KIR3.4 blocking peptide

KIR3.4 Peptide

Cat. Num. AAA3005947

• Gene Names: KCNJ5; CIR; GIRK4; KATP1; LQT13; KIR3.4
• Applications: Blocking
• Purity: Synthetic peptide KIR3.4. (Note: the amino acid sequence is proprietary).; The purity is >98%.
• Synonyms: KIR3.4; KIR3.4 Peptide; G protein-activated inward rectifier potassium channel 4; GIRK-4; GIRK4; Cardiac inward rectifier; CIR; Heart KATP channel; Inward rectifier K(+) channel Kir3.4; IRK-4; KATP-1; IRK4; KATP1; Potassium channel; inwardly rectifying subfamily J member 5; KCNJ5; KIR3.4 blocking peptide

• Specificity: This peptide can be used with studies using MBS3005946 KIR3.4 pAb.
• Purity/Purification: Synthetic peptide KIR3.4. (Note: the amino acid sequence is proprietary).; The purity is >98%.
• Form/Format: 1 mg/ml in DI water.
• Sequence Length: 418

• Applicable Applications for KIR3.4 blocking peptide: Blocking
• Preparation and Storage: Store at 4 degree C short term.; Aliquot and store at -20 degree C long term.; Avoid freeze-thaw cycles.

Related Product Information for KIR3.4 blocking peptide

G protein-coupled inwardly rectifying potassium channels (Kir3.1 through Kir3.4) are coupled to numerous neurotransmitter receptors in the brain and are abundantly expressed in the olfactory bulb, hippocampus, neocortex, dentate gyrus, cerebellar cortex and thalamus regions of the brain. Also known as GIRK, Kir3 potassium channels localize to the soma and dendrites as well as axons of neurons. Liberated Gbg subunits from G protein heterotrimers bind to and regulate Kir3 channel activity. Gb3- and Gb4-containing Gbg dimers bind directly to cytoplasmic domains of Kir3 proteins and increase the K+ current while Gb5-containing Gbg dimers inhibit Kir3 K+ current. Kir3 activity is also inhibited by tyrosine phosphorylation. Brain-derived neurotrophic factor activates receptor tyrosine kinase B, which then phosphorylates Kir3 tyrosine residues, effectively inactivating the Kir3 channels.

NCBI and Uniprot Product Information

• NCBI GI #: 67677839
• NCBI GeneID: 3762
• UniProt Accession #: P48544
• NCBI Official Full Name: KCNJ5 protein, partial
• NCBI Official Synonym Full Names: potassium inwardly rectifying 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
• 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