Mouse KCNJ5 Monoclonal Antibody | anti-KCNJ5 antibody

KCNJ5 (Potassium inwardly-rectifying Channel, Subfamily J, Member 5, CIR, GIRK4, KATP1, KIR3.4) (HRP)

Cat. Num. AAA6183371

• Gene Names: KCNJ5; CIR; GIRK4; KATP1; LQT13; KIR3.4
• Applications: Western Blot
• Purity: Purified
• Synonyms: KCNJ5; Monoclonal Antibody; KCNJ5 (Potassium inwardly-rectifying Channel; Subfamily J; Member 5; CIR; GIRK4; KATP1; KIR3.4) (HRP); Potassium inwardly-rectifying Channel; KIR3.4; anti-KCNJ5 antibody

• Host: Mouse
• Clonality: Monoclonal
• Isotype: IgG2a,k
• Clone Number: 8D2
• Specificity: Recognizes KCNJ5.
• Purity/Purification: Purified
• Form/Format: Supplied as a liquid in PBS, pH 7.2. No preservative added. Labeled with horseradish peroxidase (HRP).

• Applicable Applications for anti-KCNJ5 antibody: Western Blot (WB)
• Application Notes: Applications are based on unconjugated antibody.
• Immunogen: KCNJ5 (NP_000881.3, 321aa-419aa) partial recombinant protein with GST tag. MW of the GST tag alone is 26kD.
• Immunogen Sequence: SYMDTEVLWGHRFTPVLTLEKGFYEVDYNTFHDTYETNTPSCCAKELAEMKREGRLLQYLPSPPLLGGCAEAGLDAEAEQNEEDEPKGLGGSREARGSV
• Conjugate: HRP
• Preparation and Storage: Store product at 4 degree C if to be used immediately within two weeks. For long-term storage, aliquot to avoid repeated freezing and thawing and store at -20 degree C. Aliquots are stable at -20 degree C for 12 months after receipt. Dilute required amount only prior to immediate use. Further dilutions can be made in assay buffer. Note: Sodium azide is a potent inhibitor of peroxidase and should not be added to HRP conjugates. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap.

Western Blot (WB)

(KCNJ5 monoclonal antibody (M01), clone 8D2. Western Blot analysis of KCNJ5 expression in K-562.)

Testing Data

(Detection limit for recombinant GST tagged KCNJ5 is 0.03 ng/ml as a capture antibody.)

Product Categories/Family for anti-KCNJ5 antibody

Antibodies; Ion Channel

NCBI and Uniprot Product Information

• NCBI GI #: 24797141
• NCBI GeneID: 3762
• NCBI Accession #: NP_000881.3
• NCBI GenBank Nucleotide #: NM_000890.4
• UniProt Accession #: P48544; Q6DK13; Q6DK14; Q92807; B2R744
• Molecular Weight: 47,668 Da
• NCBI Official Full Name: G protein-activated inward rectifier potassium channel 4
• NCBI Official Synonym Full Names: potassium voltage-gated channel subfamily J member 5
• NCBI Official Symbol: KCNJ5
• NCBI Official Synonym Symbols: CIR; GIRK4; KATP1; LQT13; KIR3.4
• NCBI Protein Information: G protein-activated inward rectifier potassium channel 4
• UniProt Protein Name: G protein-activated inward rectifier potassium channel 4
• Protein Family: G protein-activated inward rectifier potassium channel
• UniProt Gene Name: KCNJ5
• UniProt Synonym Gene Names: GIRK4; GIRK-4; CIR; IRK-4
• UniProt Entry Name: KCNJ5_HUMAN

NCBI Description

This gene encodes an integral membrane protein which belongs to one of seven subfamilies of inward-rectifier potassium channel proteins called potassium channel subfamily J. The encoded protein is a subunit of the potassium channel which is homotetrameric. It is controlled by G-proteins and has a greater tendency to allow potassium to flow into a cell rather than out of a cell. Naturally occurring mutations in this gene are associated with aldosterone-producing adenomas. [provided by RefSeq, Aug 2017]

Uniprot Description

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: 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