Similar Datasets
Project description:DROSHA complementation experiments were performed to check whether dsRBD of DROSHA recognizes the lower stem of pri-miRNAs and affects miRNA biogenesis.
2018-12-13 | GSE117603 | GEO
Project description:The experiments were conducted to check whether mismatches and wobble base pairs in the upper stem of pri-miRNAs affects the DROSHA cleavage and thereby miRNA biogenesis.
2020-02-28 | GSE142136 | GEO
Project description:Our previous study has showed that complex of NF90 and nuclear factor 45 (NF45) (NF90-NF45) inhibits miRNA biogenesis through negative regulation of primary-miRNA processing step. On the other hand, miRNAs, the biogenesis of which is regulated by NF90-NF45 in hepatocellular carcinoma, are not clear. Thus, to identify the miRNAs, we performed a miRNA array using RNAs extracted from control Huh7 cells and the cells depleted of NF90.
2015-03-31 | GSE67411 | GEO
Project description:The experiments were conducted to examine the effects of DROSHA mutations on miRNA biogenesis
2023-08-01 | GSE215796 | GEO
Project description:MicroRNA (miRNA) is a type of non-coding RNA that regulates the expression of its target genes by interacting with the complementary sequence of the target mRNA molecules. Recent evidence has shown that genotoxic stress induces miRNA expression, but the target genes involved and role in cellular responses remain unclear. We examined the role of miRNA in the cellular response to X-ray irradiation by studying the expression profiles of radio-responsive miRNAs and their target genes in cultured human cell lines. We found that expression of miR-574-3p was induced in the lung cancer cell line A549 by X-ray irradiation. Overexpression of miR-574-3p caused delayed growth in A549 cells. A predicted target site was detected in the 3'-untranslated region of the enhancer of the rudimentary homolog (ERH) gene, and transfected cells showed an interaction between the luciferase reporter containing the target sequences and miR-574-3p. Overexpression of miR-574-3p suppressed ERH protein production and delayed cell growth. This delay was confirmed by knockdown of ERH expression. Our study suggests that miR-574-3p may contribute to the regulation of the cell cycle in response to X-ray irradiation via suppression of ERH protein production. miRNA expression were measured at 1 and 3 h after exposure to doses of 0, 2 or 20 Gy. Microarray experiments were performed with duplicate for each experiment.
2014-03-14 | E-GEOD-30130 | biostudies-arrayexpress
Project description:In this study, we aim at understanding which RNA degradation pathways are involved in keeping the secondary siRNA production in check in Arabidopsis thaliana. We have sequenced small RNAs from various T-DNA insertation single mutants and compared their capability of producing ectopic secondary siRNAs from endogenous miRNA targets. The mutants used in the work stem from three library pools from three different experiments. Libraries from all three experiments are submitted together here. The experiments can be distinguished by their title and their tag:experiment. There is a matrix of normalized reads from each pool of library as well called normalizedExp1.txt, normalizedExp2.txt and normalizedExp3.txt
2021-04-28 | GSE173426 | GEO
Project description:Our previous study has showed that complex of NF90 and nuclear factor 45 (NF45) (NF90-NF45) inhibits miRNA biogenesis through negative regulation of primary-miRNA processing step. On the other hand, miRNAs, the biogenesis of which is regulated by NF90-NF45 in hepatocellular carcinoma, are not clear. Thus, to identify the miRNAs, we performed a miRNA array using RNAs extracted from control Huh7 cells and the cells depleted of NF90. Comparison of miRNA expression profile in one non-targeting control siRNA (siNTC)- or two independent siNF90-treated Huh7 cells.
2015-03-31 | E-GEOD-67411 | biostudies-arrayexpress
Project description:'MicroRNA (miRNA) is a type of non-coding RNA that regulates the expression of its target genes by interacting with the complementary sequence of the target mRNA molecules. Recent evidence has shown that genotoxic stress induces miRNA expression, but the target genes involved and role in cellular responses remain unclear. We examined the role of miRNA in the cellular response to X-ray irradiation by studying the expression profiles of radio-responsive miRNAs and their target genes in cultured human cell lines. We found that expression of miR-574-3p was induced in the lung cancer cell line A549 by X-ray irradiation. Overexpression of miR-574-3p caused delayed growth in A549 cells. A predicted target site was detected in the 3''-untranslated region of the enhancer of the rudimentary homolog (ERH) gene, and transfected cells showed an interaction between the luciferase reporter containing the target sequences and miR-574-3p. Overexpression of miR-574-3p suppressed ERH protein production and delayed cell growth. This delay was confirmed by knockdown of ERH expression. Our study suggests that miR-574-3p may contribute to the regulation of the cell cycle in response to X-ray irradiation via suppression of ERH protein production. mRNA expression were compared between the A549 cell overexpressing a radio-responsive miRNA and in the A549 cells suppressing the miRNA. Five miRNAs (miR-181d, miR-565, miR-574-3p, miR-629* and miR-766) were examined. Microarray experiments were performed with triplicate for each experiment.'
2014-03-14 | E-GEOD-30131 | biostudies-arrayexpress
Project description:Global downregulation of microRNAs (miRNAs) is commonly observed in human cancers and can have a causative role in tumorigenesis. The mechanisms responsible for this phenomenon remain poorly understood. Here we show that YAP, the downstream target of the tumor-suppressive Hippo signaling pathway regulates miRNA biogenesis in a cell density-dependent manner. At low cell density, nuclear YAP binds and sequesters p72 (DDX17), a regulatory component of the miRNA processing machinery. At high cell density, Hippo-mediated cytoplasmic retention of YAP facilitates p72 association with Microprocessor and binding to a specific sequence motif in pri-miRNAs. Inactivation of the Hippo pathway or expression of constitutively active YAP causes widespread miRNA suppression in cells and tumors and a corresponding post-transcriptional induction of MYC expression. Thus, the Hippo pathway links contact-inhibition regulation to miRNA biogenesis and may be responsible for the widespread miRNA repression observed in cancer.
2014-03-03 | GSE52188 | GEO
Project description:Global downregulation of microRNAs (miRNAs) is commonly observed in human cancers and can have a causative role in tumorigenesis. The mechanisms responsible for this phenomenon remain poorly understood. Here we show that YAP, the downstream target of the tumor-suppressive Hippo signaling pathway regulates miRNA biogenesis in a cell density-dependent manner. At low cell density, nuclear YAP binds and sequesters p72 (DDX17), a regulatory component of the miRNA processing machinery. At high cell density, Hippo-mediated cytoplasmic retention of YAP facilitates p72 association with Microprocessor and binding to a specific sequence motif in pri-miRNAs. Inactivation of the Hippo pathway or expression of constitutively active YAP causes widespread miRNA suppression in cells and tumors and a corresponding post-transcriptional induction of MYC expression. Thus, the Hippo pathway links contact-inhibition regulation to miRNA biogenesis and may be responsible for the widespread miRNA repression observed in cancer. Two conditions (siCtrl and siYAP) were analyzed in duplicate.
2014-03-03 | E-GEOD-52188 | biostudies-arrayexpress