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Analysis for expression of genes in human leukemic cell line Jurkat treated with Me6TREN or Phosphate Buffered Saline (PBS) control

ABSTRACT: mRNA from cells treated with or without small molecule Me6TREN for 24 hour was analyzed for differential gene expression. The hypothesis tested in the present study was that specific genes were up- or down-regulated via certain signaling pathways. Results provide important information to study the response of cellular functions triggered by Me6TREN. Total RNA obtained from human Jurkat cells subjected to 24 hours in vitro Me6TREN and PBS-treated control cells was amplified and hybridized to Illumina HT12 human whole-genome arrays.

ORGANISM(S): Homo sapiens

SUBMITTER: Jing Zhang

PROVIDER: E-GEOD-51974 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Analysis for expression of genes in human leukemic cell line Jurkat treated with Me6TREN or Phosphate Buffered Saline (PBS) control

Project description:mRNA from cells treated with or without small molecule Me6TREN for 24 hour was analyzed for differential gene expression. The hypothesis tested in the present study was that specific genes were up- or down-regulated via certain signaling pathways. Results provide important information to study the response of cellular functions triggered by Me6TREN.

2013-11-01 | GSE51974 | GEO

Avoid Using Phosphate Buffered Saline (PBS) as an Electrolyte for Accurate OER Studies.

Project description: Not available

| S-EPMC11320652 | biostudies-literature

Expression data from Staphylococcus aureus and Phosphate buffered saline (PBS) treated mouse wound bed

Project description:Environmental factors that enhance regeneration are largely unknown. We hypothesized that skin bacteria modulate regeneration. Here, we assessed low, medium, and high levels of bacterial burden in Wound Induced Hair follicle Neogenesis (WIHN), a rare adult organogenesis model. WIHN levels and stem cell markers indeed correlated with bacterial counts, being lowest in germ free (GF), intermediate in conventional specific pathogen free (SPF), and highest even in mice infected with pathogenic Staphylococcus aureus. We identified IL-1β and keratinocyte-dependent IL-1R-MyD88 signaling as necessary and sufficient for bacteria to promote regeneration. Finally, in a small clinical trial, we found that a topical broad-spectrum antibiotic slowed skin wound healing. These results counter conventional notions that infection inhibits regeneration and the need for full sterility of small wounds.

2021-04-01 | GSE158614 | GEO

TAL1 knock down in Jurkat cells

Project description:We used microarray profiling in Jurkat cells to uncover TAL1 dependent genes in a leukemic context. Clonal Jurkat lines expressing a Doxycycline (Dox) -inducible shRNA against TAL1 coding sequence were generated. A clone in which Dox treatment led to 80% decrease of TAL1 mRNA was chosen.

2010-12-14 | E-GEOD-20544 | biostudies-arrayexpress

Platelet-derived sphingosine 1-phosphate induces migration of Jurkat T cells.

Project description:BACKGROUND: The migration of T cell to atherosclerotic lesions is proposed to be involved in the pathogenesis of the atherosclerosis. Sphingosine 1-phosphate (S1P), a bioactive lysophospholipid released from activated platelets, exerts a variety of responses such as cell migration and proliferation, and reportedly induces T cell migration. Accordingly, platelet-T cell interactions may exist based on T cell responses triggered by platelet-derived S1P. METHODS: S1P was measured using two-step lipid extraction followed by high-performance liquid chromatography (HPLC) separation while other phospholipids were determined by an enzymatic assay. The expression of S1P and lysophosphatidic acid receptors on Jurkat T cells was examined by RT-PCR and flow cytometry. Jurkat cell migration by S1P and the supernatant of activated platelets (SAP) was evaluated by a modified Boyden's chamber assay. RESULTS: S1P1 receptor was confirmed to be expressed on Jurkat T cell by RT-PCR and flow cytometry. S1P at 10-100 nM induced strong Jurkat cell migration, which was inhibited by the S1P1 (and S1P3) antagonist VPC23019 and the Gi inactivator pertussis toxin (PTX). We found that the supernatant (releasate) of human platelets activated by collagen stimulation, which contains S1P abundantly, induced Jurkat cell migration and that the migration was inhibited by VPC23019 and PTX. In addition, human serum, into which platelet contents (including S1P) are fully released, induced the Jurkat cell migration, which was also inhibited by VPC23019. CONCLUSIONS: Our findings suggest that platelet-derived S1P induces Jurkat T cell migration possibly via S1P1. S1P may be a key molecule involved in the responses triggered by platelet-T cell interactions, including atherosclerosis.

| S-EPMC4193286 | biostudies-literature

ArtinM Mediates Murine T Cell Activation and Induces Cell Death in Jurkat Human Leukemic T Cells.

Project description:The recognition of cell surface glycans by lectins may be critical for the innate and adaptive immune responses. ArtinM, a d-mannose-binding lectin from Artocarpus heterophyllus, activates antigen-presenting cells by recognizing TLR2 N-glycans and induces Th1 immunity. We recently demonstrated that ArtinM stimulated CD4? T cells to produce proinflammatory cytokines. Here, we further studied the effects of ArtinM on adaptive immune cells. We showed that ArtinM activates murine CD4? and CD8? T cells, augmenting their positivity for CD25, CD69, and CD95 and showed higher interleukin (IL)-2 and interferon (IFN)-? production. The CD4? T cells exhibited increased T-bet expression in response to ArtinM, and IL-2 production by CD4? and CD8? T cells depended on the recognition of CD3??-chain glycans by ArtinM. The ArtinM effect on aberrantly-glycosylated neoplastic lymphocytes was studied in Jurkat T cells, in which ArtinM induced IL-2, IFN-?, and IL-1? production, but decreased cell viability and growth. A higher frequency of AnnexinV- and propidium iodide-stained cells demonstrated the induction of Jurkat T cells apoptosis by ArtinM, and this apoptotic response was reduced by caspases and protein tyrosine kinase inhibitors. The ArtinM effects on murine T cells corroborated with the immunomodulatory property of lectin, whereas the promotion of Jurkat T cells apoptosis may reflect a potential applicability of ArtinM in novel strategies for treating lymphocytic leukemia.

| S-EPMC5535893 | biostudies-literature

Transcriptome profile of GEN2.2 cell line

Project description:Analysis of expression profile of human GEN2.2 cell line RNA expression profile of the human pDC cell line GEN2.2 Total RNA was isolated from GEN2.2 cells growing at log phase with High Pure RNA isolation Kit (Roche Diagnostics, Mannheim, Germany), according with the manufacturer´s instructions in quintuplicate. A total of 300 ng of total RNA was processed using Illumina TotalPrep RNA Amplification Kit. Hybridization of human samples was performed on Illumina Human-HT12 Version 4.

2014-07-30 | E-GEOD-59887 | biostudies-arrayexpress

Transcription profiling of mouse pre-leukemic stem cells and leukemic stem cells

Project description:The molecular pathways mediating unlimited self-renewal and alleged drug resistant properties that are believed to be key for maintenance and re-initiation of leukemia during relapse are largely unexplored area. To gain further insights into the potential pathways responsible for the conversion and establishment of leukemic stem cells (LSC), we molecularly dissected and compared the cell populations enriched in pre-LSC and LSC. In this model, pre-LSC were identified as early transduced primary cells carrying the initiating event and endowed with the ability to induce leukemia in vivo with a long latency. LSC were defined as leukemic cells harvested from primary mice transplanted with pre-LSC that had then acquired additional events and were capable of inducing leukemia in secondary mice with a very short latency. <br><br>Pre-LSC were generated by transformation of cKit+ purified cells derived from mouse bone marrow with MLL-ENL retrovirus and subjected to several rounds of replating in methylcellulose. A cell line (pre-LSC bulk population) was subsequently generated and injected into mice. Cells derived from a leukemic mouse were used to generate the LSC cell line (LSC bulk population). Pre-LSC and LSC bulk populations and their clonal deriviatives were used in microarray experiments to help identify key events which convert pre-LSC to LSC.

2011-03-12 | E-MEXP-2618 | biostudies-arrayexpress

Gene expression analysis of DBC1 KO B cells

Project description:DBC1 KO B cells were either unstimulated, activated with anti-IgM, anti-CD40 of LPS for 4 hours. Genes differentially expressed in DBC1 KO B cells were compared to WT B cells. RNA was collected from unstimulated for stimulated B cells, and gene expression between WT and DBC1 KO B cells were compared

2014-09-04 | E-GEOD-61029 | biostudies-arrayexpress

Transcription profiling by array of human PMA-activated Jurkat cells

Project description:Cyclin T1-dependent genes in activated Jurkat cells. HIV-1 is dependent upon cellular co-factors to mediate its replication cycle in CD4+ T cells and macrophages, the two major cell types infected by the virus in vivo. One critical co-factor is Cyclin T1, a subunit of a general RNA polymerase II elongation factor known as P-TEFb. Cyclin T1 is targeted directly by the viral Tat protein to activate proviral transcription. Cyclin T1 is up-regulated when resting CD4+ T cells are activated and during macrophage differentiation or activation, conditions that are also necessary for high levels of HIV-1 replication. Because Cyclin T1 is a subunit of a transcription factor, the up-regulation of Cyclin T1 in these cells results in the induction of cellular genes, some of which might be HIV-1 co-factors. Using shRNA depletions of Cyclin T1 and transcriptional profiling, we identified 54 cellular mRNAs that are Cyclin T1-dependent for their induction in activated CD4+ T cells and during macrophage differentiation and activation. The promoters for these Cyclin T1-dependent genes (CTDGs) are over-represented in two transcription factor binding sites, SREBP1 and ARP1. Notably, 10 of these CTDGs have been reported to be involved in HIV-1 replication, a significant over-representation of such genes when compared to randomly generated lists of 54 genes (p value < 0.00021). SiRNA depletions of two CTDGs identified here, CDK11 and Casein kinase1gamma1, suggest that these genes are also involved in HIV-1 replication. It is therefore likely that the 54 CTDGs identified here include novel HIV-1 co-factors. The presence of CTDGs in the protein space that was available for HIV-1 to sample during its evolution and acquisition of Tat function may provide an explanation for why CTDGs are enriched in viral co-factors. Experiment Overall Design: Using shRNA knockdown of cyclin T1, cyclin T1-dependent genes were identified in activated Jurkat cells.

2008-10-20 | E-GEOD-10232 | biostudies-arrayexpress

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