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Mouse Anti-KCNJ2 Recombinant Antibody (S21-32) (CBMAB-K0570-LY)

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Summary

Host Animal
Mouse
Specificity
Mouse, Human, Rat
Clone
S21-32
Antibody Isotype
IgG1
Application
IHC-Fr, WB

Basic Information

Immunogen
Fusion protein amino acids 41-64 and 189-428 of mouse Kir2. 1
Specificity
Mouse, Human, Rat
Antibody Isotype
IgG1
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

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

Format
Liquid
Concentration
1 mg/mL
Purity
> 95% Purity determined by SDS-PAGE.
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freezethaw cycles.

Target

Full Name
potassium inwardly rectifying channel subfamily J member 2
Introduction
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, probably participates in establishing action potential waveform and excitability of neuronal and muscle tissues. Mutations in this gene have been associated with Andersen syndrome, which is characterized by periodic paralysis, cardiac arrhythmias, and dysmorphic features. [provided by RefSeq, Jul 2008]
Entrez Gene ID
Human3759
Mouse16518
Rat29712
UniProt ID
HumanP63252
MouseP35561
RatQ64273
Alternative Names
IRK1; Kcnf1; Kir2.1
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.
More Infomation

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

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