MiR-146a Pulldown-sequencing data
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ABSTRACT:
PROVIDER: PRJNA675568 | ENA |
REPOSITORIES: ENA
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Project description:Human CD4+ Total memory cells (CD4+CD25-CD45RA-CCR7+/-) were activated with anti-CD3/anti-CD28 antibodies and transfected with biotinylated miR-146a mimic or biotinylated mimic negative control by Exiqon. After 24h cells were lysed and miRNA:mRNA complexes pulled-down with streptavidin agarose O/N at 4°C. RNA was then purified using TRI-reagent and RNA zymospin columns. Four independent donors were used for this experiment. Total RNA was sequenced in 2 lanes, paired ends. This experiment is assessing direct targets bound by miR-146a in human T cells.
2022-01-10 | GSE161094 | GEO
Project description:miR-150 Pulldown-sequencing data
| PRJNA675569 | ENA
Project description:Here we show that biotin-labelled miR-34a can be loaded to AGO2, and AGO2 immunoprecipitation can pulldown biotinylated miR-34a (Bio-miR pulldown). RNA-sequencing (RNA-seq) of the Bio-miR pulldown RNAs efficiently identified miR-34a mRNA targets, which could be verified with luciferase assays. In contrast to the approach of Bio-miR pulldown, RNA-seq of miR-34a overexpression samples had limited value in identifying direct targets of miR-34a. It seems that pulldown of 30 -Biotin-tagged miRNA can identify bona fide microRNA targets at least for miR34a.
2019-02-27 | GSE127211 | GEO
Project description:A long-prevailing model has held that the “seed” region (nucleotides 2-8) of a microRNA is typically sufficient to mediate target recognition and repression. However, numerous recent studies, both within the context of defining miRNA/target pairs by direct physical association and by directly assessing this model in vivo in C. elegans have brought this model into question. To test the importance of miRNA 3' pairing in vivo, in a mammalian system, we engineered a mutant murine mir-146a allele in which the 5' half of the mature microRNA retains the sequence of the wild-type mir-146a but the 3ʹ half has been altered to be anti-complementary to the wild-type miR-146a sequence. Mice homozygous or hemizygous for this mutant allele are phenotypically indistinguishable from wild-type controls and do not recapitulate any of the immunopathology previously described for mir-146a-null mice. Our results strongly support the conclusion that 3ʹ pairing is dispensable in the context of the function of a key mammalian microRNA.
2019-02-09 | PXD011413 | Pride
Project description:MiR-146a is an important regulator of innate inflammatory responses and is also implicated in cell death and survival. Here, we identified microglia as the main cellular source of miR-146a among mouse CNS resident cells. We further characterized the phenotype of miR-146a KO microglia cells during in vivo demyelination induced by cuprizone (CPZ) and found reduced number of CD11c+ microglia in the KO compared to WT mice. Microglia were also isolated from the brain, and the proteome was analyzed by liquid chromatography mass spectrometry.
2020-06-29 | PXD015939 | Pride
Project description:miR-146a is a known anti-inflammatory miRNA. Intringuigly, it is overexpressed in RAS-induced senescent cells which is accompanied with a rich pro-inflammatoy secretpry phenotype. We aim to study possible sponges for miR-146a.
2021-05-11 | GSE150325 | GEO
Project description:miR-146a acts as a negative feedback regulator of inflammation. To investigate the role of miR-146a in psoriasis psoriasiform skin inflammation was indeuced in Mir-146a-/- and wild type mice (C57BL6J) by topical applciation of imiquimod (IMQ)-cream (Aldara). Gene expression profiling (Affymetrix) was used to identify transcriptomic changes associated with psoriasis-like skin inflammation in wild type vs. miR-146a -/-mice.
2016-02-19 | GSE78057 | GEO
Project description:MicroRNAs (miRNAs) are small non-coding RNAs that function as modulators of gene expression. We previously showed that miR-146a-5p is upregulated in pancreatic islets treated with pro-inflammatory cytokines and in pancreatic sections from organ donors with type 1 diabetes (T1D). Other studies have associated overexpression of miR-146a-5p with β cell apoptosis and impaired insulin secretion; however, the molecular mechanisms mediating these effects remain elusive. To investigate the role of miR-146a-5p in β cell function, we developed stable MIN6 cell lines transduced with lentiviral vectors to either overexpress or inhibit the expression of miR-146a-5p. Monoclonal cell populations were treated with pro-inflammatory cytokines (IL1β, IFNg, and TNFα) to model T1D in vitro. We found that overexpression of miR-146a-5p increased the cell death of MIN6 cells under inflammatory stress, whereas inhibition of miR-146a-5p reversed these effects. Additionally, inhibition of miR-146a-5p increased mitochondrial DNA copy number, respiration rate, and ATP production, suggesting that miR-146a-5p inhibition improves mitochondrial function. In support of this finding, we also observed that miR-146a-5p is enriched in the mitochondria of MIN6 cells treated with cytokines. Consistently, bioinformatic analysis of RNA sequencing data using MIN6 stable cells showed enrichment of pathways related to insulin secretion, apoptosis, and mitochondrial function when the expression levels of miR-146a-5p were altered. Overall, the findings from our study show for the first time that miR-146a-5p upregulation during inflammatory stress may promote β cell dysfunction and death by suppressing mitochondrial function.
2024-04-10 | GSE255756 | GEO
Project description:We have found expression of miR-146a up-regulated in gastric cancer. To identify new targets of miR-146a we profiled the transcriptome after miR-146a over-expression in the human gastric cancer cell line SNU638. SNU638 cells were transfected in triplicates with 50 nM miR-146a or control (siGlo) using Lipofectamine 2000. Total RNA was harvested 24 h after transfection using Trizol reagent. There are a total of six arrays included in this experiment, including three biological replicates of mRNA expression after miR-146a over-expression and three controls in SNU638 cells.
2012-07-01 | E-MEXP-3479 | biostudies-arrayexpress
Project description:Screening the differetial expressed genes with Jurkat-146a(miR-146a over expression),Jurkat-sponge(miR-146a knockdown),Jurkat-FF3(vector control)
2010-03-24 | E-MEXP-2627 | biostudies-arrayexpress