Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA117193 | ENA |
REPOSITORIES: ENA
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Project description:Analysis of miRNA-targeted cellular NMD substrates in HeLa cell. The hypothesis tested in the present study was that endogenous NMD substrates containing long 3' untranslated region may targeted for miRNA. Results provide important information expanding the roles of miRISC in the posttranscriptional regulation of gene expression: a new cross-talk between miRNA-mediated gene silencing and NMD. ABSTRACT: Imperfect base-pairing between microRNA (miRNA) and the 3â-untranslated region (3âUTR) of target mRNA triggers translational repression of the target mRNA. Here, we provide evidence that human Argonaute 2 (Ago2) targets cap-binding protein (CBP)80/20- and exon junction complex (EJC)-bound mRNAs and inhibits nonsense-mediated mRNA decay (NMD), which is tightly restricted to CBP80/20-bound mRNAs. Furthermore, microarray analyses reveal that a subset of cellular transcripts, which are expected to be targeted for NMD, is stabilized by miRNA-mediated gene silencing. The regulation of NMD by miRNAs will shed light on a new post-transcriptional regulation mechanism of gene expression in mammalian cells Total RNA obtained from HeLa cells with downregulation of Ago2 or Ago2/UPF1 by siRNA. The up- or down-regulated transcripts were compared to control siRNA treated HeLa cell RNA extract. Significant transcripts were confirmed by replication.
2010-04-09 | E-GEOD-16170 | biostudies-arrayexpress
Project description:Analysis of miRNA-targeted cellular NMD substrates in HeLa cell. The hypothesis tested in the present study was that endogenous NMD substrates containing long 3' untranslated region may targeted for miRNA. Results provide important information expanding the roles of miRISC in the posttranscriptional regulation of gene expression: a new cross-talk between miRNA-mediated gene silencing and NMD. ABSTRACT: Imperfect base-pairing between microRNA (miRNA) and the 3’-untranslated region (3’UTR) of target mRNA triggers translational repression of the target mRNA. Here, we provide evidence that human Argonaute 2 (Ago2) targets cap-binding protein (CBP)80/20- and exon junction complex (EJC)-bound mRNAs and inhibits nonsense-mediated mRNA decay (NMD), which is tightly restricted to CBP80/20-bound mRNAs. Furthermore, microarray analyses reveal that a subset of cellular transcripts, which are expected to be targeted for NMD, is stabilized by miRNA-mediated gene silencing. The regulation of NMD by miRNAs will shed light on a new post-transcriptional regulation mechanism of gene expression in mammalian cells
2010-03-08 | GSE16170 | GEO
Project description:Analysis 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. 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 replication
2012-02-28 | E-GEOD-26781 | biostudies-arrayexpress
Project description:Analysis 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.
2012-02-28 | GSE26781 | GEO
Project description:Analysis of cellular NMD (Nonsense-mediated mRNA decay) substrates that regulated by Upf1, SMG5, SMG7 and/or PNRC2 in HeLa cell. The hypothesis tested in the present study was that endogenous NMD substrates may co-regulated by Upf1, SMG5, SMG7 and PNRC2.
2012-11-01 | GSE34876 | GEO
Project description:Analysis of cellular NMD (Nonsense-mediated mRNA decay) substrates that regulated by Upf1, SMG5, SMG7 and/or PNRC2 in HeLa cell. The hypothesis tested in the present study was that endogenous NMD substrates may co-regulated by Upf1, SMG5, SMG7 and PNRC2. Total RNA obtained from HeLa cells with downregulation of Upf1, SMG5, PNRC2 or SMG7 by siRNA. The up- or down-regulated transcripts were compare to control siRNA treated HeLa cell RNA extract. Significant transcripts were confirmed by replication
2012-11-01 | E-GEOD-34876 | biostudies-arrayexpress
Project description:Genome-wide analysis of cellular NMD substrates that regulated by Upf1, PNRC2 or CTIF in HeLa cell
| PRJNA161531 | ENA
Project description:Genome-wide analysis of cellular SMD or NMD substrates that regulated by Upf1 or PNRC2 in HeLa cell
| PRJNA136279 | ENA
Project description:The first round of translation occurs on mRNAs bound by nuclear cap-binding complex (CBC), which is composed of nuclear cap-binding protein (CBP) 80 and 20. During this round of translation, aberrant mRNAs are recognized and downregulated in abundance by nonsense-mediated mRNA decay (NMD), which is one of the mRNA quality control mechanisms. Here our microarray analysis reveals that the level of cyclin-dependent kinase inhibitor 1A (CDKN1A) mRNAs increases in the cells depleted of cellular NMD factors. Intriguingly, CDKN1A mRNA contains an upstream open reading frame (uORF), which is one of NMD-inducing features. Using chimeric reporter constructs and confocal microscopy, we find that the uORF of CDKN1A mRNA is actively translated and modulates a translational efficiency of the main downstream ORF. Our findings provide the biological insights into the possible role of NMD in diverse pathways mediated by CDKN1A. The microarray analysis performed to analize the cellular NMD substrates that regulated by Upf1, PNRC2 and/or CTIF in HeLa cell. The hypothesis tested in the present study was that endogenous NMD substrates may co-regulated by Upf1, PNRC2 and CTIF. Results provide important information that vast range of cellular NMD substrates are reqired CTIF. Total RNA obtained from HeLa cells with downregulation of Upf1, PNRC2 or CTIF by siRNA. The up- or down-regulated transcripts were compare to control siRNA treated HeLa cell RNA extract. Significant transcripts were confirmed by replication.
2012-07-22 | E-GEOD-37538 | biostudies-arrayexpress
Project description:The first round of translation occurs on mRNAs bound by nuclear cap-binding complex (CBC), which is composed of nuclear cap-binding protein (CBP) 80 and 20. During this round of translation, aberrant mRNAs are recognized and downregulated in abundance by nonsense-mediated mRNA decay (NMD), which is one of the mRNA quality control mechanisms. Here our microarray analysis reveals that the level of cyclin-dependent kinase inhibitor 1A (CDKN1A) mRNAs increases in the cells depleted of cellular NMD factors. Intriguingly, CDKN1A mRNA contains an upstream open reading frame (uORF), which is one of NMD-inducing features. Using chimeric reporter constructs and confocal microscopy, we find that the uORF of CDKN1A mRNA is actively translated and modulates a translational efficiency of the main downstream ORF. Our findings provide the biological insights into the possible role of NMD in diverse pathways mediated by CDKN1A. The microarray analysis performed to analize the cellular NMD substrates that regulated by Upf1, PNRC2 and/or CTIF in HeLa cell. The hypothesis tested in the present study was that endogenous NMD substrates may co-regulated by Upf1, PNRC2 and CTIF. Results provide important information that vast range of cellular NMD substrates are reqired CTIF.
2012-07-23 | GSE37538 | GEO