Human KCNJ2 ELISA Kit (V2LY-0626-LY2035)

Name: Human KCNJ2 ELISA Kit
SKU: V2LY-0626-LY2035
Rating: 5 (1 reviews)

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Tested Data

Datasheet

SDS

Request for COA

Datasheet Target References Q & As Review & reward Protocols Associated Products

Basic Information

Sensitivity

0.047 ng/mL

Detection Range

0.1-35 ng/mL

Sample Type

Serum, Plasma, cell culture supernates

Specificity

Human

Assay Type

Sandwich

Reactivity

Human

Assay Time

1.5 h

Molecule Mass

48.3 kDa

Components

Pre-coated ELISA plate: 12 wells * 8 detachable strips
Standard solution: 0.5ml x1
Standard diluent: 3ml x1
Streptavidin-HRP: 6ml x1
Stop solution: 6ml x1
Substrate solution A: 6ml x1
Substrate solution B: 6ml x1
Wash buffer concentrate (25x): 20ml x1
Biotinylated antibody: 1ml x1

Formulations & Storage [For reference only, actual COA shall prevail!]

Storage

Store at 2-8°C

More Infomation

Target

Full Name

potassium inwardly rectifying channel subfamily J member 2

Function

Probably participates in establishing action potential waveform and excitability of neuronal and muscle tissues. 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 extracellular barium or cesium.

Biological Process

Cardiac muscle cell action potential involved in contractionManual Assertion Based On ExperimentIMP:BHF-UCL
Cellular potassium ion homeostasisManual Assertion Based On ExperimentTAS:BHF-UCL
Cellular response to mechanical stimulusIEA:Ensembl
Magnesium ion transportIEA:Ensembl
Membrane depolarization during cardiac muscle cell action potentialManual Assertion Based On ExperimentTAS:BHF-UCL
Membrane repolarization during action potentialManual Assertion Based On ExperimentIMP:BHF-UCL
Membrane repolarization during cardiac muscle cell action potentialManual Assertion Based On ExperimentIMP:BHF-UCL
Positive regulation of potassium ion transmembrane transportIEA:Ensembl
Potassium ion import across plasma membraneManual Assertion Based On ExperimentIDA:BHF-UCL
Potassium ion transmembrane transportManual Assertion Based On ExperimentIDA:BHF-UCL
Potassium ion transportManual Assertion Based On ExperimentIDA:UniProtKB
Protein homotetramerizationManual Assertion Based On ExperimentIDA:UniProtKB
Regulation of cardiac muscle cell contractionIEA:Ensembl
Regulation of heart rate by cardiac conductionManual Assertion Based On ExperimentIMP:BHF-UCL

Cellular Location

Membrane

Involvement in disease

Long QT syndrome 7 (LQT7):
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 exercise or emotional stress, and can present with a sentinel event of sudden cardiac death in infancy. Long QT syndrome type 7 manifests itself as a clinical triad consisting of potassium-sensitive periodic paralysis, ventricular ectopy and dysmorphic features.
Short QT syndrome 3 (SQT3):
A heart disorder characterized by idiopathic persistently and uniformly short QT interval on ECG in the absence of structural heart disease in affected individuals. It causes syncope and sudden death. SQT3 has a unique ECG phenotype characterized by asymmetrical T waves.
Atrial fibrillation, familial, 9 (ATFB9):
A familial form of atrial fibrillation, a common sustained cardiac rhythm disturbance. Atrial fibrillation is characterized by disorganized atrial electrical activity and ineffective atrial contraction promoting blood stasis in the atria and reduces ventricular filling. It can result in palpitations, syncope, thromboembolic stroke, and congestive heart failure.

Topology

Cytoplasmic: 2-81
Helical: 82-106
Extracellular: 107-128
Helical: 129-140
Pore-forming: 141-147
Extracellular: 148-156
Helical: 157-178
Cytoplasmic: 179-427

PTM

S-nitrosylation increases the open probability and inward rectifying currents.

Shen, M., Pan, R., Lei, S., Zhang, L., Zhou, C., Zeng, Z., ... & Tian, X. (2023). KCNJ2/HIF1α positive-feedback loop promotes the metastasis of osteosarcoma. Cell Communication and Signaling, 21(1), 46.

Ozekin, Y. H., Saal, M. L., Pineda, R. H., Moehn, K., Ordonez-Erives, M. A., Figueroa, M. F. D., ... & Vladar, E. K. (2023). Intrauterine exposure to nicotine through maternal vaping disrupts embryonic lung and skeletal development via the Kcnj2 potassium channel. Developmental Biology, 501, 111-123.

Zhou, J., Cui, B., Wang, X., Wang, H., Zheng, J., Guo, F., ... & Liang, P. (2023). Overexpression of KCNJ2 enhances maturation of human-induced pluripotent stem cell-derived cardiomyocytes. Stem Cell Research & Therapy, 14(1), 92.

Yim, J., Kim, K. B., Kim, M., Lee, G. D., & Kim, M. (2022). Andersen–Tawil Syndrome With Novel Mutation in KCNJ2: Case Report. Frontiers in Pediatrics, 9, 790075.

Ferraris, C., Turner, A., Scarlett, C., Veysey, M., Lucock, M., Bucher, T., & Beckett, E. L. (2021). Association between sour taste SNP KCNJ2-rs236514, diet quality and mild cognitive impairment in an elderly cohort. Nutrients, 13(3), 719.

Le Tanno, P., Folacci, M., Revilloud, J., Faivre, L., Laurent, G., Pinson, L., ... & Fauré, J. (2021). Characterization of Loss-Of-Function KCNJ2 Mutations in Atypical Andersen Tawil Syndrome. Frontiers in Genetics, 12, 773177.

Chen, S., Huang, M., & Hu, X. (2021). Interference with KCNJ2 inhibits proliferation, migration and EMT progression of apillary thyroid carcinoma cells by upregulating GNG2 expression. Molecular Medicine Reports, 24(3), 1-10.

Jeong, D. U., Lee, J., & Lim, K. M. (2020). Computational study to identify the effects of the KCNJ2 E299V mutation in cardiac pumping capacity. Computational and Mathematical Methods in Medicine, 2020.

Despang, A., Schöpflin, R., Franke, M., Ali, S., Jerković, I., Paliou, C., ... & Ibrahim, D. M. (2019). Functional dissection of the Sox9–Kcnj2 locus identifies nonessential and instructive roles of TAD architecture. Nature genetics, 51(8), 1263-1271.

Binda, A., Rivolta, I., Villa, C., Chisci, E., Beghi, M., Cornaggia, C. M., ... & Combi, R. (2018). A novel KCNJ2 mutation identified in an autistic proband affects the single channel properties of Kir2. 1. Frontiers in cellular neuroscience, 12, 76.

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Please try the standard protocols which include: protocols, troubleshooting and guide.

Enzyme-linked Immunosorbent Assay (ELISA)
Flow Cytometry
Immunofluorescence (IF)
Immunohistochemistry (IHC)
Immunoprecipitation (IP)
Western Blot (WB)
Enzyme Linked Immunospot (ELISpot)
Proteogenomic
Other Protocols

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Isotype control

For research use only. Not intended for any clinical use.

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