KCNJ5 sirna

KCNJ5 siRNA (Rat)

Cat. Num. AAA8215226

• Reactivity: Rat
• Applications: RNA Interference (RNAi)
• Purity: > 97%
• Synonyms: KCNJ5; KCNJ5 siRNA (Rat); GIRK4; G protein-activated inward rectifier potassium channel 4; GIRK-4; Cardiac inward rectifier; CIR; Heart KATP channel; Inward rectifier K(+) channel Kir3.4; KATP-1; Potassium channel. inwardly rectifying subfamily J member 5; KCNJ5 sirna

• Host: Synthetic
• Reactivity: Rat
• Specificity: KCNJ5 siRNA (Rat) is a target-specific 19-23 nt siRNA oligo duplexes designed to knock down gene expression.
• Purity/Purification: > 97%
• Form/Format: Lyophilized powder
• Sequence Length: 419

• Applicable Applications for KCNJ5 sirna: RNA Interference (RNAi)
• Quality Control: Oligonucleotide synthesis is monitored base by base through trityl analysis to ensure appropriate coupling efficiency. The oligo is subsequently purified by affinity-solid phase extraction. The annealed RNA duplex is further analyzed by mass spectrometry to verify the exact composition of the duplex. Each lot is compared to the previous lot by mass spectrometry to ensure maximum lot-to-lot consistency.
• Directions for Use: We recommends transfection with 100 nM siRNA 48 to 72 hours prior to cell lysis. Before resuspending, briefly centrifuge the tube to ensure the lyophilized siRNA is at the bottom of the tube. Resuspend the siRNA oligos to an appropriate concentration with DEPC water. For each vial, suitable for 250 transfections in 24 well plate (20 pmol for each well).
• Components: We offer pre-designed sets of 3 different target-specific siRNA oligo duplexes of rat KCNJ5 gene. Each vial contains 5 nmol of lyophilized siRNA. The duplexes can be transfected individually or pooled together to achieve knockdown of the target gene, which is most commonly assessed by qPCR or western blot. Our siRNA oligos are also chemically modified (2'-OMe) at no extra charge for increased stability and enhanced knockdown in vitro and in vivo.
• Preparation and Storage: Shipped at 4 degree C. Store at -20 degree C for one year.

Related Product Information for KCNJ5 sirna

siRNA to inhibit KCNJ5 expression using RNA interference

NCBI and Uniprot Product Information

• NCBI GI #: 8393654
• NCBI GeneID: 29713
• NCBI Accession #: NP_058993.1
• NCBI GenBank Nucleotide #: NM_017297.2
• UniProt Accession #: P48548
• Molecular Weight: 47,783 Da
• NCBI Official Full Name: G protein-activated inward rectifier potassium channel 4
• NCBI Official Synonym Full Names: potassium channel, inwardly rectifying subfamily J, member 5
• NCBI Official Symbol: Kcnj5
• 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
• UniProt Entry Name: KCNJ5_RAT

NCBI Description

inwardly-rectifying potassium channel which is controlled by G proteins [RGD, Feb 2006]

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

Cellular Component: integral to plasma membrane; T-tubule; integral to membrane; external side of plasma membrane

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

Biological Process: potassium ion import