DDX5 RNA interactome in cultured T cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA660665 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12563740_1.fastq.gz | Fastqsanger.gz | |||
| SRR12563740_2.fastq.gz | Fastqsanger.gz | |||
| SRR12563741_1.fastq.gz | Fastqsanger.gz | |||
| SRR12563741_2.fastq.gz | Fastqsanger.gz | |||
| SRR12563742_1.fastq.gz | Fastqsanger.gz |
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Project description:RAR-related orphan receptor gamma (ROR t)-expressing regulatory T (ROR t+ Treg) cells play pivotal roles in preventing T cell hyperactivation and maintaining tissue homeostasis, in part, by secreting the anti-inflammation cytokine interleukin 10 (IL-10). Here, we report that Hypoxia Induced Factor 1a (HIF1alpha) is the master transcription factor for *Il10* in ROR t+ Tregs. Interestingly, this critical anti-inflammatory pathway is negatively regulated by an RNA-binding protein DEAD box helicase 5 (DDX5). As a transcriptional corepressor, DDX5 restricts the expression of HIF1 and its downstream target gene *Il10* in ROR t+ Tregs. T cell specific *Ddx5* knockout (DDX5 T) mice have augmented ROR t+ Treg suppressor activities and are better protected from intestinal inflammation. Genetic ablation or pharmacologic inhibition of HIF1a restores enteropathy susceptibility in DDX5 T mice. The DDX5-HIF1 -IL-10 pathway is conserved in mice and humans. These findings reveal potential therapeutic targets for intestinal inflammatory diseases.
2022-12-21 | GSE157259 | GEO
Project description:DDX5 is a multifunctional RNA helicase that regulates RNA metabolism and gene expression programs relevant to cancer and antiviral responses. Despite its importance, the RNA-binding landscape of DDX5 remains poorly defined. Here, we use CLIP-seq to systematically map the endogenous RNA interactome of DDX5 and to determine how it is altered by the K144N point mutation within the conserved RNA helicase domain.
2025-07-31 | GSE303849 | GEO
Project description:Purpose: The goals of this study are to compare RNAs bound by DDX5 and RORgt in cultured T helper 17 cell in wildtype background. Methods: Th17 mRNA profiles of 48hrs in vitro cultured T helper 17 cells from wild-type mice were generated by deep sequencing, using Illumina HighSeq. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: BurrowsâWheeler Aligner (BWA) and TopHat followed by CuffDiff. qRTâPCR validation was performed using SYBR Green assays. Results: Among the 3444 RefSeq non-coding RNAs and 46449 NONCODE non-coding RNAs, 2533 were found to be expressed in Th17 cells (FPKM>1). 210 of them were enriched in DDX5 pull-down and 119 of them were enriched in RORgt pull-down. Conclusions: Our study suggest that a subset of 31 ncRNAs were co-enriched in DDX5 and RORgt pull-down. DDX5 or RORgt-associated-RNA profiles of 48hr in vitro cultured Th17 from wild type (WT) mice were generated by deep sequencing using Illumina HighSeq
2015-12-21 | E-GEOD-70109 | biostudies-arrayexpress
Project description:The small heat shock protein Hsp27 has been long demonstrated as a major driver of Castration Resistant Prostate Cancer (CRPC) progression via an androgen receptor-independent pathway. In the light of identification of its molecular mechanisms, we found that the RNA helicase protein DDX5 was an interactor of Hsp27 and DDX5 expression was regulated by Hsp27 through its cytoprotective function. We showed that DDX5 was overexpressed in a large collection of human samples in aggressive PCs, especially CRPC. Here, we described the protein-protein interaction network of DDX5 which were identified in four human prostate cell lines (PNT1A, LNCaP, DU-145 and PC-3) representing different disease stages using immunoaffinity purification and quantitative mass spectrometry. The DDX5 interactome in CRPC cells was enriched in several functions (DNA damage response, translation, transcription, RNA stability, and DNA conformation changes) involved in disease progression. Furthermore, we found a new critical function of DDX5 in DNA damage repair in CRPC and validated the interaction of DDX5 with the DNA repair complex Ku70/Ku86 which plays a pivotal role in the NHEJ process. We also showed that DDX5 overexpression conferred resistance to DNA damage poisoners (such as irradiation and cisplatin) in CRPC, a feature that could lead to genome maintenance, tumor progression and treatment resistance.
2022-08-21 | PXD023252 | Pride
Project description:Purpose: The goals of this study are to identify chromatin loci bound by DDX5 in cultured T helper 17 cell in wildtype and DDX5 deficient background. Methods: ChIP-seq profiles of 48hrs in vitro cultured T helper 17 cells from wild-type mice were generated by deep sequencing, using Illumina HighSeq. The sequence reads that passed quality filters were mapped by Bowtie2.0. Results: DDX5 were found to be enriched on a subset of previously characterized RORgt occupied sites on the chromatin. Conclusions: Our study suggest that a subset of RORgt occupied regions were co-bound by DDX5.
2015-12-21 | GSE73913 | GEO
Project description:The maintenance of spermatogenesis in adult males is dependent on a population of mitotic germ cells with self-renewal potential known as undifferentiated spermatogonia. Regulation of undifferentiated spermatogonia function is dependent on transcriptional and post-transcriptional mechanisms. We have identified an essential role for the RNA helicase DDX5 in undifferentiated spermatogonia through generation of a UBC-CreERT2;Ddx5flox/flox mouse model that allows tamoxifen-dependent Ddx5 ablation. To identify genes regulated by DDX5, we generated lines of cultured undifferentiated spermatogonia from these mice and treated cells with tamoxifen (TMX) to induce Ddx5 knockout or vehicle (VEH) as a control, and performed RNA-sequencing analysis to compare these conditions.
2019-04-02 | GSE127275 | GEO
Project description:Mapping the RNA interactome of DDX5 and its rewiring by the K144N mutation in the RNA helicase domain
| PRJNA1297760 | ENA
Project description:RNA helicases DDX5 and DDX17 are members of a large family of highly conserved proteins involved in gene expression regulation, although their in vivo targets and activities in biological processes like cell differentiation, that requires reprogramming of gene expression programs at multiple levels, are not well characterized. In this report, we uncovered a new mechanism by which DDX5 and DDX17 cooperate with hnRNP H/F splicing factors to define epithelial- and myoblast-specific splicing subprograms. We next observed that downregulation of DDX5 and DDX17 protein expression during epithelial to mesenchymal transdifferentiation and during myogenesis contributes to switching splicing programs during these processes. Remarkably, this downregulation is mediated by the production of microRNAs induced upon differentiation in a DDX5/DDX17-dependent manner. Since DDX5 and DDX17 also function as coregulators of master transcriptional regulators of differentiation, we propose to name these proteins M-bM-^@M-^\master orchestratorsM-bM-^@M-^] of differentiation, that dynamically orchestrate several layers of gene expression. 6 samples of MCF7 cells exposed to different treatments were analyzed: 3 x siCTRLM-BM- ; 3 x si(DDX5-17) AND 6 samples of MCF10 cells exposed to different treatments were analyzed: 3 x siCTRLM-BM- ; 3 x si(DDX5-17)
2014-05-06 | E-GEOD-57281 | biostudies-arrayexpress
Project description:Purpose: The goals of this study are to compare in vitro polarized T helper 17 cell transcriptome profiling (RNA-seq) in different genetic background. Methods: Th17 mRNA profiles of 96hrs in vitro cultured T helper 17 cells from wild-type and mutant mice were generated by deep sequencing, using Illumina RapidRun. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: BurrowsâWheeler Aligner (BWA) and TopHat followed by CuffDiff. qRTâPCR validation was performed using SYBR Green assays. Results: Among the 325 genes that were significantly dysregulated in DDX5-deficient T cells, approximately 40% were previously identified as RORγt targets in Th17 cells. 96 RORγt-dependent Th17 cell genes co-regulated by Rmrp together with DDX5. Conclusions: Our study suggest that the DDX5-Rmrp axis is critical for expression of a critical subset of the RORγt transcriptional targets in Th17 cells. mRNA profiles of 96hr in vitro cultured Th17 from wild type (WT) and mutant mice were generated by deep sequencing using Illumina RapidRun.
2015-12-21 | E-GEOD-70108 | biostudies-arrayexpress
Project description:Purpose: The goals of this study are to compare RNAs bound by DDX5 and RORgt in cultured T helper 17 cell in wildtype background. Methods: Th17 mRNA profiles of 48hrs in vitro cultured T helper 17 cells from wild-type mice were generated by deep sequencing, using Illumina HighSeq. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) and TopHat followed by CuffDiff. qRT–PCR validation was performed using SYBR Green assays. Results: Among the 3444 RefSeq non-coding RNAs and 46449 NONCODE non-coding RNAs, 2533 were found to be expressed in Th17 cells (FPKM>1). 210 of them were enriched in DDX5 pull-down and 119 of them were enriched in RORgt pull-down. Conclusions: Our study suggest that a subset of 31 ncRNAs were co-enriched in DDX5 and RORgt pull-down.
2015-12-21 | GSE73912 | GEO