IL-4 stimulation of Dicer deficient bone-marrow derived macrophages in vitro
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE36585 | GEO | 2012/03/17
SECONDARY ACCESSION(S): PRJNA153753
REPOSITORIES: GEO
Similar Datasets
Project description:Macrophages were derived from the bone-marrow of 3 x fl/+ Dicer LysCre +/- (wild-type) and 3 x fl/fl Dicer LysCre +/- mice and stimulated with IL-4 (50ng/mL) for 72h. Total RNA was isolated and analyzed by gene array. In this experiment, we derived Dicer deficient bone-marrow macrophages using Dicer fl/+ LysM-Cre by Dicer fl/+ crossed mice to obtain Dicer fl/fl LysM-cre progeny (and Dicer deficient macrophages). Next, we studied the effects of IL-4 stimulation in macrophage with a deficiency in Dicer/microRNAs.
2012-03-17 | E-GEOD-36585 | biostudies-arrayexpress
Project description:Transcriptional profiling of Langerhans cells isolated from CD11c-Cre x Dicer wt/wt (Dicer +/+ ) and CD11c-Cre x Dicer fl/fl (Dicer-/-) mice. Langerhans cells are isolated via enzymatic digestion of skin followed by antibody staining and FACS sorting
2010-06-17 | E-MEXP-2387 | biostudies-arrayexpress
Project description:To determine genes regulated independently of microRNAs in early haematopoietic progenitors (LSKs) we compared the expression profiles of Drosha or Dicer deficient LSKs and control. Those genes differentially expressed between Drosha or Dicer deficient LSKs are likely regulated indepedently of microRNAs as either Drosha or Dicer deletion will lead to a complete and equivalent loss of microRNAs. LSKs were sorted from control, Drosha fl/fl of Dicer fl/fl mice.These cells were activated in vitro for 72 hours to induce total and equivalent deletion of Drosha or Dicer. RNA was extracted after 72 hours.3 repeats of the three groups were analyzed.
2015-09-10 | E-GEOD-61305 | biostudies-arrayexpress
Project description:Small RNAs, such as miRNAs and siRNAs, are involved in gene regulation in a variety of systems, including mouse oocytes. Dicer is a ribonuclease III enzyme essential for miRNA and siRNA biosynthesis. In an effort to uncover the function of small RNAs during oocyte growth, we specifically deleted Dicer in growing oocytes and analyzed the global pattern of gene expression in these Dicer-deficient oocytes.
2010-03-05 | GSE17985 | GEO
Project description:Background & Aims: MiRNAs are small (~22 nucleotide), non-coding RNA molecules that regulate gene expression through imperfect complementarity with target messenger RNAs. The function of miRNA in mammalian organogenesis is largely unknown. Conditional loss-of-function of Dicer, the enzyme that processes precursor miRNA transcripts into their mature, active form, has been shown to cause severe defects in a number of organ systems. Here we address the role of Dicer in liver development and function. Methods: Mice lacking Dicer function in hepatocytes were generated using an Afp-Cre strain to drive deletion of a floxed Dicer allele. Deletion of the flox-dicer allele was confirmed by quantitative PCR. Decreased miRNA levels detected by quantitative RT-PCR and in situ hybridization confirmed loss of Dicer function. Gene expression microarray analysis was performed on liver RNA from P28 mutant and control mice. Liver sections from mutant and control mice ranging from embryonic stages through 3-4 months of age were examined and liver function tests were performed on adult mice. Results: Mice lacking hepatocyte Dicer function were born alive at the expected frequency, and had grossly normal appearance and behavior. Despite the loss of mature miRNA, hepatic function was normal, as reflected by normal blood gludose, albumin, cholesterol, and bilirubin. However, mutant mice between 2-4 months of age exhibit progressive hepatocyte damage, elevated ALT/AST, with evidence of balanced proliferation and apoptosis in the lobule. Microarray analysis indicates large-scale changes in gene expression, with increased expression of many miRNA targets, as well as imprinted genes. Conclusions: Loss of miRNA processing in the liver at late gestation has a remarkably mild phenotype, suggesting that miRNAs do not play an essential role in hepatic physiology. However, miRNA deficiency results in hepatocyte apoptosis and balanced hepatocyte regeneration. Finally, microarray analysis of gene expression in mutant liver suggests a previously unrecognized role for Dicer in the repression of imprinted genes. Keywords: Genetic modification
2008-12-31 | GSE11899 | GEO
Project description:The role of microRNAs in the inflammatory response of macrophages to LPS was adressed by expression analysis in DicerKO (LysMcre/+;Dicerfl/fl;ApoE-/-) vs wildtype (LysMcre/+;Dicer+/+ApoE-/-) macrophages when challenged either with vehicle (PBS) or LPS.
2018-05-25 | GSE106854 | GEO
Project description:DICER has a well-characterized role in the processing of microRNAs (miRNAs) and small interfering RNAs (siRNA) that are important for post-transcriptional gene regulation. Emerging evidence suggests that DICER also has several non-canonical functions beyond miRNA/siRNA biogenesis, for example in transcriptional gene silencing at the chromatin level, as well as in RNA degradation and maintenance of genomic integrity. We have shown that the function of DICER in germ cells is essential for normal spermatogenesis; male mice lacking DICER in postnatal male germ cells are infertile due to severe defects in haploid differentiation. To better understand the function of DICER in male germ cells, we immunoprecipitated DICER from juvenile mouse testes and performed mass spectrometric analysis to identify DICER-interacting proteins.
2020-06-03 | PXD017772 | Pride
Project description:Small RNAs, such as miRNAs and siRNAs, are involved in gene regulation in a variety of systems, including mouse oocytes. Dicer is a ribonuclease III enzyme essential for miRNA and siRNA biosynthesis. In an effort to uncover the function of small RNAs during oocyte growth, we specifically deleted Dicer in growing oocytes and analyzed the global pattern of gene expression in these Dicer-deficient oocytes. Germinal vesicle-intact, fully grown oocytes were collected from eCG-primed wild-type or Dicer-deficient female mice and freed of attached cumulus cells by pipetting. Twenty oocytes per mouse were used for RNA extraction and hybridization on the MOE430 v2 Affymetrix microarray platform. Oocytes from four wild-type and four Dicer-knockout mice were analyzed.
2010-04-06 | E-GEOD-17985 | biostudies-arrayexpress
Project description:Abelson virus (v-Abl)-transformed pre-B cell lines from BM of dcrfl/fl; R26R-yfp (4470; 4475) and dcrfl/+; R26R-yfp mice (4483) are treated with a transducible Cre protein (Tat-Cre) to induce deletion of the dicer-1 gene in vitro. Cre activity is conveniently monitored by concomitant expression of YFP. To obtain Dicer KO cells, YFP+ cells from dcrfl/fl; R26R-yfp (4470_YFP; 4475_YFP) cultures treated with Tat-cre were isolated by fluorescence-activated cell sorting (FACS) and further propagated in cell culture. As controls, we used non-deleted, YFP- cells sorted from dcrfl/fl; R26R-yfp cultures (4470; 4475) treated with Tat-cre, and YFP+ deleted cells from dcrfl/+; R26R-yfp cultures (4483_YFP). To validate this system, various cell populations were sorted and analyzed for Dicer protein and miRNA expression. In the Dicer KO pro-B cell lines, Western analysis indicated that Dicer protein was efficiently ablated, and Northern blots demonstrated that the levels of mature miR-17 and miR-191 were drastically reduced.
2008-03-08 | E-MEXP-1455 | biostudies-arrayexpress
Project description:Dicer is an essential ribonuclease involved in the biogenesis of miRNA. Previous studies have reported that Dicer is dysregulated in multiple types of cancers. To investigate the downstream phosphoproteome of Dicer, we carried out phosphotyrosine profiling of the liver of Dicer knockout of mice. We employed antibody-based enrichment of phosphotyrosine containing peptides coupled with spike-in SILAC-based quantitation. Over 400 phosphoisites were identified in each condition while 290 phosphosites were quantitated in common. Amongst these, several key signaling molecules like receptor tyrosine kinase MET, MET, PDGFR, EPHA2, EPHB4 and IGF1R/INSR were hyperphosphorylated. Also, non-receptor tyrosine kinases of Src family and their downstream effector signaling partners including IRS2 and STAT3were found to be hyperphosphorylated. Our study indicates that there is significant alteration in the signaling pathways upon ablation of Dicer.
2016-07-08 | PXD000927 | Pride