IndraLab

"Our data show that both LPS and Tm could induce the formation of the GRP78 and USP13 complex (Figure  xref )."

"Similarly, endogenous USP13 and GRP78 formed a complex in DSS‐induced colon tissues (Figure  xref )."

"Also, the interaction between exogenous USP13 and GRP78 was confirmed in NIH/3T3 cells co‐transfected with Flag‐USP13 and His‐GRP78 plasmids (Figure  xref ; Figure xref , Supporting Information) in a dose‐dependent manner (Figure  xref )."

"We also demonstrated the protective role of the intestinal epithelial cell‐specific USP13‐GRP78 axis in IBD, suggesting that targeting USP13 for intestinal epithelial cell‐specific gene therapy may be a potential treatment strategy for IBD."

"Mechanistically, USP13 interacted with  GRP78, attenuating ER stress‐induced apoptosis and maintaining intestinal barrier integrity by selectively removing K63‐linked ubiquitin at lysine 327."

"These observations validated that USP13 interacts with GRP78 protein both in vitro and in vivo."

"These findings underscore the protective role of the USP13‐GRP78 axis in IBD and suggest that targeting USP13 through intestinal epithelial‐specific gene therapy may be a potential therapeutic strategy for IBD."

"USP13 interacts with GRP78 and reduces its K63‐linked ubiquitination to alleviate epithelial injury."

"DUBs control cellular functions by altering the ubiquitination status of proteins, which influences protein stability and regulates signaling pathways. [ xref ] The interaction between USP13 and GRP78 raises the question of whether USP13 plays a regulatory role in GRP78."

"Anti‐ HA (51064‐2‐AP), anti‐Flag (66008‐4‐Ig), anti‐6×His (His, 10001‐0‐AP), anti‐USP13 (16840‐1‐AP), anti‐GRP78 (11587‐1‐AP, 66574‐1‐lg), anti‐eukaryotic translation initiation factor 2‐alpha kinase 3 (PERK, 24390‐1‐AP), anti‐tight junction protein (ZO‐1, 21773‐1‐AP), anti‐Claudin‐1 (28674‐1‐AP), anti‐Occludin (27260‐1‐AP), anti‐DNA‐damage‐inducible transcript 3 (CHOP, 15204‐1‐AP), anti‐Cleaved Caspase‐3 (25128‐1‐AP), anti‐Caspase‐3 (19677‐1‐AP), anti‐activating transcription factor 4 (ATF4, 10835‐1‐AP), anti‐E‐cadherin (60335‐1‐Ig), and anti‐epithelial cell adhesion molecule (EpCAM, 21050‐1‐AP) antibodies were purchased from Proteintech (Wuhan, China)."

"Restoring USP13 expression or targeting the USP13‐GRP78 axis may represent a promising strategy for treating inflammatory bowel disease by preserving mucosal barrier integrity."

"Our findings demonstrate the protective role of the intestinal epithelial cell‐specific USP13‐GRP78 axis in IBD, suggesting that targeting USP13 for intestinal epithelial cell‐specific gene therapy may be a potential treatment strategy for intestinal inflammatory diseases."

"Thus, we validated the interaction between endogenous USP13 and GRP78 in LPS‐treated NCM460 cells using co‐IP analysis (Figure  xref ), as well as in Tm‐stimulated NCM460 cells (Figure  xref )."