mProX™ Human KCNA5 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Ion Channel Cell Lines
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Published Data
Fig.1 Structure of KCNA5 gene and characteristics of Kv1.5 channel currents.
Representative single channel Kv1.5 currents from a human embryonic kidney (HEK)-293 cell, a rat PASMC, a human coronary artery smooth muscle cell (CASMC) transfected with KCNA5, and a COS-7 cell at a test potential (TP) of 100 mV.
Ref: Remillard, Carmelle V., et al. "Function of Kv1. 5 channels and genetic variations of KCNA5 in patients with idiopathic pulmonary arterial hypertension." American Journal of Physiology-Cell Physiology 292.5 (2007): C1837-C1853.
Pubmed: 17267549
DOI: 10.1152/ajpcell.00405.2006
Research Highlights
Cancer cells have PcG-dependent chromatin repressive changes that become more pronounced in hypoxic environments, marking the KCNA5 promoter. KCNA5 expression is restored by genetic and pharmacological suppression of BMI-1 and EZH2, respectively, making cells more susceptible to stress-induced death.
Ryland, Katherine E., et al. "Polycomb-dependent repression of the potassium channel-encoding gene KCNA5 promotes cancer cell survival under conditions of stress." Oncogene 34.35 (2015): 4591-4600.
Pubmed:
25435365
DOI:
10.1038/onc.2014.384
One typical feature of human or experimental pulmonary arterial hypertension (PAH) is reduced expression and/or activity of Kv1.5 channels. Similarly, genetic variations in KCNA5 have been discovered in PAH patients; however, little is known about these variants' functional implications and possible influence on the illness.
Vera-Zambrano, Alba, et al. "Novel loss-of-function KCNA5 variants in pulmonary arterial hypertension." American Journal of Respiratory Cell and Molecular Biology 69.2 (2023): 147-158.
Pubmed:
36917789
DOI:
10.1165/rcmb.2022-0245OC