HUR affected genes in human skin cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE161811 | GEO | 2020/11/20
REPOSITORIES: GEO
Similar Datasets
Project description:HUR affected genes in human skin cells
| PRJNA679558 | ENA
Project description:This study aims to evaluate the effect of AUF-1 knokdown on the function and global gene expression in human skin cells. Cells with AUF1 silencing were compared with control cells by RNA-Seq. Cell senescence is a tightly controlled, programmed process. Although the mechanism of cell senescence is unclear, the concept that cell aging is an interaction results between enviomental and genetic factors has been accepted. Changes in the expression of related genes are the genetic basis of cell senescence. AUF1 gene has been proved that can recognize classical mRNA and regulated its expression level. These classical mRNA include those encoding cecle-regulating proteins, apoptotic regulators, cytokines and proto-oncogenes. Our study use overexpression and interference lentivirus of AUF1 to transfect WS1 cell to process cell transcriptome sequencing. Through the Bioinformatics analysis results, we want to see some different expressed genes related to cell cecle, cell apoptosis and so on. Our study can provide basis research to further expound AUF1 gene, play an important role of aging mechanism.
2019-10-10 | GSE138621 | GEO
Project description:HuR is a regulator of mRNA turnover or translation of inflammatory genes through binding to adenylate-uridylate-rich elements (ARE) and related motifs present in the 3’untranslated region (UTR) of mRNAs. We aimed to identify HuR targets in the human airway epithelial cell line BEAS-2B challenged with TNFa plus IFNg, a strong stimulus for inflammatory epithelial responses. Ribonucleoprotein (RNP) complexes from resting and cytokine-treated cells were immunoprecipitated (IP) using anti-HuR and isotype-control antibody, and eluted mRNAs were reverse-transcribed and hybridized to an inflammatory-focused gene array. The chemokines CCL2, CCL8, CXCL1 and CXCL2 ranked highest among 27 signaling and inflammatory genes significantly enriched in the HuR RNP-IP from stimulated cells over the control IP. Among these, 20 displayed published HuR binding motifs. Association of HuR with the four endogenous chemokine mRNAs was validated by single-gene RNP-IP, and shown to be 3’UTR-dependent by biotin pull-down assay. Cytokine treatment increased mRNA stability only for CCL2 and CCL8, and transient silencing and overexpression of HuR affected only CCL2 and CCL8 expression in primary and transformed epithelial cells. Cytokine-induced CCL2 mRNA was predominantly cytoplasmic; conversely, CXCL1 mRNA remained mostly nuclear and unaffected, as CXCL2, by changes in HuR levels. Increase in cytoplasmic HuR and HuR target expression partially relied on the inhibition of AMP-dependent kinase, a negative regulator of HuR nucleocytoplasmic shuttling. We postulate that HuR critically regulates the epithelial response, by associating with multiple adenylate-uridylate-rich elements (ARE)-bearing, functionally related inflammatory transcripts. On the basis of genome-wide studies probing the relationship between RNA-binding proteins and the functional profile of their associated transcripts, we combined the specific HuR immunoprecipitation of RNPs and the genome-scale microarray to profile the target mRNAs of HuR in the human airway epithelial cell line BEAS-2B challenged with very strong inflammatory stimulation, TNFa plus IFNG. The array platform we used is the Human Autoimmune and Inflammatory Response Gene Array (SuperArray Bioscience, Frederick, MD). To validate the association of HuR and its target mRNAs, we planned to apply biotin pull-down assay. HuR overexpression and knockdown assays were also planned to further verify the association of HuR and its target mRNAs. Overall, we did three biological replicates for the IP array experiments, which include both IgG1 control IP and HuR IP arrays.
2010-11-10 | E-GEOD-25264 | biostudies-arrayexpress
Project description:Purpose: To determine biological impact between silencing HuR and YAP1, in MIA-PaCa2. Methods: Expression profiling of MIA-PaCa2 cells knocked-down for HuR and YAP1 and control cells transfected with scramble siRNA.
2022-06-07 | GSE167525 | GEO
Project description:HuR is a regulator of mRNA turnover or translation of inflammatory genes through binding to adenylate-uridylate-rich elements (ARE) and related motifs present in the 3’untranslated region (UTR) of mRNAs. We aimed to identify HuR targets in the human airway epithelial cell line BEAS-2B challenged with TNFa plus IFNg, a strong stimulus for inflammatory epithelial responses. Ribonucleoprotein (RNP) complexes from resting and cytokine-treated cells were immunoprecipitated (IP) using anti-HuR and isotype-control antibody, and eluted mRNAs were reverse-transcribed and hybridized to an inflammatory-focused gene array. The chemokines CCL2, CCL8, CXCL1 and CXCL2 ranked highest among 27 signaling and inflammatory genes significantly enriched in the HuR RNP-IP from stimulated cells over the control IP. Among these, 20 displayed published HuR binding motifs. Association of HuR with the four endogenous chemokine mRNAs was validated by single-gene RNP-IP, and shown to be 3’UTR-dependent by biotin pull-down assay. Cytokine treatment increased mRNA stability only for CCL2 and CCL8, and transient silencing and overexpression of HuR affected only CCL2 and CCL8 expression in primary and transformed epithelial cells. Cytokine-induced CCL2 mRNA was predominantly cytoplasmic; conversely, CXCL1 mRNA remained mostly nuclear and unaffected, as CXCL2, by changes in HuR levels. Increase in cytoplasmic HuR and HuR target expression partially relied on the inhibition of AMP-dependent kinase, a negative regulator of HuR nucleocytoplasmic shuttling.
2010-11-10 | GSE25264 | GEO
Project description:FLASH, a novel method, was utilized to identify binding sites of RNA-binding proteins (RBPs) with single-nucleotide resolution (Nucleic Acids Res 2020;48:e15). In order to identify HuR target genes in THP-1 macrophages after circARCN1 regulation, we performed FLASH experiments using the anti-HuR antibody on THP-1 macrophages with circARCN1 knockdown or overexpression. The resulting FLASH products were then subjected to RNA sequencing.
2024-06-01 | GSE254370 | GEO
Project description:The effect of HuR silencing in breast epithelial cells
2010-12-14 | E-MEXP-3035 | biostudies-arrayexpress
Project description:IL-20 cytokines are involved in the establishment of psoriasis, a common chronic skin inflammation epidemiologically associated with metabolic syndrome, but molecular mechanisms underlying their over-expression remain to be elucidated. We find that keratinocytes (KCs) expressed IL-20 and lymphocytes expressed IL-22 cytokines up-regulation occurs at post-transcriptional level with stabilization of their RNA messengers. Looking at psoriatic epidermis, we observe that the p38/MK2 pathway is not activated but that the RNA-binding protein (RBP) HuR re-localizes in keratinocytes cytoplasm, suggesting post-transcriptional regulation of numerous mRNAs. HuR ribonucleoprotein immunoprecipitations analyzed by high-throughput sequencing (RIP-Seq) identify potential pre-mature and mature RNA targets for uninvolved and involved skin and confirms that HuR activity is displaced from the nucleus to the cytoplasm. Numerous psoriasis up-regulated transcripts are HuR targets and HuR knockdown reduces expression of transcripts like beta-defensin-2, CXCL-10 or IL-2, suggesting an implication of HuR in pathophysiological processes such as morphological, immune and metabolic inflammatory responses. Finally, metabolic disorders affecting psoriatic keratinocytes are responsible for HuR cytoplasmic localization since a decreased activity of the cellular metabolic sensor AMPK, that is observed in human psoriatic epidermis, is sufficient to promote HuR cytosolic localization as well as IL-20 over-production both in human keratinocytes and in vivo in mouse epidermis where it then initiates psoriasis-like histological changes. These results may provide insights into molecular links between metabolism and post-transcriptional networks during chronic inflammation, as illustrated in psoriasis by mechanisms connecting AMPK, HuR and IL-20. Analysis of HuR-binding RNA in uninvolved versus involved psoriatic samples by RIP-Seq. Samples from five different patients were used for both uninvolved and involved skin. RIP-Seq was also made using a control IgG.
2015-09-08 | E-GEOD-50598 | biostudies-arrayexpress
Project description:mRNA TE and steady-state levels were measured in hypoxic U87MG cells treated with non-silencing control or HuR-specific siRNA pools followed by ribosome density fractionation.
2020-04-23 | GSE128541 | GEO
Project description:The progressive development of T-cells in the thymus is a highly regulated process that aims to arm the body with T-cells against pathogens whilst maintaining tolerance to self. Although the role of gene transcription in this process has been extensively studied, little is known about the significance of associated post-transcriptional mechanisms. Post-transcriptional control is imposed by the dynamic interactions of RNA-binding proteins (RBPs) with RNA molecules which destine mRNA molecules towards translation or destruction. In this study we focus on the functions of an RBP called HuR. We made use of novel transgenic systems in which HuR is deleted in thymic T-cells to test whether HuR is involved in their developmental maturation. We show that HuR controls the generation and provision of T-cells competent for the proper recognition of antigens in the body and the elimination of harmfull cells. We further show that HuR controls T-cell development through its involvement in basic cellular processes like cell cycle regulation, cellular activation, death and migration which were associated to HuR’s efficacy in regulating the expression or function of key signaling components. Our studies provide important insight on the post-transcriptional regulation of fundamental cellular processes and identify HuR as an important modulator of adaptive immunity and autoimmunity.
2009-05-20 | GSE9174 | GEO