Differentially expressed mRNA profiles between LPS and LPS + Tat (48-60) YVEEL induced FHC cells.
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PROVIDER: PRJNA886976 | ENA |
REPOSITORIES: ENA
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Project description:To further explore the underlying mechanisms of the protection functions of Tat (48-60) YVEEL, high throughput sequencings were used to identify differentially expressed mRNA profiles between LPS and LPS + Tat (48-60) YVEEL induced FHC cells.
2022-10-06 | GSE214736 | GEO
Project description:RNA sequencing was performed to compare levels of intracellular transcripts in HL-60 WT and HL-60 HAX1 KO cells. Experiment was performed to check influence of HAX1 protein on cellular transcriptome (in HL-60 cell line)
2022-09-21 | GSE189609 | GEO
Project description:Our previous work demonstrated that HIV-1 infection progressively reduces TCR/CD3 expression due to a defect in CD3g gene transcripts. We further found that knocking down expression of the viral tat and/or nef genes was correlated with CD3g transcript and TCR/CD3 surface receptor levels on HIV-1 infected cells. This study was undertaken to investigate the direct effect of HIV-1 Tat expression on the TCR/CD3 machinery. Progressive downregulation from TCR/CD3hi to TCR/CD3lo to TCR/CD3− was observed on Tat expressing cells in a manner that emulated HIV-1 infection, with a lack of CD3g transcripts again responsible for the defect. When Tat cell cultures containing a mixture of TCR/CD3 surface densities were separated into TCR/CD3hi and TCR/CD3lo/− populations, they quickly reverted to a mixed CD3 phenotype. Thus, the progression TCR/CD3hi to TCR/CD3lo to TCR/CD3− is an active, reversible process with receptor levels fluctuating in response to intracellular dynamics. Examination of tat mutants found that the regions involved in Tat-mediated transactivation and TAR binding are required for TCR/CD3 downregulation while the lysine at position 28 and Tat exon 2 are dispensable. Global gene expression, assessed in association with TCR/CD3 downregulation in HIV-1 infected and Tat expressing cells, detected broad suppression of TCR/CD3 signaling, co-stimulation and negative regulatory genes along with target transcription factors, ligands and receptors. A significant subset of the genes altered in HIV-1 infected cells was specifically targeted by Tat in association with TCR/CD3 loss. Our finding that Tat negatively regulates many facets of the TCR/CD3 machinery has important implications for disease pathogenesis. We used microarrays to investigate changes in CD4+ T cell gene expression induced by expression of the HIV-1 Tat protein.
2015-12-31 | GSE33705 | GEO
Project description:Our previous work demonstrated that HIV-1 infection progressively reduces TCR/CD3 expression due to a defect in CD3g gene transcripts. We further found that knocking down expression of the viral tat and/or nef genes was correlated with CD3g transcript and TCR/CD3 surface receptor levels on HIV-1 infected cells. This study was undertaken to investigate the direct effect of HIV-1 Tat expression on the TCR/CD3 machinery. Progressive downregulation from TCR/CD3hi to TCR/CD3lo to TCR/CD3â was observed on Tat expressing cells in a manner that emulated HIV-1 infection, with a lack of CD3g transcripts again responsible for the defect. When Tat cell cultures containing a mixture of TCR/CD3 surface densities were separated into TCR/CD3hi and TCR/CD3lo/â populations, they quickly reverted to a mixed CD3 phenotype. Thus, the progression TCR/CD3hi to TCR/CD3lo to TCR/CD3â is an active, reversible process with receptor levels fluctuating in response to intracellular dynamics. Examination of tat mutants found that the regions involved in Tat-mediated transactivation and TAR binding are required for TCR/CD3 downregulation while the lysine at position 28 and Tat exon 2 are dispensable. Global gene expression, assessed in association with TCR/CD3 downregulation in HIV-1 infected and Tat expressing cells, detected broad suppression of TCR/CD3 signaling, co-stimulation and negative regulatory genes along with target transcription factors, ligands and receptors. A significant subset of the genes altered in HIV-1 infected cells was specifically targeted by Tat in association with TCR/CD3 loss. Our finding that Tat negatively regulates many facets of the TCR/CD3 machinery has important implications for disease pathogenesis. We used microarrays to investigate changes in CD4+ T cell gene expression induced by expression of the HIV-1 Tat protein. Examine changes in gene expression in HIV-1 Tat transduced cells compared with cells transduced with an antisense Tat sequence used as a control.
2015-12-31 | E-GEOD-33705 | biostudies-arrayexpress
Project description:The effect of LPS and LPS+antiCD40 on the Transcriptome of IgD+ B Cells was analysed here at 48 hours after the stimulation B-lymphocytes constitute an important aspect of mammalian immune systems by virtue of their ability to produce highly specific antibodies in response to foreign antigens and pathogens. When B-lymphocytes encounter the particular antigen that they are responsive to, they differentiate into two types of cells: short-lived antibody-secreting plasma cells and long-lived memory cells. While the plasma B cells are responsible for the rapid resolution of a current infection or immune challenge, the memory B cells are responsible for mounting a rapid response to subsequent exposures. Previous work had demonstrated that treatment of mice with a single dose of anti-CD40 at the time of immunization leads to improved secondary responses, suggesting an enhancement of the memory B cell pool. We are currently studying the molecular mechanisms underlying the generation of memory B cells, using CD40 signalling as a tool. We have carried out a Microarray analyses of genome wide gene expression patterns in naïve B-lymphocytes following CD40 signalling, over multiple time points.
2012-12-25 | GSE30170 | GEO
Project description:Molecular mechanisms of anti-cancer activities of BG-P1600-TAT were explored employing genome-wide expression profiling experiments. Human neuroblastoma cell line SK-N-FI and primary cells SKNAS were treated with 30µM of the BG-P1600-TAT for 48 hours, harvested, and total RNA was immediately isolated from three biological replicates of control (vehicle-treated) and BG-P1600-TAT-treated cells. Gene expression profiling experiments identified 14-gene BG-P1600-TAT molecular interference signature captured most biologically important significantly enriched records reflecting the putative molecular mechanisms of anti-cancer activities of the BG-P1600-TAT. In BG-P1600-TAT treated SK-N-FI cells, 753 differentially expressed genes (DEGs) were identified compared to control vehicle-treated cells. Among 753 DEGs, 427 genes were down-regulated and 326 genes were up-regulated. In SKNAS cells, BG-P1600-TAT showed a significant effects on signal transduction pathways activated during cellular responses to IL-1alpha, TNF-alpha, EGF, TGF, PDGF, and AR. Further BG-P1600-TAT also showed a significant effect on multiprotein complexes of potential biological and therapeutic significance, including several complexes engaged during apoptosis (BCL-2 family protein complex; Survivin complex; BAX complex; Caspase complex), angiogenesis (VEGF-A complex; Thrombospondin complex), and cell adhesion (Galectin complex; Integrin alpha/beta complexes).
2021-09-06 | GSE183482 | GEO
Project description:HIV-1 Tat can modulate the expression of both HIV and cellular genes. In antigen-presenting cells Tat induces the expression of a subset of interferon-stimulated genes (ISGs) in the absence of interferons (IFNs). We investigated the genome-wide Tat association with cellular promoters in immature dendritic cells (iDC) and in monocyte derived macrophages (MDM). Chromatin immunoprecipitation (ChIP) of Tat together with chromatin profiling by ChIP-on-chip analysis demonstrated that Tat associates with the MAP2K6 and MAP2K3 promoters and mediates its increase, which also affects the induction of some ISGs.
2013-05-31 | GSE42191 | GEO
Project description:Microarray analysis was carried out on human GBM primary cells (GBM 10181360) and GBM cell line (U87) exposed to P-bi-TAT (10-6 M tetrac equivalent) for 24 h and 48 h. P-bi-TAT significantly downregulated electron transport chain genes ATP5A1 (ATP synthase A1), ATP51, ATP5G2, COX6B1 (cytochrome c oxidase subunit 6B1), NDUFA8 (NADH dehydrogenase [ubiquinone] FA8), NDUFV2 and other NDUF genes, SLC25A6 (solute carrier group 2), UCP2 ([mitochondrial] uncoupling protein 2) and COX5A. The NDUF and ATP genes are also relevant to control of oxidative phosphorylation and transcription. Six additional NDUF genes linked to oxidative phosphorylation were affected. Conclusions. P-bi-TAT caused downregulation of expression of a panel of genes involved in electron transport, oxidative phosphorylation, and cytoplasmic ribosomal protein generation in GBM cells. A key component of the anticancer activity of P-bi-TAT relates to disordering of ATP generation mechanisms in tumor cells
2021-09-11 | GSE183776 | GEO
Project description:Purpose: To investigate the impact of HIV protein Tat on macrophage transcriptome related to atherosclerosis development Methods: Peritoneal macrophages were isolated from myeloid specific IKKβ deficient LDLR-/- (IKKβΔMyeLDLR-/-) mice and their littermates (IKKβF/FLDLR-/-). Then the macrophages were treated with HIV protein Tat or control for 12 hr. Total RNA was extracted for RNAseq Results: HIV protein Tat treatment induces 2640 differentially expressed genes (DEGs) with false discovery rate (FDR) < 1 % and fold change > 3 in control macrophages. Those DEGs enriched in several biological processes that may contribute to atherogenesis. FAIME analysis demonstrated higher geneset scores of those GO terms in the Tat-treated macrophages from IKKβF/FLDLR-/- mice compared with the control ones. IKKβ deletion resulted in loss of geneset score in the macrophages of IKKβΔMyeLDLR-/- treated with HIV Tat. Conclusions: These results indicate that HIV protein Tat may affect many genes in macrophages related atherosclerosis development through IKKβ signaling.
2021-07-21 | GSE157833 | GEO
Project description:Xanthomonas sp. 60 strain:60 Genome sequencing
| PRJNA547317 | ENA