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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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ChIP-chip from KG-1 cells with HIV Tat

ABSTRACT: 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. comparison of KG-1 cells expressing tTA control vs Tat or mutant TatSF2G48R57A

ORGANISM(S): Homo sapiens

SUBMITTER: NAYOUNG KIM

PROVIDER: E-GEOD-42191 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Tat engagement of p38 MAP kinase and IRF7 pathways leads to activation of interferon-stimulated genes in antigen-presenting cells.

Kim Nayoung N Kukkonen Sami S Martinez-Viedma Maria Del Pilar Mdel P Gupta Sumeet S Aldovini Anna A

Blood 20130327 20

As a result of its interaction with transcription factors, HIV type 1 (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 (IFN)-stimulated genes (ISGs) in the absence of IFNs. We investigated the genome-wide Tat association with promoters in immature dendritic cells and in monocyte-derived macrophages. Among others, Tat associated with the MAP2K6, MAP2K3, and IRF7 promoters that are functionally ...[more]

PMID: 23535064

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Expression data from human antigen presenting cells expressing HIV-1 Tat alleles and mutants

Project description:HIV-1 Tat induces the expression of interferon (IFN)-inducible genes in immature dendritic cells (iDC) in the absence of IFN production. We evaluated how three alleles of Tat and some Tat mutants differ in cellular gene modulation and whether a similar gene induction pattern could be detected by treating cells with IFNM-bM-^@M-^Ys. The three alleles and mutants, with the exception of mutants TatSF21-47 and TatSF2G48-R57A that do not localize in the nucleous, modulated to different degrees IFN-inducible genes without concomitant induction of IFNM-bM-^@M-^Ys. The first exon TatSF21-72 and the minimal transactivator TatSF21-58, all induced genes to a significantly greater extent than full-length Tat. The 2nd exon appears to diminish the gene modulation that can be observed when the first exon alone is expressed. To investigate what domain of Tat are critical to the host-pathogen interactions that are Tat-dependent during HIV infection, we evaluated a variety of Tat-mutants and found that in antigen presenting cells, blood-derived myeloid iDC and macrophages, the second exon of Tat reduces innate immunological responses which are maximal when a Single exon Tat is expressed. 1X10e6 macrophages were infected with HIVBal (20 ng of p24/ 106 cells) for 10 days and with adenoviruses expressing TatHXB2 or LacZ control (5 pfu per cell). Cells infected with Ad-Tat or Ad-LacZ were collected at 24 hours and cells infected with HIV or treated with medium were harvested at 7d and 10d post-infection. THP-Mac were infected with Ad-Tat or Ad-tTA control for 24 hours. RNA was isolated and mRNA expression levels were analyzed by microarrays. adenovirus expressing HIV Tat for 30 hours. and then RNA was isolated, labeled, and prepared for hybridization on Affymetrix microarrays.

2013-06-01 | E-GEOD-42925 | biostudies-arrayexpress

Genome-wide recruitment profile of Tat protein on cellular genes in HIV-1 infected T-cells

Project description:HIV-1 Tat is a multifunctional protein, that in addition to its primary function of transactivating viral transcription also tends to modulate cellular gene expression, the molecular mechanism of which remains to be clearly elucidated. We have reported earlier NFÎºB enhancer binding activity of Tat and proposed its potential role in regulation of cellular gene expression. In the present study, we have analysed genome wide occupancy of Tat protein in HIV-1 infected cells. Our results identify an entire spectrum of binding sites of Tat protein on chromatin and also reveal that Tat is recruited majorly on gene promoters indicating its possible involvement in the regulation of cellular gene expression. Agilent two-color ChIP-on-Chip experiment, Organism: Homo sapiens ,Genotypic Technology designed Custom Human Promoter 244k ChIP-on-chip Array (AMADID-019469)

2014-12-15 | E-GEOD-37183 | biostudies-arrayexpress

Tat controls RNA Polymerase II and the epigenetic landscape to precisely rewire cellular transcriptional programs (ChIP-Seq)

Project description:Transcription factors mediate precise regulation of gene expression programs to modulate key biological processes. In addition to controlling HIV transcription, Tat appears to modulate cellular transcription to alter the biology of target immune cells and generate a permissive state for HIV infection. However, the molecular mechanisms of transcriptional control have remained elusive. Here, we identified the direct target genes of Tat using genomics and defined mechanisms by which Tat selectively rewires cellular transcriptional programs. Interestingly, Tat functions as both transcriptional activator and repressor of a defined set of genes sharing functional annotations and regulated by master transcriptional regulators such as T-cell identity factors. Tat is recruited to precise genomic domains (promoters and intragenic enhancers) through interaction with master transcriptional regulators to control both the transcription initiation and elongation steps. Tat mediates transcription initiation by modulating Pol II recruitment to promoters and intragenic enhancers and fine-tuning chromatin looping. Tat stimulates or blocks RNA Polymerase (Pol) II recruitment or promoter-proximal pause release thereby promoting gene activation or repression, respectively. Global analysis of chromatin signatures revealed correlation of transcription activity marks with Pol II recruitment or pause release status at gene promoters and enhancers, and transcription elongation at coding units. We propose that Tat has evolved these unique properties to hijack precise genomic domains to control cellular transcription using unexpected regulatory mechanisms, which showed marked differences to the regulation of the HIV genome. Our studies also reveal that Tat can be used as a molecular probe to decode general principles of transcriptional regulation. ChIP of various DNA binding proteins

2015-06-15 | E-GEOD-65687 | biostudies-arrayexpress

Human Immunodeficiency Virus Tat Directly Interacts with a Specific Set of Cellular RNAs

Project description:We have used RNA immunoprecipitation to identify the set of mRNAs that HIV-1 Tat interacts with in T-cells. We have also performed measurements of relative RNA abundance to determine if Tat binding is associated with an increase in RNA abundance in Tat-expressing T-cells and during HIV infection of primary T-cells. We have also used RNA IP and ChIP-Chip to compare the RNAs with which Tat interacts with to the RNAs that RISC interacts with and the genes associated with pTEF-b.

2013-11-05 | E-MEXP-3199 | biostudies-arrayexpress

ChIP-chip analysis for H-NS binding sites in wild type and hhaydgT cells

Project description:Analysis of the distribution of the binding regions of the H-NS protein in E. coli W3110 and W3110hhaydgT mutant cells.

2013-04-04 | E-MEXP-3812 | biostudies-arrayexpress

ChIP-seq analysis of H3K9me3 levels across the genome for one copy of H3K9M mutant in pombe

Project description:We performed ChIP-seq analyses for WT, H3K9M mutant and clr4 mutant in Schizosaccharomyces pombe, and showed that H3K9me3 level was reduced to background levels across the entire genome, similar to clr4 mutant.

2016-10-03 | E-MTAB-4776 | biostudies-arrayexpress

Lhx2 ChIP-chip from primary mouse keratinocytes

Project description:The Lhx2 transcription factor plays essential roles in morphogenesis and patterning of ectodermal derivatives, as well as in controlling stem cell activity. Lhx2 is expressed in the hair follicle (HF) buds, while in postnatal telogen HFs Lhx2+ cells reside in the stem cell-enriched epithelial compartments (bulge, secondary hair germ) and co-express selected stem cell markers (Sox9, Tcf4 and Lgr5). Lhx2+ cells represent the vast majority of cells in the bulge and secondary hair germ that proliferate in response to skin injury. This is functionally important, since the wound re-epithelialization is significantly retarded in heterozygous Lhx2 knockout (+/-) mice, while anagen onset in the HFs located closely to the wound is accelerated compared to wild-type mice. Cell proliferation in the bulge and the number of Sox9+ and Tcf4+ cells in the HFs closely adjacent to the wound in Lhx2+/- mice are decreased in comparison to wild-type controls, while expression of Lgr5 and cell proliferation in the secondary hair germ are increased. Furthermore, acceleration of wound-induced anagen development in Lhx2+/- mice is inhibited by administration of Lgr5 siRNA. In addition, Chip-on-chip/ChIP-qPCR and reporter assay analyses reveal Sox9, Tcf4 and Lgr5 as direct Lhx2 targets in keratinocytes. These data strongly suggest that Lhx2 positively regulates Sox9 and Tcf4 in the bulge cells and promotes wound re-epithelization, while it simultaneously negatively regulates Lgr5 in the secondary hair germ and inhibits HF cycling. Thus, Lhx2 operates as a regulator of epithelial stem cell activity during skin response to injury. Chromatin form primary mouse keratinocytes (PMK) was subjected to ChIP analysis with Lhx2 antibody; input and ChIP DNA were labelled with Cy3 and Cy5 respectivly and used form Nimblegen MM8 Mouse Promoter Array

2011-10-03 | E-GEOD-32514 | biostudies-arrayexpress

ChIP-on-chip with anti-RBPj antibody from embryonic AGM E11.5

Project description:Hematopoietic Stem Cells (HSC) are originated during embryonic development from endothelial-like cells located in the ventral side of the dorsal aorta around day E10-12 of murine development. This region is called AGM for Aorta/Gonad/Mesonephros refering to the tissues around the hemogenic aorta. Hematopoiesis depends on the Notch pathway and the identification of Notch-targets is important for the understanding of blood origin. Hematopoietic Stem Cells (HSCs) specification occurs in the embryonic aorta and requires Notch activation, however which are the elements regulated by Notch that control this process are mainly unknown. Here, we took a genome-wide approach to identify putative direct Notch targets by precipitating the chromatin that binds to the Notch partner RBPj in the Aorta-Gonad-Mesonephros (AGM) tissue from E11.5 mouse embryos. This assay revealed 701 gene promoter regions as candidates to be regulated by Notch in the AGM. Chromatin was obtained from a pool of 40 dissected AGMs at E11.5. Chromatin immunoprecipitation (ChIP) was performed as previously described (Aguilera et al, PNAS 2004) with minor modifications. In brief, cross-linked chromatin was sonicated for 10 minutes, medium-power, 0.5-interval; with a Bioruptor (Diagenode) and precipitated with anti-RBPJ (Chu and Bresnick, 2004). After crosslinkage reversal, DNA was used as a template for PCR or for array hybridization. Mouse promoter chip on chip microarray SET (Agilent) was used to identify RBPj targets. It covers 70,000 best identified gene regions with a-5.5 kb to + 2.5 kb range, and has on average 25 probes per gene with an average probe to probe distance of 200 bp. The ChIP-on-chip was performed with dye swaps and one IgG control was brought along. Enrichment analysis was done by comparing the precipitation normalized dye swap signal with input control signal.

2014-10-22 | E-GEOD-52094 | biostudies-arrayexpress

Genome wide screen reveals WNT11, a noncanonical WNT gene, as a target of ETS transcription factor ERG

Project description:ERG is a transcription factor that is involved in leukomogenesis and its mRNA overexpression has been associated with poor prognosis in a subset of patients with T-cell acute lymphoblastic leukemia (T-ALL) and acute myeloid leukemia (AML). Herein, a genome-wide screen of ERG target genes was conducted by chromatin immunoprecipitation-on-chip (ChIP-chip) in Jurkat cells. 342 significant annotated regions were derived from ChIP-chip experiments. Seventeen candidate promoter regions resulted in at least two-fold enrichment by quantitative PCR. Notably, ERG potential targets included WNT signaling genes: WNT2, WNT9A, WNT11, CCND1, and FZD7. Functionally, expression of WNT11 was downregulated with siRNA ERG knockdown and substantially upregulated in a tet-on ERG-inducible assay in K562 cells. To investigate a role for ERG in WNT signaling, a WNT agonist was used to inhibit glycogen synthase kinase (GSK-3). This treatment resulted in an ERG-dependent proliferative growth advantage in the tet-on ERG-inducible system. Lastly, chromatin immunoprecipitation assays of primary leukemia blasts confirmed WNT11 promoter enrichment dependent on ERG mRNA expression. In conclusion, ERG transcriptional networks in leukemia are revealed. Specifically, WNT11 emerged as a target of ERG. We propose that overexpression of ERG in acute leukemia may lead to a proliferative advantage upon activation of WNT signals. ChIP-chip with ERG antibody C20 and combined C17/20 and nonspecificic IgG in Jurkat

2010-12-10 | E-GEOD-21495 | biostudies-arrayexpress

A Unifying Model for Molecular Determinants of the Pre-selection VÎ² Repertoire [ChIP-chip]

Project description:Chip-chip from pro-T(DN) cells from Rag1KO mice for H3K27ac, P300 and FAIRE The primary antigen receptor repertoire is sculpted by the process of V(D)J recombination, which must strike a balance between diversification and favoring gene segments with specialized functions. The precise determinants of how often gene segments are chosen to complete variable region coding exons remain elusive. We have quantified VÎ² usage in the pre-selection Tcrb repertoire and report relative contributions of 14 distinct features in shaping their recombination efficiencies, including transcription, chromatin environment, spatial proximity to their DÎ²JÎ² targets, and quality of recombinase recognition elements. Computational analyses provide a unifying model, revealing a minimal set of eight parameters that are predictive of VÎ²usage, dominated by chromatin modifications associated with transcription, but largely independent of the precise spatial proximity to DÎ²JÎ²clusters. Rag1KO DN epigenetic landscape at Tcrb

2013-08-14 | E-GEOD-42851 | biostudies-arrayexpress

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