestinal secretion of chloride ions, which is reduced in cystic fibrosis and pathologically stimulated in cholera and other forms of secretory diarrhea.
Involvement in disease: Function: Probably important in cardiac repolarization. Associates with KCNE1 (MinK) to form the I(Ks) cardiac potassium current. Elicits a rapidly activating, potassium-selective outward current. Muscarinic agonist oxotremorine-M strongly suppresses KCNQ1/KCNE1 current in CHO cells in which cloned KCNQ1/KCNE1 channels were coexpressed with M1 muscarinic receptors. May associate also with KCNE3 (MiRP2) to form the potassium channel that is important for cyclic AMP-stimulated intestinal secretion of chloride ions, which is reduced in cystic fibrosis and pathologically stimulated in cholera and other forms of secretory diarrhea. Subunit: Heterotetramer with KCNE1 (MinK) or KCNE3 (MiRP2). Interacts with CALM. Subcellular Location: Cell membrane; Multi-pass membrane protein. Cytoplasmic vesicle membrane; Multi-pass membrane protein. Tissue Specificity: Abundantly expressed in heart, pancreas, prostate, kidney, small intestine and peripheral blood leukocytes. Less abundant in placenta, lung, spleen, colon, thymus, testis and ovaries. DISEASE: Defects in KCNQ1 are the cause of long QT syndrome type 1 (LQT1) ; also known as Romano-Ward syndrome (RWS). 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 exercise or emotional stress. LQT1 inheritance is an autosomal dominant. Defects in KCNQ1 are the cause of Jervell and Lange-Nielsen syndrome type 1 (JLNS1) . JLNS1 is an autosomal recessive disorder characterized by congenital deafness, prolongation of the QT interval, syncopal attacks due to ventricular arrhythmias, and a high risk of sudden death. Defects in KCNQ1 are the cause of atrial fibrillation familial type 3 (ATFB3) . Atrial fibrillation is a common disorder of cardiac rhythm that is hereditary in a small subgroup of patients. It is characterized by disorganized atrial electrical activity and ineffective atrial contraction promoting blood stasis in the atria and reduces ventricular filling. It can result in palpitations, syncope, thromboembolic stroke, and congestive heart failure. Similarity: Belongs to the potassium channel family. KQT (TC 1.A.1.15) subfamily. Kv7.1/KCNQ1 sub-subfamily. SWISS: P51787 Gene ID: 3784 Database links: UniProtKB/Swiss-Prot: P51787.3 |
| 1、抗體溶解方法 | |
| 2、抗體修復方式 | |
| 3、常用試劑的配制 | |
| 4、免疫組化操作步驟 | |
| 5、免疫組化問題解答 | |
| 6、Western Blotting 操作步驟 | |
| 7、Western Blotting 問題解答 | |
| 8、關(guān)于肽鏈的設(shè)計 | |
| 9、多肽的溶解與保存 | |
| 10、酶標抗體效價測定程序 | |
