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U1 cells stimulated with the TLR8 agonist 3M-002 at 10 microM show a prominent activation of TLR-dependent genes as assessed by "Human toll-like Receptor PCR array pathway" over time

ABSTRACT: We investigated the effects of the TLR8 agonist 3M-002 on latently HIV infected U1 cells. We found a prominent upregulation of TLR-dependent genes. Notably, the TLR8 agonist resulted in a marked activation of HIV.

ORGANISM(S): Homo sapiens

PROVIDER: GSE26469 | GEO | 2011/01/11

SECONDARY ACCESSION(S): PRJNA136541

REPOSITORIES: GEO

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U1 cells stimulated with the TLR8 agonist 3M-002 at 10 microM show a prominent activation of TLR-dependent genes as assessed by "Human toll-like Receptor PCR array pathway" over time

Project description:We investigated the effects of the TLR8 agonist 3M-002 on latently HIV infected U1 cells. We found a prominent upregulation of TLR-dependent genes. Notably, the TLR8 agonist resulted in a marked activation of HIV. We stimulated U1 cells for 6 or 10 hours with 3M-002 and subsequently harvested the cells, extracted total RNA. RNA was then used for quantifiying TLR-dependent gene upregulation using a commercial PCR array pathway

2011-01-11 | E-GEOD-26469 | biostudies-arrayexpress

Monocyte-derived macrophages stimulated with the TLR8 agonist 3M-002 at 10 microM show a prominent activation of TLR-dependent genes as assessed b "Human Toll-like Receptor PCR array pathway" over time

Project description:We were interested in the effects of TLR8 triggering of human monocyte-derived macrophages. We observed a striking upregulation of those genes. This work was done in the context of examining the effects of TLR8 triggering for the activation of HIV. We generated monocyte-derived macrophages (MDM) by initially isolating monocytes and subsequently culturing them in RPMI supplemented with human AB serum. MDM were stimulated for 18 h with the TLR8 agonist 3M-002, and subsequently harvested for extraction of total RNA. Total RNA was then used to quantify the TLR-dependent genes using a PCR array pathway.

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Project description:This phase Ib trial studies the best way of TLR8 Agonist VTX-2337 and cyclophosphamide in treating patients with a solid tumor that has spread from the primary site (place where it started) to other places in the body (metastatic), progressed for a long time (persistent), come back (recurrent), or is growing, spreading, or getting worse (progressed). TLR8 Agonist VTX-2337 may stimulate the immune system in different ways and stop tumor cells from growing. Drugs used in chemotherapy, such as cyclophosphamide, work in different ways to stop the growth of tumor cells, either by killing the cells, by stopping them from dividing, or by stopping them from spreading. Giving TLR8 Agonist VTX-2337 together with cyclophosphamide may be a better treatment for solid tumors.

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Project description:Setaria viridis strain:NMU.00626. 3m | cultivar:NMU.00626. 3m Genome sequencing

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BET inhibitor UM-002 reduces GBM proliferation and invasion

Project description:Bromodomain and extraterminal domain (BET) proteins have emerged as therapeutic targets in multiple cancers, including the most common primary adult brain tumor glioblastoma (GBM). Although several bet inhibitors have entered clinical trials, few are brain penetrant. We have generated UM-002, a novel brain penetrant BET inhibitor that reduces GBM cell proliferation in vitro and in a human cerebral brain organoid model. Since UM-002 is more potent than other BET inhibitors, it could potentially be developed for GBM treatment. Furthermore, UM-002 treatment reduces the expression of cell-cycle related genes in vivo, and reduces the expression of invasion related genes within the non-proliferative cells present in tumors as measured by single cell RNAsequencing. These studies suggest that BET inhibition alters the transcriptional landscape of GBM tumors, which has implications for designing combination therapies. Importantly, they also provide an integrated dataset that combines in vitro and ex vivo studies with in vivo single-cell RNA-sequencing to characterize a novel BET inhibitor in GBM.

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Reversal of human regulatory T cell suppression throgh TLR8 signaling

Project description:Analyses of gene alterations of human Treg cells treated with or without TLR8 ligand using the Illumina whole-genome Human HT-12 BeadChips. The study will provide important information for the molecular signature changes during the reversal of human Treg suppression mediated by activation of TLR8 signaling.

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Project description:BP-002

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