Sign in or Register   Sign in or Register
  |  

Mouse Anti-KCNJ5 Recombinant Antibody (2E11) (CBMAB-K0584-LY)

This product is antibody recognizes KCNJ5. The antibody 2E11 immunoassay techniques such as: ELISA, WB.
See all KCNJ5 antibodies

Summary

Host Animal
Mouse
Specificity
Human
Clone
2E11
Antibody Isotype
IgG1, κ
Application
ELISA, WB

Basic Information

Immunogen
CIR (136 a.a. ~ 204 a.a) partial recombinant protein with GST tag. MW of the GST tag alone is 26 KDa.Immunogen sequence: HVNTDRECPL FGLSGINASS VPTDGSGPSM HPSELIAEMR NSGFALKRNV LGRNLTANDP SQEYVASEG
Specificity
Human
Antibody Isotype
IgG1, κ
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
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 5
Introduction
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]
Entrez Gene ID
3762
UniProt ID
P48544
Alternative Names
Potassium Voltage-Gated Channel Subfamily J Member 5; Potassium Inwardly-Rectifying Channel; Subfamily J; Member 5; Heart KATP Channel; IRK-4; GIRK4; CIR; Potassium Channel; Inwardly Rectifying Subfamily J; Member 5; Potassium Channel; Inwardly Rectifying Subfamily J Member 5; G Protein-Activated Inward Rectifier Potassium Channel 4; Cardiac ATP-Sensitive Potassium Channel;
Function
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.
Biological Process
Membrane repolarization during atrial cardiac muscle cell action potentialManual Assertion Based On ExperimentIMP:BHF-UCL
Potassium ion import across plasma membraneManual Assertion Based On ExperimentIDA:BHF-UCL
Potassium ion transportManual Assertion Based On ExperimentTAS:ProtInc
Regulation of heart rate by cardiac conductionManual Assertion Based On ExperimentIMP:BHF-UCL
Regulation of ion transmembrane transportManual Assertion Based On ExperimentIBA:GO_Central
Ventricular cardiac muscle cell membrane repolarization1 PublicationIC:BHF-UCL
Cellular Location
Membrane
Involvement in disease
Long QT syndrome 13 (LQT13):
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.
Hyperaldosteronism, familial, 3 (HALD3):
A form of hyperaldosteronism characterized by hypertension secondary to massive adrenal mineralocorticoid production. HALD3 patients present with childhood hypertension, elevated aldosteronism levels, and high levels of the hybrid steroids 18-oxocortisol and 18-hydroxycortisol. 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. APAs 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. The precise role of KCNJ5 mutations in APA is under debate. They produce increased sodium conductance and cell depolarization, which in adrenal glomerulosa cells produces calcium entry, the signal for aldosterone production and cell proliferation. However, they may not be causative of APA development but may be a consequence of tumorigenesis, playing only a contributory role toward aldosterone overproduction and tumor growth (PubMed:22275527). Somatic mutations in KCNJ5 have not been found in non-aldosterone secreting adrenal adenomas suggesting that they are specifically associated with APA (PubMed:22275527 and PubMed:22848660).
Mutations in KCNJ5 are involved in the pathogenesis of hypertension without primary aldosteronism but with increased aldosterone response to ACTH stimulation.
Topology
Cytoplasmic: 1-86
Helical: 87-111
Extracellular: 112-135
Helical: 136-147
Pore-forming: 148-154
Extracellular: 155-163
Helical: 164-185
Cytoplasmic: 186-419

Meyer, K. M., Malhotra, N., Kwak, J. S., & El Refaey, M. (2023). Relevance of KCNJ5 in Pathologies of Heart Disease. International Journal of Molecular Sciences, 24(13), 10849.

Chang, Y. Y., Lee, B. C., Chen, Z. W., Tsai, C. H., Chang, C. C., Liao, C. W., ... & TAIPAI study group. (2023). Cardiovascular and metabolic characters of KCNJ5 somatic mutations in primary aldosteronism. Frontiers in Endocrinology, 14, 1061704.

Kitamoto, T., & Nishikawa, T. (2022). Clinical translationality of KCNJ5 mutation in aldosterone producing adenoma. International Journal of Molecular Sciences, 23(16), 9042.

Adolf, C., Murck, H., Sarkis, A. L., Schneider, H., Heinrich, D. A., Williams, T. A., ... & Künzel, H. (2022). Differential central regulatory mineralocorticoidreceptor systems for anxiety and depression–Could KCNJ5 be an interesting target for further investigations in major depression?. Journal of Psychiatric Research, 156, 69-77.

Peng, K. Y., Liao, H. W., Chueh, J. S., Pan, C. Y., Lin, Y. H., Chen, Y. M., ... & Wu, V. C. (2021). Pathophysiological and pharmacological characteristics of KCNJ5 157-159delITE somatic mutation in aldosterone-producing adenomas. Biomedicines, 9(8), 1026.

Yamada, N., Asano, Y., Fujita, M., Yamazaki, S., Inanobe, A., Matsuura, N., ... & Takashima, S. (2019). Mutant KCNJ3 and KCNJ5 potassium channels as novel molecular targets in bradyarrhythmias and atrial fibrillation. Circulation, 139(18), 2157-2169.

Yang, Y., Gomez-Sanchez, C. E., Jaquin, D., Aristizabal Prada, E. T., Meyer, L. S., Knösel, T., ... & Williams, T. A. (2019). Primary aldosteronism: KCNJ5 mutations and adrenocortical cell growth. Hypertension, 74(4), 809-816.

Vilela, L. A., Rassi-Cruz, M., Guimaraes, A. G., Moises, C. C., Freitas, T. C., Alencar, N. P., ... & Almeida, M. Q. (2019). KCNJ5 somatic mutation is a predictor of hypertension remission after adrenalectomy for unilateral primary aldosteronism. The Journal of Clinical Endocrinology & Metabolism, 104(10), 4695-4702.

Kitamoto, T., Omura, M., Suematsu, S., Saito, J., & Nishikawa, T. (2018). KCNJ5 mutation as a predictor for resolution of hypertension after surgical treatment of aldosterone-producing adenoma. Journal of Hypertension, 36(3), 619-627.

Yamazaki, Y., Omata, K., Tezuka, Y., Ono, Y., Morimoto, R., Adachi, Y., ... & Sasano, H. (2018). Tumor cell subtypes based on the intracellular hormonal activity in KCNJ5-mutated aldosterone-producing adenoma. Hypertension, 72(3), 632-640.

Ask a question We look forward to hearing from you.
0 reviews or Q&As

Purchasing FAQs
Technical FAQs

Loading...
Have you used Mouse Anti-KCNJ5 Recombinant Antibody (2E11)?
Submit a review and get a Coupon or an Amazon gift card. 20% off Coupon $30 eGift Card
Submit a review
Loading...
For research use only. Not intended for any clinical use.

Custom Antibody Labeling

We also offer labeled antibodies developed using our catalog antibody products and nonfluorescent conjugates (HRP, AP, Biotin, etc.) or fluorescent conjugates (Alexa Fluor, FITC, TRITC, Rhodamine, Texas Red, R-PE, APC, Qdot Probes, Pacific Dyes, etc.).

Online Inquiry

Documents

Contact us

  • Tel: (USA)
  • (UK)
  • Fax:
  • Email:

Submit A Review

Go to
Compare