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Retinoic acid enhances HIV-1 reverse transcription and transcription in macrophages via mTOR-modulated mechanisms

ABSTRACT: Retinoic acid enhances HIV-1 reverse transcription and transcription in macrophages via mTOR-modulated mechanisms

PROVIDER: PRJNA941056 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23701903_1.fastq.gz	Fastqsanger.gz
	SRR23701903_2.fastq.gz	Fastqsanger.gz
	SRR23701904_1.fastq.gz	Fastqsanger.gz
	SRR23701904_2.fastq.gz	Fastqsanger.gz
	SRR23701905_1.fastq.gz	Fastqsanger.gz

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Retinoic acid enhances HIV-1 reverse transcription and transcription in macrophages via mTOR-modulated mechanisms

Project description:The intestinal environment facilitates HIV-1 infection via mechanisms involving the gut-homing vitamin A-derived retinoic acid (RA), which transcriptionally reprograms CD4+ T cells for increased HIV-1 replication/outgrowth. Consistently, colon-infiltrating CD4+ T cells carry replication-competent viral reservoirs in people with HIV-1 (PWH) receiving antiretroviral therapy (ART). Intriguingly, integrative infection in colon macrophages, a pool replenished by monocytes, represents a rare event in ART-treated PWH, thus questioning the effect of RA on macrophages. Here, we demonstrate that RA enhances R5 but not X4 HIV-1 replication in monocyte-derived macrophages (MDMs). RNA sequencing, gene set variation analysis, and HIV interactor NCBI database interrogation reveal RA-mediated transcriptional reprogramming associated with metabolic/inflammatory processes and HIV-1 resistance/dependency factors. Functional validations uncover post-entry mechanisms of RA action including SAMHD1-modulated reverse transcription and CDK9/RNA polymerase II (RNAPII)-dependent transcription under the control of mammalian target of rapamycin (mTOR). These results support a model in which macrophages residing in the intestine of ART-untreated PWH contribute to viral replication/dissemination in an mTOR-sensitive manner.

2023-12-31 | GSE226653 | GEO

Retinoic acid enhances HIV-1 reverse transcription and transcription in macrophages via mTOR-modulated mechanisms.

| S-EPMC11341200 | biostudies-literature

Reverse transcription comparison

Project description:Commercially available reverse transcription enzyme and temperature comparison in high throughput sequencing of bacterial ribosomal 16S rRNA.

| PRJEB32237 | ENA

Comparative study of a mTOR inhibitor, a pan-PI3K inhibitor and a dual PI3K/mTOR inhibitor in MCL

Project description:Phosphatidylinositol-3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway activation contributes to mantle cell lymphoma (MCL) pathogenesis and drug resistance. However, the use of mTOR inhibitors as single agents have shown limited clinical efficacy in relation with drug activation of feedback loops. Selective PI3K inhibition or dual PI3K/mTOR catalytic inhibition are different therapeutic approaches developed to achieve effective pathway blockage. Here, we evaluated the antitumor activity of a mTOR inhibitor, a pan-PI3K inhibitor and a dual PI3K/mTOR inhibitor in primary MCL cells. We found that dual PI3K/mTOR inhibitor modulated angiogenesis, tumor invasiveness and cytokine signaling compared to a mTOR inhibitor and a pan-PI3K inhibitor in MCL. We used microarrays to compare the effect of these three compounds in MCL and identified distinct classes of down-regulated genes modulated by each compound. Global RNA expression in primary cells from two MCL patients treated with a mTOR inhibitor, a pan-PI3K inhibitor and a dual PI3K/mTOR inhibitor for 8 hours

2013-12-14 | E-GEOD-53309 | biostudies-arrayexpress

mTOR

Project description:mTOR

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Comparative study of a mTOR inhibitor, a pan-PI3K inhibitor and a dual PI3K/mTOR inhibitor in MCL

2013-12-14 | GSE53309 | GEO

Anomalous reverse transcription through chemical modifications in polyadenosine stretches

Project description:Anomalous reverse transcription through chemical modifications in polyadenosine stretches

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The alarmin S100A9 hampers retroviral infection by limiting reverse transcription

Project description:The alarmin S100A9 hampers retroviral infection by limiting reverse transcription

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Impact of post-lysis stopping point prior to reverse transcription

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Notoginsenoside R1 regulates ischemic myocardial lipid metabolism through activating AKT/mTOR signaling pathway

Project description:Radix notoginseng is widely used to treat ischemic heart disease in China and other Asian countries, and notoginsenoside R1 (NGR1) is its characteristic and large-amount ingredient. However, the potential molecular mechanisms of NGR1 improving ischemic heart diseases are unclear. Our results revealed that NGR1 improved the echocardiographic, tissue pathological and serum biochemical perturbations in myocardial ischemic rats. The network pharmacology studies indicated that NGR1 mainly regulated smooth muscle cell proliferation, vasculature development and lipid metabolism signaling, especially PI3K/AKT pathway. The myocardial proteomics revealed that the function of NGR1 was focused on regulating metabolic progresses and energy supply processes. The combining research of reverse-docked targets and differential proteins demonstrated that NGR1 modulated lipid metabolism in ischemic myocardial and mTOR and AKT were key targets. Conventional MD simulation was adopted to investigate the interference effect of NGR1 on the structure stabilization of mTOR and AKT complex. The results suggested that NGR1 can strengthen the affinity stabilization of mTOR and AKT.

2022-08-12 | PXD032814 | Pride

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