G蛋白激活内向钾通道5抗体
规格：1mg/1ml
英文名： KCNJ5
别名： inwardly rectifying subfamily J member 5; Cardiac ATP sensitive potassium channel; Cardiac inward rectifier; CIR; G protein activated inward rectifier potassium channel 4; G protein-activated inward r
分子量： 48kDa
储存液：0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glyce
克隆类型：Polyclonal
亚型：IgG
纯化方法：affinity purified by Protein A
**原：KLH conjugated synthetic peptide derived from human KCNJ5
交叉反应：Human, Mouse, Rat, Chicken, Pig, Cow, Horse, Rabbit, Sheep,
细胞定位：细胞膜
G蛋白激活内向钾通道5抗体产品介绍：background: 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, is controlled by G-proteins. It may associate with two other G-protein-activated potassium channels to form a heteromultimeric pore-forming complex. [provided by RefSeq, Jul 2008]. Function: This potassium channel is controlled by G proteins. 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 external barium. Subunit: May associate with GIRK1 and GIRK2 to form a G-protein-activated heteromultimer pore-forming unit. The resulting inward current is much larger (By similarity). Subcellular Location:G蛋白激活内向钾通道5抗体 Membrane; Multi-pass membrane protein. Tissue Specificity: Islets, exocrine pancreas and heart. DISEASE: Defects in KCNJ5 are the cause of long QT syndrome type 13 (LQT13) [MIM:613485]. It is a heart disorder 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, and can present with a sentinel event of sudden cardiac death in infancy. Defects in KCNJ5 are the cause of familial hyperaldosteronism type 3 (FH3) [MIM:613677]. A form of hyperaldosteronism characterized by hypertension secondary to massive adrenal mineralocorticoid production. Like patients with familial hyperaldosteronism type 1 (glucocorticoid-remediable aldosteronism), patients with FH3 present with childhood hypertension, elevated aldosteronism levels,G蛋白激活内向钾通道5抗体 and high levels of the hybrid steroids 18-oxocortisol and 18-hydroxycortisol. However, hypertension and aldosteronism are not reversed by administration of exogenous glucocorticoids and patients require adrenalectomy to control hypertension. Note=Somatic mutations in KCNJ5 have been found in aldosterone-producing adrenal adenomas and can be responsible for aldosteronism associated with cell autonomous proliferation. These are typically solitary, well circumscribed tumors diagnosed between ages 30 and 70. They come to medical attention due to new or worsening hypertension, often with hypokalemia. KCNJ5 mutations produce increased sodium conductance and cell depolarization, which in adrenal glomerulosa cells produces calcium entry, the signal for aldosterone production and cell proliferation. Similarity: Belongs to the inward rectifier-type potassium channel (TC 1.A.2.1) family. KCNJ5 subfamily. Database links: Entrez Gene: 3762 Human Entrez Gene: 16521 Mouse Entrez Gene: 29713 Rat Omim: 600734 Human SwissProt: P48544 Human SwissProt: P48545 Mouse SwissProt: P48548 Rat Unigene: 632109 Human Unigene: 69472 Mouse Unigene: 10047 Rat Important Note: This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. Involvement in disease; Defects in KCNJ5 are the cause of long QT syndrome type 13 (LQT13). It is a heart disorder 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, and can present with a sentinel event of sudden cardiac death in infancy.
G蛋白激活内向钾通道5抗体产品应用：WB=1:100-500 ELISA=1:500-1000 IHC-P=1:100-500 IHC-F=1:100-500 ICC=1:100-500 IF=1:50-200 （石蜡切片需做抗原修复） not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user.
研究领域：肿瘤 心血管 神经生物学 通道蛋白 G蛋白信号
储存条件： Store at -20 °C for one year. Avoid repeated freeze/thaw cycles.
来源： Rabbit
外观： Lyophilized or Liquid