GSE169623
The human monocyte model BLaER1 exhibits an epigenetic GPI anchor defect that impairs TLR4 signaling
We show that the human monocyte model BLaER1 contains GPI-anchor-deficient cells, which lack CD14 surface expression when differentiated to monocytes, resulting in diminished LPS/TLR4 responsiveness. We found that this GPI anchor defect is caused by epigenetic silencing of the PIGH gene, leading to a random distribution of intact and PIGH-deficient clones after single-cell cloning. Overall design: Comparison of mRNA expression profiles of 3 undifferentiated GPI-positive and 4 undifferentiated GPI-negative BLaER1 monoclonal cell lines