IndraLab

"39 , 42 USP29 promotes HSV-1-triggered innate antiviral signaling in THP-1 cells Because USP29 interacted with cGAS and was upregulated by HSV-1 infection , we investigated its role in regulating HSV-1-or cytoplasmic DNA-triggered innate immune signaling ."

"Sequence analysis of USP29 promoter ( -5000 bp ~ +100 bp ) failed to identify any recognizable IRF , NF-kappaB , or STAT binding sites , indicating that the transcriptional regulation of USP29 by viral infection is different from that of OTUD4 , USP25 or INKIT previously reported.37 ,40,41 In this context , it has been shown that transcription factors JTV1 and FBP co-activate USP29 transcription in response to oxidative stress and that one of the evolutionarily conserved sequence elements ( CSE1 ) on Usp29 promoter suppresses its transcription.39 ,42 Because USP29 interacted with cGAS and was upregulated by HSV-1 infection , we investigated its role in regulating HSV-1 - or cytoplasmic DNA-triggered innate immune signaling ."

"Sequence analysis of USP29 promoter ( -5000 bp ~ +100 bp ) failed to identify any recognizable IRF , NF-kappaB , or STAT binding sites , indicating that the transcriptional regulation of USP29 by viral infection is different from that of OTUD4 , USP25 or INKIT previously reported.37 ,40,41 In this context , it has been shown that transcription factors JTV1 and FBP co-activate USP29 transcription in response to oxidative stress and that one of the evolutionarily conserved sequence elements ( CSE1 ) on Usp29 promoter suppresses its transcription.39 ,42 USP29 promotes HSV-1-triggered innate antiviral signaling in THP-1 cells Because USP29 interacted with cGAS and was upregulated by HSV-1 infection , we investigated its role in regulating HSV-1 - or cytoplasmic DNA-triggered innate immune signaling ."

"Our results suggest that HSV-1 infection upregulated USP29 , which might be responsible for increased USP29-cGAS association after HSV-1 infection ."