Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA117575 | ENA |
REPOSITORIES: ENA
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Project description:Expression data from HeLa cells treated with V-ATPase inhibitors or with desoxyferramine compared to HeLa treated with DMSO or medium with low LDL To determine which genes respond first to low concentrations of V-ATPase inhibition, we treated HeLa cells with two different V-ATPase inhibitors, bafilomycin and phenylsalicylihalamide (LX1077) at concentrations that slow cell growth by only 20%. To identify genes responding to expected effects of inhibiting the V-ATPase, expression data from inhibiting the V-ATPase was compared to that of chelating iron or incubating cells in medium with low LDL.
2010-07-22 | GSE16870 | GEO
Project description:Expression data from HeLa cells treated with V-ATPase inhibitors or with desoxyferramine compared to HeLa treated with DMSO or medium with low LDL To determine which genes respond first to low concentrations of V-ATPase inhibition, we treated HeLa cells with two different V-ATPase inhibitors, bafilomycin and phenylsalicylihalamide (LX1077) at concentrations that slow cell growth by only 20%. To identify genes responding to expected effects of inhibiting the V-ATPase, expression data from inhibiting the V-ATPase was compared to that of chelating iron or incubating cells in medium with low LDL. We used microarrays to detail the global programme of gene expression in HeLa cells at 6, 12 & 24 hours culture in the presence of V-ATPase inhibitors. For each drug treatment, control cells were incubated at the same time with the same concentration of DMSO used as carrier for the drugs. HeLa cells were also treated with the iron chelator, desoxiferamine for 6 or 12 hours or with medium with low LDL for 12 hours to identify genes that respond to low iron or low cholesterol. Each timepoint and each treatment has two independent replicates. Experimental samples were compared to control samples grown on the same day.
2010-07-22 | E-GEOD-16870 | biostudies-arrayexpress
Project description:3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, statins, are known to exert endothelial athero-protective effects through the induction of specific transcriptional factors and their downstream target genes besides lowering LDL-cholesterol. However its critical mechanism has not still been elucidated. Here we report the comprehensive change of transcripts induced by pitavastatin. We used repeated microarray analysis of HUVECs treated with pitavastatin for 4-hours, we identified a group of consistently up - or down - regulated genes. HUVECs were used within the first 6 passages. For studies, HUVECs were cultivated in medium EGM2MV containing pitavastatin at a concentration of 1 μM, and same concentration of DMSO was used as a control sample.
2013-01-01 | E-GEOD-32547 | biostudies-arrayexpress
Project description:HeLa cells were synchronized with a double thymidine block procedure. Briefly, the exponentially growing HeLa cells were maintained with 2 mM thymidine for 18 h, followed by a release of 9 h in fresh medium, and then cells were re-cultured in 2 mM thymidine for additional 15 h. After a release of 7.5 h in fresh medium, DMSO or G6PD inhibitor was added to the medium. 1 h later, the cells entered into M phase. Mitotic cells were harvested by mitotic shake-off. Then, the samples were subjected to LC-MS/MS analysis. Finally, a Kinase-Substrate Enrichment was performed, which could infer the changes of upstream kinase activity upon the treatment of G6PD inhibitors.
2023-05-18 | PXD033825 | Pride
Project description:We used phosphoproteomics to compare the responses of the ERK1/2 inhibitors, SCH772984 and GDC0994, and the MKK1/2 inhibitor, trametinib. These are compared with responses to the MKK1/2 inhibitor, selumetinib (AZD6244), previously measured by our lab in the same metastatic melanoma cell line. In three replicate experiments, we quantified a total of 12,805 class I phosphosites on 3,819 proteins in the trametinib-SCH772984-DMSO experiment, and 7,074 class I phosphosites on 2,453 in the GDC0994-SCH772984-DMSO experiment. This included 466 phosphosites that reproducibly decreased in response to at least one inhibitor in the trametinib-SCH772984-DMSO experiment and 414 phosphosites in the GDC0994-SCH772984-DMSO experiment. The results demonstrate linearity in signaling through the MAP kinase pathway. By comparing multiple inhibitors targeted to multiple tiers of protein kinases in the MAPK pathway, we gain insight into regulation and new targets of the oncogenic BRAF driver pathway in cancer cells, and a useful approach for evaluating the specificity of drugs and drug candidates. SILAC Experimental Design Experiment 1 Replicate 1: Heavy – DMSO, Medium – SCH772984, Light – Trametinib Replicate 2: Heavy – SCH772984, Medium – Trametinib, Light – DMSO Replicate 3: Heavy – Trametinib, Medium – DMSO, Light – SCH772984 SILAC Experimental Design Experiment 2 Replicate 1: Heavy – DMSO, Medium – SCH772984, Light – GDC0994 Replicate 2: Heavy – SCH772984, Medium – GDC0994, Light – DMSO Replicate 3: Heavy – GDC0994, Medium – DMSO, Light – SCH772984 File List 1. Zipped MaxQuant search results folder containing index and output folders for each raw file, ‘combined’ output folder, and mqpar.xml MaxQuant search parameters file 2. Individual raw files of phosphopeptide-enriched ERLIC fractions 3. Zipped MaxQuant version used for analysis 4. FASTA file containing Uniprot human identifications 5. Instructions for viewing annotated spectra
2018-01-02 | PXD007621 | Pride
Project description:We used phosphoproteomics to compare the responses of the ERK1/2 inhibitors, SCH772984 and GDC0994, and the MKK1/2 inhibitor, trametinib. These are compared with responses to the MKK1/2 inhibitor, selumetinib (AZD6244), previously measured by our lab in the same metastatic melanoma cell line. In three replicate experiments, we quantified a total of 12,805 class I phosphosites on 3,819 proteins in the trametinib-SCH772984-DMSO experiment, and 7,074 class I phosphosites on 2,453 in the GDC0994-SCH772984-DMSO experiment. This included 466 phosphosites that reproducibly decreased in response to at least one inhibitor in the trametinib-SCH772984-DMSO experiment and 414 phosphosites in the GDC0994-SCH772984-DMSO experiment. The results demonstrate linearity in signaling through the MAP kinase pathway. By comparing multiple inhibitors targeted to multiple tiers of protein kinases in the MAPK pathway, we gain insight into regulation and new targets of the oncogenic BRAF driver pathway in cancer cells, and a useful approach for evaluating the specificity of drugs and drug candidates. SILAC Experimental Design Experiment 1 Replicate 1: Heavy – DMSO, Medium – SCH772984, Light – Trametinib Replicate 2: Heavy – SCH772984, Medium – Trametinib, Light – DMSO Replicate 3: Heavy – Trametinib, Medium – DMSO, Light – SCH772984 SILAC Experimental Design Experiment 2 Replicate 1: Heavy – DMSO, Medium – SCH772984, Light – GDC0994 Replicate 2: Heavy – SCH772984, Medium – GDC0994, Light – DMSO Replicate 3: Heavy – GDC0994, Medium – DMSO, Light – SCH772984 File List 1. Zipped MaxQuant search results folder containing index and output folders for each raw file, ‘combined’ output folder, and mqpar.xml MaxQuant search parameters file 2. Individual raw files of phosphopeptide-enriched ERLIC fractions and total protein fractions 3. Zipped MaxQuant version used for analysis 4. FASTA file containing Uniprot human identifications 5. Instructions for viewing annotated spectra
2018-01-02 | PXD007620 | Pride
Project description:Primary human AML cells (newly diagnosed, prior to treatment initation) was obtained from donor after consent and AML blasts were isolated by standard Ficoll centrifugation. Cells were treated ex vivo with DMSO vehicle control or 10 nM FLT3 inhibitors quizartinib, crenolanib, gilteritinib for 6 hours in SILAC medium and processed for LC/MS.
2022-08-25 | PXD034081 | Pride
Project description:RKO cells were treated with low doses of aphidicolin (0,2µM) that inhibit replicative DNA polymerases and induce a mild replication stress. Expression data were analysed on control cells (DMSO), 16h of treatment (t0) and after release in complete new culture medium of 13h (N+1) using microarray (affymetrix Clarion S) We used microarray to analyse the impact of low replication stress on gene expression comparing DMSO or aphidicolin-treated cells at the end of the treatment (t0) and in daughter cells released from the replication stress (N+1).
2021-05-19 | GSE156521 | GEO
Project description:Target genes regulated by ox-LDL treatment in bladder cancer cells T24 were identified by microarrays. In this dataset, we include the expression data obtained from bladder cancer cells T24 starved with serum-free medium and then treated with 20 μg/mL ox-LDL or vehicle for 24 h. These data are used to obtain genes that are differentially expressed in response to ox-LDL treatment.
2022-02-18 | GSE134530 | GEO
Project description:Although the mechanisms underlying development of atherosclerosis are not well understood, LDL-C is known to influence expression of endothelial microRNAs (miRNAs) and gene-targets of miRNAs to promote cell senescence. However, the impact of LDL-C on expression of PBMC miRNAs and miRNA targeted genes in response to an atherogenic diet is not known. We hypothesized that miRNA expression profiles differ between baboons with low and high serum low-density lipoprotein cholesterol (LDL-C) concentrations in response to diet, and that microRNA-gene networks in baboons discordant for LDL-Cholesterol We generated small RNA libraries from baboons differing in their LDL-C response to dietary fat and cholesterol (low LDL-C, n = 3; high LDL-C, n = 3) using liver biopsies collected before and after a high-cholesterol, high-fat (HCHF) challenge diet. We sequenced the libraries using Next-Generation Illumina sequencing methods, analyzed the data using mirTools software and identified 517 baboon miRNAs: 490 homologous to human and 27 novel miRNAs. HCHF diet elicited expression of more miRNAs compared to baseline (chow) diet for both low and high LDL-C baboons. Seventeen miRNAs exhibited significant differential expression in response to HCHF diet in high LDL-C baboons compared to nine miRNAs in low LDL-C baboons. Putative miRNA targets were identified with TargetScan/Base tools. miRNAs significantly targeted more genes in high LDL-C baboons compared to low LDL-C responders. Further, we identified miRNA isomers and other non-coding RNAs that were differentially expressed in response to the challenge diet.Our discovery of differentially expressed baboon miRNAs and their targets is a fundamental step in understanding the role of non-coding RNAs in the modulation of dsylipidemia.
2019-03-20 | GSE114722 | GEO