Why the study?
Half of reported KCNH2 variants in ClinVar are classified as variants of uncertain significance, creating a need for functional phenotyping to determine their clinical significance.
This high-throughput automated patch-clamp assay enables rapid functional phenotyping of KCNH2 variants, which may help reclassify variants of uncertain significance in Long QT Syndrome type 2.
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May aid reclassification of KCNH2 VUS in LQTS2; leaves open prospective clinical validation.
KCNH2 is one of the 59 medically actionable genes recommended by the American College of Medical Genetics for reporting of incidental findings from clinical genomic sequencing. However, half of the reported KCNH2 variants in the ClinVar database are classified as variants of uncertain significance. In the absence of strong clinical phenotypes, there is a need for functional phenotyping to help decipher the significance of variants identified incidentally. Here, we report detailed methods for assessing the molecular phenotype of any KCNH2 missense variant. The key components of the assay include quick and cost-effective generation of a bicistronic vector to co-express WT and any KCNH2 variant allele, generation of stable Flp-In HEK293 cell lines and high-throughput automated patch-clamp electrophysiology analysis of channel function. Stable cell lines take 3-4 weeks to produce and can be generated in bulk, which will then allow up to 30 variants to be phenotyped per week after 48 hours of channel expression. This high throughput functional genomics assay will enable a much more rapid assessment of the extent of loss of function of any KCNH2 variant.
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Ng et al. (2021) studied this question.
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