CLCN2 Knockout Cell Line (HEK293)

The choice depends on whether you are studying CLCN2 (chloride channel 2, CLC-2)'s role as a plasma membrane voltage-gated Cl⁻ channel or modeling leukoencephalopathy and CLCN2-mediated aldosteronism. The Knockout line is the standard tool for asking whether CLCN2 is required for these processes — CLCN2 is a CLC family member that, unlike CLC-7, functions as a true plasma membrane voltage-gated Cl⁻ channel activated by hyperpolarization, cell swelling, and acidic pH; CLCN2 has roles in maintaining cellular Cl⁻ homeostasis, brain extracellular ion balance, and aldosterone production. Overexpression is useful for studying CLCN2 gain-of-function effects. For neurological and endocrine research, the EDITGENE CLCN2 Knockout in HEK293 enables structure-function studies — CLCN2 biallelic loss-of-function mutations cause leukoencephalopathy with ataxia (LKPAT, brain white matter disease) and infertility; gain-of-function mutations cause familial hyperaldosteronism type II. Rescue with wild-type, channel-dead, or disease-mutant CLCN2 enables comprehensive disease modeling. The knockout is valuable for studying voltage-gated Cl⁻ channel biology, leukoencephalopathy mechanisms, and aldosterone production regulation.

Primary applications: • Voltage-gated Cl⁻ current: whole-cell patch clamp analysis of hyperpolarization-activated Cl⁻ currents in CLCN2-null cells. • LKPAT leukoencephalopathy modeling: rescue with biallelic loss-of-function patient mutations for genotype-function studies. • Familial hyperaldosteronism modeling: rescue with gain-of-function CLCN2 mutations (e.g., G24D, R172Q, Y26N) for type II hyperaldosteronism studies. • Aldosterone production: in heterologous adrenocortical-relevant contexts, CLCN2-induced membrane depolarization and aldosterone synthesis. EDITGENE recommends this model for researchers investigating voltage-gated Cl⁻ channel biology and CLCN2-related neurological/endocrine disease.

Yes. CLCN2 rescue experiments require attention to plasma membrane voltage-gated channel architecture: • Construct design: use a codon-modified CLCN2 sequence with a small intracellular tag (FLAG, HA). CLCN2 has the canonical CLC architecture — preserve membrane topology. • Surface localization validation: confirm plasma membrane localization before electrophysiology assays. • Channel-dead rescue: gating residue mutations abolish hyperpolarization-activated Cl⁻ currents. • Familial hyperaldosteronism mutation rescue: gain-of-function mutations (G24D, R172Q, Y26N) enable disease modeling. • Functional readout: rescue should restore hyperpolarization-activated Cl⁻ currents by patch clamp. HEK293 transduces efficiently with lentivirus and supports stable rescue line generation for systematic CLCN2 mutation analysis.