mProX™ Human CLCN2 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Ion Channel Cell Lines
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Published Data
Fig.1 Sertoli cell-specific Clcn2 disruption causes testicular degeneration in mice.
Membrane fractions obtained from the whole testis of adult Clcn2lox/lox, GC-ΔC2 (Clcn2 knockout specific to germ cells), Clcn2-/-, and SC-ΔC2 animals were subjected to Western blot examination of ClC-2. The BCA assay was used to determine the protein loading levels.
Ref: Göppner, Corinna, et al. "Cellular basis of ClC-2 Cl− channel-related brain and testis pathologies." Journal of Biological Chemistry 296 (2021).
Pubmed: 33187987
DOI: 10.1074/jbc.RA120.016031
Research Highlights
These results reveal the involvement of anion channels in the determination of the glomerulosa membrane potential, aldosterone production, and hypertension for the first time. They determine the etiology of a significant portion of primary aldosteronism with early onset.
Scholl, Ute I., et al. "CLCN2 chloride channel mutations in familial hyperaldosteronism type II." Nature genetics 50.3 (2018): 349-354.
Pubmed:
29403011
DOI:
10.1038/s41588-018-0048-5
The most prevalent and treatable type of secondary arterial hypertension is primary aldosteronism. Hyperpolarization-activated Cl-currents were seen in patch-clamp examination of glomerulosa cells in mouse adrenal gland slices; these currents were eliminated in Clcn2-/-mice.
Fernandes-Rosa, Fabio L., et al. "A gain-of-function mutation in the CLCN2 chloride channel gene causes primary aldosteronism." Nature genetics 50.3 (2018): 355-361.
Pubmed:
29403012
DOI:
10.1038/s41588-018-0053-8