When they conducted the study, the slowing down of translational elongation rate actually partially reverted the folding and processing defects of ΔF508-CFTR. But the tests did not stop there. Other experiments conducted for study include silencing human homologs of yeast Yor-1-ΔF670 biogenesis modifier genes by using the human CF bronchial epithelial CFBE cell line with CFTRΔF508/ΔF508 genetic background, SiRNA-mediated knockdown of RPL12, RPL12 knockdown, RPL12 silencing, and SiRNA-mediated silencing of ribosomal stalk proteins, among other things. RPL12 knockdown confirmed the relevance of RPL12 silencing on correcting misprocessing of ΔF508-CFTR and increased the ΔF508-CFTR efficiency at the Endoplasmic Reticulum. RPL12 silencing in combination with VX-809, a corrector drug, increased the functional expression of ΔF508-CFTR in “immortalized and primary human bronchial epithelia.” And last but not least, SiRNA-mediated silencing of ribosomal stalk proteins resulted in an increase in the functional expression of ΔF508-CFTR, as well as its
When they conducted the study, the slowing down of translational elongation rate actually partially reverted the folding and processing defects of ΔF508-CFTR. But the tests did not stop there. Other experiments conducted for study include silencing human homologs of yeast Yor-1-ΔF670 biogenesis modifier genes by using the human CF bronchial epithelial CFBE cell line with CFTRΔF508/ΔF508 genetic background, SiRNA-mediated knockdown of RPL12, RPL12 knockdown, RPL12 silencing, and SiRNA-mediated silencing of ribosomal stalk proteins, among other things. RPL12 knockdown confirmed the relevance of RPL12 silencing on correcting misprocessing of ΔF508-CFTR and increased the ΔF508-CFTR efficiency at the Endoplasmic Reticulum. RPL12 silencing in combination with VX-809, a corrector drug, increased the functional expression of ΔF508-CFTR in “immortalized and primary human bronchial epithelia.” And last but not least, SiRNA-mediated silencing of ribosomal stalk proteins resulted in an increase in the functional expression of ΔF508-CFTR, as well as its