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货号： bs-9931R-HRP 基本售价： 2980.0 元 规格： 100ul
产品信息
- 产品编号
- bs-9931R-HRP
- 英文名称
- Anti-KCNJ5/HRP
- 中文名称
- 辣根过氧化物酶标记的G蛋白激活内向钾通道5抗体
- 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 rectifier potassium channel 4; GIRK 4; GIRK-4; GIRK4; Heart KATP channel; Inward rectifier K(+) channel Kir3.4; Inward rectifier K+ channel KIR3.4; IRK-4; IRK5_HUMAN; KATP 1; KATP-1; KATP1; KCNJ 5; Kcnj5; KIR 3.4; KIR3.4; Potassium channel; Potassium channel inwardly rectifying subfamily J member 5; Potassium inwardly rectifying channel J5; Potassium inwardly rectifying channel subfamily J member 5.
- 规格价格
- 100ul/2980元购买 大包装/询价
- 说 明 书
- 100ul
- 研究领域
- 肿瘤 心血管 神经生物学 通道蛋白 G蛋白信号
- 抗体来源
- Rabbit
- 克隆类型
- Polyclonal
- 交叉反应
- Human, Mouse, Rat, Chicken, Pig, Cow, Horse, Rabbit, Sheep,
- 产品应用
- WB=1:50-200 ELISA=1:100-1000 IHC-P=1:50-200 IHC-F=1:50-200 ICC=1:50-200
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
- 分 子 量
- 48kDa
- 性 状
- Lyophilized or Liquid
- 浓 度
- 1mg/ml
- 免 疫 原
- KLH conjugated synthetic peptide derived from human KCNJ5
- 亚 型
- IgG
- 纯化方法
- affinity purified by Protein A
- 储 存 液
- 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
- 保存条件
- Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C.
- 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:
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, 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.