other

CXCR4 Positive Control

MBS542666

5 Applications

290 USD

Positive Control

CXCR4 Positive Control

[CXCR4]

[Cardiac ATP sensitive potassium channel; Cardiac inward rectifier; CIR; G protein activated inward rectifier potassium channel 4; GIRK 4; Heart KATP channel; Inward rectifier K(+) channel Kir3.4; inwardly rectifying subfamily J member 5; IRK-4; IRK5_HUMAN; KATP 1; KCNJ 5; KIR 3.4; Potassium channel; Potassium channel inwardly rectifying subfamily J member 5 antibody]

[G protein-activated inward rectifier potassium channel 4; G protein-activated inward rectifier potassium channel 4; G protein-activated inward rectifier potassium channel 4; potassium voltage-gated channel subfamily J member 5; Cardiac inward rectifier; CIR; Heart KATP channel; Inward rectifier K(+) channel Kir3.4; IRK-4; KATP-1; Potassium channel, inwardly rectifying subfamily J member 5]

[CXCR4]

[KCNJ5; KCNJ5; CIR; GIRK4; KATP1; LQT13; KIR3.4; GIRK4; GIRK-4; CIR; IRK-4]

KCNJ5_HUMAN

Rabbit

419

Western Blot Positive Control

Store at -20°C for long term storage

Western Blot (WB)

Western Blot: 1:250

Immunogen: Purified Protein. Volume: 20ul per lane

Molecular Function: Potassium. Structure: Belongs to inward rectifier-type potassium channel family. Subcellular Location: Membrane; Multi-pass membrane protein

Western Blot Positive Control G protein-activated inward rectifier potassium channel 4 Antibody

24797141

NP_000881

NM_000890.3

P61073

Activation Of G Protein Gated Potassium Channels Pathway (1268826); Activation Of GABAB Receptors Pathway (1268816); Calcium Regulation In The Cardiac Cell Pathway (198906); Circadian Entrainment Pathway (698773); Circadian Entrainment Pathway (699872); Dopaminergic Synapse Pathway (469199); Dopaminergic Synapse Pathway (469185); Estrogen Signaling Pathway (799177); Estrogen Signaling Pathway (799197); G Protein Gated Potassium Channels Pathway (1268825)

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]

GIRK4: 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. 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. Defects in KCNJ5 are the cause of familial hyperaldosteronism type 3 (FH3). 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. 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. Belongs to the inward rectifier-type potassium channel (TC 1.A.2.1) family. KCNJ5 subfamily. Protein type: Membrane protein, multi-pass; Membrane protein, integral; Channel, potassium. Chromosomal Location of Human Ortholog: 11q24. Cellular Component: external side of plasma membrane; plasma membrane; T-tubule; voltage-gated potassium channel complex. Molecular Function: G-protein activated inward rectifier potassium channel activity; inward rectifier potassium channel activity; protein binding. Biological Process: potassium ion import; potassium ion transport. Disease: Hyperaldosteronism, Familial, Type Iii; Long Qt Syndrome 13

5 Applications

290 USD