Jason Wong
@jwhwong.bsky.social
Professor at the School of Biomedical Sciences, University of Hong Kong. Uses genomics data to understand DNA repair and cancer.
In addition to cell type specificity, the promoter of ERVK-7.long is driven by NF-κB, likely via TNF-α, while ERVK-7.short is already known to be regulated by IRFs. (7/n)
March 17, 2025 at 6:36 AM
In addition to cell type specificity, the promoter of ERVK-7.long is driven by NF-κB, likely via TNF-α, while ERVK-7.short is already known to be regulated by IRFs. (7/n)
The promoter of ERVK-7.long was found to be lineage-specific, with H3K4me3 deposition in LUAD cells. ScRNA-seq confirmed that ERVK-7.long expression is restricted largely to LUAD cells, fibroblasts, and AT-2 cells, which may be the cell type of origin of LUAD cells. (6/n)
March 17, 2025 at 6:36 AM
The promoter of ERVK-7.long was found to be lineage-specific, with H3K4me3 deposition in LUAD cells. ScRNA-seq confirmed that ERVK-7.long expression is restricted largely to LUAD cells, fibroblasts, and AT-2 cells, which may be the cell type of origin of LUAD cells. (6/n)
ERVK-7.long is highly expressed in LUAD, contributing significantly to the overall expression of ERVK-7. This suggests that the epigenetic regulation of ERVK-7.long may be key to ERVK-7 overexpression in patients. (5/n)
March 17, 2025 at 6:36 AM
ERVK-7.long is highly expressed in LUAD, contributing significantly to the overall expression of ERVK-7. This suggests that the epigenetic regulation of ERVK-7.long may be key to ERVK-7 overexpression in patients. (5/n)
HERVs and retroviruses are transcribed from the 5'LTR. Yet PacBio Iso-seq revealed alternative transcripts for ERVK-7 arising from upstream promoters, with the canonical TSS of the 5'LTR heavily methylated in A549 (ONT WGS) along with TFBS mutations. (4/n)
March 17, 2025 at 6:36 AM
HERVs and retroviruses are transcribed from the 5'LTR. Yet PacBio Iso-seq revealed alternative transcripts for ERVK-7 arising from upstream promoters, with the canonical TSS of the 5'LTR heavily methylated in A549 (ONT WGS) along with TFBS mutations. (4/n)
A key motivation for us is to understand the epigenetic regulation of ERVK-7 as it is frequently over-expressed but only amplified in ~10% of LUAD patients. (3/n)
March 17, 2025 at 6:36 AM
A key motivation for us is to understand the epigenetic regulation of ERVK-7 as it is frequently over-expressed but only amplified in ~10% of LUAD patients. (3/n)