ENA0000GenomicsMolecular Genomics, School of Life Sciences and Biotechnology, Korea Universityhttps://www.ebi.ac.uk/ena/browser/view/PRJNA136279Homo sapiensAnalysis of cellular SMD or NMD substrates that regulated by Upf1 and/or PNRC2 in HeLa cell. The hypothesis tested in the present study was that endogenous SMD or NMD substrates may co-regulated by Upf1 and PNRC2. Results provide important information that vast range of cellular SMD or NMD substrates are reqired PNRC2 for decay. Overall design: Total RNA obtained from HeLa cells with downregulation of Upf1 or PNRC2 by siRNA. The up- or down-regulated transcripts were compare to control siRNA treated HeLa cell RNA extract. Significant transcripts were confirmed by replicationENAtype 1, B430202H16Rik, MQD22.15, SEMDSTWK, wide/broad, Strudwick syndrome, determination, SmD, ATUPF1, 0610011E17Rik, MQD22_15, broad, dappled metaphysis syndrome, DmUpf1, spondyloepimetaphyseal dysplasia Strudwick type, UPF1, pNORF1, spondylometaphyseal dysplasia, Upflp, chemical analysis, smg-2, LOW-LEVEL BETA-AMYLASE 1, Semdc, HELA cell., spondyloepimetaphyseal dysplasia congenita, RENT1, Smed, IFS2, SMED type 1, Upf1p, Genomes, Rent1, DmelCG1559, SEMD, SUP113, HUPF1, upf1, HeLa, spondylometaepiphyseal dysplasia congenita, Strudwick type, Dm-Upf1, wide, spondyloepimetaphyseal dysplasia, PNORF-1, NORF1, MOF4, assay, SMED Strudwick type, CG1559, D4Bwg0593ehuman being, human., man0.00.00.00.00.00falseHomo sapiensGenome-wide analysis of cellular SMD or NMD substrates that regulated by Upf1 or PNRC2 in HeLa cell2022-07-192014-02-11PRJNA136279GSE26781225031029606