mProX™ Human KCNJ2 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Ion Channel Cell Lines
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Published Data
Fig.1 KCNJ2/Kir2.1 expressionin SCLC cells.
In comparison to H69 and H446 cells, respectively, KCNJ2/Kir2.1 expression was considerably higher in H69AR and H446AR cells both at the mRNA and protein levels. Kir2.1 expression was elevated in H69AR and H44AR cells as compared with H69 and H446 cells, according to Western blotting and immunofluorescence studies.
Ref: Liu, Huanxin, et al. "Upregulation of the inwardly rectifying potassium channel Kir2. 1 (KCNJ2) modulates multidrug resistance of small-cell lung cancer under the regulation of miR-7 and the Ras/MAPK pathway." Molecular cancer 14.1 (2015): 1-19.
Pubmed: 25880778
DOI: 10.1186/s12943-015-0298-0
Research Highlights
Numerous cardiovascular diseases have previously been linked to inwardly rectifying potassium channels (Kir). Specifically, patients with Andersen-Tawil syndrome have been linked to loss-of-function mutations in the Kir2.1 channel, whereas short QT3 syndrome is caused by gain-of-function mutations in the same channel.
Binda, Anna, et al. "A novel KCNJ2 mutation identified in an autistic proband affects the single channel properties of Kir2. 1." Frontiers in cellular neuroscience 12 (2018): 76.
Pubmed:
29615871
DOI:
10.3389/fncel.2018.00076
The autosomal dominant hereditary or sporadic Andersen-Tawil syndrome (ATS) is typified by dysmorphic features, ventricular arrhythmias (VAs), and recurrent paralyses. It is unknown what the best pharmaceutical regimen is for treating VAs in patients with ATS.
Miyamoto, Koji, et al. "Efficacy and safety of flecainide for ventricular arrhythmias in patients with Andersen-Tawil syndrome with KCNJ2 mutations." Heart Rhythm 12.3 (2015): 596-603.
Pubmed:
25496985
DOI:
10.1016/j.hrthm.2014.12.009