Description
To exploit the potential function of PARP1 during renal IRI by binding target RNA to regulate its expression, we obtained PARP1 bound peaks in proximal tubular epithelial cell (HK-2) by iRIP-seq for the first time, which showed that the bind peaks of PARP1_IP group is more enriched at GGUAA-rich motifs and PARP1 preferentially bound to the downstream of TSS (transcription start site) and upstream of TTS (transcription termination site). iRIP-seq analysis was used to decipher RBP binding sites and revealed the RNA that interacts with PARP1 within the genome of HK-2 cells.
Overall Design
RIP-seq analysis of PARP1 IP versus input in HK-2 cells
Curator
xm_li