mProX™ Human KCNQ4 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Ion Channel Cell Lines
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Published Data
Fig.1 Effects of DFNA2 mutations on KCNQ4 subunit interaction
DFNA2 mutations' effects on KCNQ4 subunit interaction In HEK293T cells, each HA-tagged mutant KCNQ4 channel was co-expressed at a 1:1 ratio with the Myc-tagged WT KCNQ4. As positive and negative controls, the vector and the WT HA-KCNQ4 were likewise co-expressed with the WT Myc-KCNQ4 channel. 24 hours after the transfections, the cell lysates were extracted and utilized in the reciprocal co-immunoprecipitation experiment.
Ref: Gao, Yanhong, et al. "Impaired surface expression and conductance of the KCNQ 4 channel lead to sensorineural hearing loss." Journal of cellular and molecular medicine 17.7 (2013): 889-900.
Pubmed: 23750663
DOI: 10.1111/jcmm.12080
Research Highlights
Genetic abnormalities causing a decrease in KCNQ4 channel activity are the cause of nonsyndromic hearing loss, which is usually a late-onset, high-frequency loss that gradually gets worse.
Rim, John Hoon, et al. "Activation of KCNQ4 as a therapeutic strategy to treat hearing loss." International journal of molecular sciences 22.5 (2021): 2510.
Pubmed:
33801540
DOI:
10.3390/ijms22052510
According to these results, genetic screening for KCNQ4 variations is crucial for the prevention and treatment of non-severe hearing loss (NSHL) since it suggests that these variants may contribute more to late-onset NSHL than previously thought.
Jung, Jinsei, et al. "Rare KCNQ4 variants found in public databases underlie impaired channel activity that may contribute to hearing impairment." Experimental & molecular medicine 51.8 (2019): 1-12.
Pubmed:
31434872
DOI:
10.1038/s12276-019-0300-9