Fig. 5.

Loss of CBS is also associated with an inflammatory response. a Overlap of upregulated MSigDB hallmark pathways in GES1 and HFE145 CBS-deficient clones and the list of shared pathways; “k” is the number of genes in the intersection of the MSigDB hallmark query set (q-value < 0.01). b Relative H₂S levels in GES1 CBS-deficient clone 1 [28%] and clone 2 [54%] compared to CRISPR control cells [n = 3] (*P < 0.05). c NF-κB luminescence reporter assay in GES1 CBS-deficient cells, and in d HFE145 CBS-deficient cells, at 48 h [n = 3] and in 0.5 mM GYY 4137-treated cells at 24 h [1 = 3]. Control represents data pooled from parental and CRISPR control cells (*P < 0.05). e Upregulated MSigDB hallmark pathways (q-value < 0.01) in genes negatively correlated to CBS gene expression in gastric TCGA (q-value < 0.05) and in f CCLE (q-value < 0.05). g Upregulated MSigDB hallmark pathways (q-value < 0.01) in mouse CBS-deficient stomachs (FD (≥ 1.5))