G protein-activated inward rectifier potassium channel 4 (KCNJ5), ELISA Kit

For Research Use Only. Not for use in diagnostic procedures.

Store all reagents at 2-8 degree C.

We suggest pre-experimenting with neat (undiluted) samples, 1:2 or 1:4 dilutions. Please avoid diluting your samples more than 1:10 as it would exceed the dilution limit set for this kit. If the expected concentration of the target is beyond the detection range of the kit, please contact our technical support team

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Small volumes of KCNJ5 elisa kit vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

MBS7237100 is a ready-to-use microwell, strip plate ELISA (enzyme-linked immunosorbent assay) Kit for analyzing the presence of the G protein-activated inward rectifier potassium channel 4 (KCNJ5) ELISA Kit target analytes in biological samples. The concentration gradients of the kit standards or positive controls render a theoretical kit detection range in biological research samples containing KCNJ5. The ELISA analytical biochemical technique of the MBS7237100 kit is based on KCNJ5 antibody-KCNJ5 antigen interactions (immunosorbency) and an HRP colorimetric detection system to detect KCNJ5 antigen targets in samples. The ELISA Kit is designed to detect native, not recombinant, KCNJ5. Appropriate sample types may include undiluted body fluids and/or tissue homogenates, secretions. Quality control assays assessing reproducibility identified the intra-assay CV (%) and inter-assay CV(%).

47,668 Da

potassium inwardly-rectifying channel, subfamily J, member 5

G protein-activated inward rectifier potassium channel 4; IRK-4; heart KATP channel; inward rectifier K+ channel KIR3.4; cardiac ATP-sensitive potassium channel

G protein-activated inward rectifier potassium channel 4

GIRK4; GIRK-4; CIR; IRK-4  [Similar Products]

KCNJ5_HUMAN

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: Channel, potassium; Membrane protein, multi-pass; Membrane protein, integral

Chromosomal Location of Human Ortholog: 11q24

Cellular Component: voltage-gated potassium channel complex; plasma membrane

Molecular Function: protein binding; G-protein activated inward rectifier potassium channel activity; inward rectifier potassium channel activity

Biological Process: synaptic transmission; potassium ion import; potassium ion transport

Disease: Hyperaldosteronism, Familial, Type Iii; Long Qt Syndrome 13

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