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Mouse Anti-KCNK3 Recombinant Antibody (S374-48) (CBMAB-K0057-LY)

This product is antibody recognizes KCNK3. The antibody S374-48 immunoassay techniques such as: ICC, IHC, WB.
See all KCNK3 antibodies

Summary

Host Animal
Mouse
Specificity
Rat
Clone
S374-48
Antibody Isotype
IgG2b
Application
ICC, IHC, WB

Basic Information

Specificity
Rat
Antibody Isotype
IgG2b
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
Buffer
50% Glycerol
Preservative
0.1% sodium azide
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 Two Pore Domain Channel Subfamily K Member 3
Introduction
This gene encodes a member of the superfamily of potassium channel proteins that contain two pore-forming P domains. The encoded protein is an outwardly rectifying channel that is sensitive to changes in extracellular pH and is inhibited by extracellular acidification. Also referred to as an acid-sensitive potassium channel, it is activated by the anesthetics halothane and isoflurane. Although three transcripts are detected in northern blots, there is currently no sequence available to confirm transcript variants for this gene. [provided by RefSeq, Aug 2008]
Entrez Gene ID
29553
UniProt ID
O54912
Alternative Names
Task-1; rTASK
Function
pH-dependent, voltage-insensitive, background potassium channel protein. Rectification direction results from potassium ion concentration on either side of the membrane. Acts as an outward rectifier when external potassium concentration is low. When external potassium concentration is high, current is inward.
Biological Process
Brain developmentIEA:Ensembl
Cellular response to hypoxiaIEA:Ensembl
Cellular response to zinc ionIEA:Ensembl
Chemical synaptic transmissionManual Assertion Based On ExperimentTAS:ProtInc
Cochlea developmentIEA:Ensembl
Ion transmembrane transportManual Assertion Based On ExperimentIMP:UniProtKB
Negative regulation of cytosolic calcium ion concentrationIEA:Ensembl
Potassium ion transmembrane transportManual Assertion Based On ExperimentIBA:GO_Central
Potassium ion transportManual Assertion Based On ExperimentTAS:ProtInc
Response to xenobiotic stimulusIEA:Ensembl
Stabilization of membrane potentialManual Assertion Based On ExperimentIBA:GO_Central
Cellular Location
Cell membrane
Involvement in disease
Pulmonary hypertension, primary, 4 (PPH4):
A rare disorder characterized by plexiform lesions of proliferating endothelial cells in pulmonary arterioles. The lesions lead to elevated pulmonary arterial pression, right ventricular failure, and death. The disease can occur from infancy throughout life and it has a mean age at onset of 36 years. Penetrance is reduced. Although familial pulmonary hypertension is rare, cases secondary to known etiologies are more common and include those associated with the appetite-suppressant drugs.
Topology
Cytoplasmic: 1-8
Helical: 9-29
Pore-forming: 78-101
Helical: 108-128
Cytoplasmic: 129-158
Helical: 159-179
Pore-forming: 184-207
Helical: 223-243
Cytoplasmic: 244-394

Saint‐Martin Willer, A., Santos‐Gomes, J., Adão, R., Brás‐Silva, C., Eyries, M., Pérez‐Vizcaino, F., ... & Antigny, F. (2023). Physiological and pathophysiological roles of the KCNK3 potassium channel in the pulmonary circulation and the heart. The Journal of Physiology, 601(17), 3717-3737.

Sörmann, J., Schewe, M., Proks, P., Jouen-Tachoire, T., Rao, S., Riel, E. B., ... & Tucker, S. J. (2022). Gain-of-function mutations in KCNK3 cause a developmental disorder with sleep apnea. Nature Genetics, 54(10), 1534-1543.

Lin, G., Lin, L., Lin, H., Chen, W., Chen, L., Chen, X., ... & Zeng, Y. (2022). KCNK3 inhibits proliferation and glucose metabolism of lung adenocarcinoma via activation of AMPK-TXNIP pathway. Cell Death Discovery, 8(1), 360.

Lambert, M., Mendes-Ferreira, P., Ghigna, M. R., LeRibeuz, H., Adao, R., Boet, A., ... & Antigny, F. (2021). Kcnk3 dysfunction exaggerates the development of pulmonary hypertension induced by left ventricular pressure overload. Cardiovascular Research, 117(12), 2474-2488.

West, J. D., Austin, E. D., Rizzi, E. M., Yan, L., Tanjore, H., Crabtree, A. L., ... & Rathinasabapathy, A. (2021). KCNK3 mutation causes altered immune function in pulmonary arterial hypertension patients and mouse models. International journal of molecular sciences, 22(9), 5014.

Le Ribeuz, H., Dumont, F., Ruellou, G., Lambert, M., Balliau, T., Quatredeniers, M., ... & Antigny, F. (2020). Proteomic analysis of KCNK3 loss of expression identified dysregulated pathways in pulmonary vascular cells. International Journal of Molecular Sciences, 21(19), 7400.

Le Ribeuz, H., Courboulin, A., Ghigna, M. R., Lambert, M., Hautefort, A., Humbert, M., ... & Antigny, F. (2020). In vivo miR-138-5p inhibition alleviates monocrotaline-induced pulmonary hypertension and normalizes pulmonary KCNK3 and SLC45A3 expression. Respiratory Research, 21(1), 1-14.

Lambert, M., Capuano, V., Boet, A., Tesson, L., Bertero, T., Nakhleh, M. K., ... & Antigny, F. (2019). Characterization of Kcnk3-mutated rat, a novel model of pulmonary hypertension. Circulation research, 125(7), 678-695.

Babicheva, A., Zhao, T., & Yuan, J. X. J. (2019). KCNK3 channel: a new player in the field of pulmonary vascular disease. Circulation Research, 125(7), 696-698.

Lambert, M., Boet, A., Rucker-Martin, C., Mendes-Ferreira, P., Capuano, V., Hatem, S., ... & Antigny, F. (2018). Loss of KCNK3 is a hallmark of RV hypertrophy/dysfunction associated with pulmonary hypertension. Cardiovascular research, 114(6), 880-893.

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

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