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Specific modulation of HIV RNA splicing and upregulation of anti-inflammatory miR-124 by the new drug candidate ABX464

ABSTRACT: Specific modulation of HIV RNA splicing and upregulation of anti-inflammatory miR-124 by the new drug candidate ABX464

PROVIDER: PRJNA476952 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7405120.fastq.gz	Fastqsanger.gz
	SRR7405130.fastq.gz	Fastqsanger.gz
	SRR7405140.fastq.gz	Fastqsanger.gz
	SRR7405121.fastq.gz	Fastqsanger.gz
	SRR7405131.fastq.gz	Fastqsanger.gz

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Specific modulation of HIV RNA splicing and upregulation of anti-inflammatory miR-124 by the new drug candidate ABX464

Project description:Purpose: To ensure that ABX464 acted specifically on HIV splicing and did not significantly or globally affect the splicing events of human genes, we used a high-throughput RNAseq approach. Many genome-wide expression studies of HIV infection are based on analyses of total peripheral blood mononuclear cells (PBMCs), which consist of over a dozen cell subsets, including T cells, B cells, NK cells and monocytes Methods: The CD4 T cells were uninfected or infected with the YU2 strain and were untreated or treated for 6 days with ABX464, followed by high-throughput RNAseq. Each raw dataset of the samples contained between 44 and 105 million single-end reads (50 bp), with an average of approximately 60 million raw reads per sample Results: Approximately 98% of the total raw reads were mapped to the human genome sequence (GRCh38), giving an average of 60 million human reads per sample for further analyses. The reads that were correctly mapped (approximately 98% of total input reads) to the gene and transcript locations (GTF annotation file) Conclusions: The MDS of our gene expression data showed, without any outliers, that the different donors segregated well and distributed into the DMSO (untreated) and ABX464 treatments that were infected or uninfected. The displayed variance was donor-dependent (clustered by donor) but treatment-independent (no data structure related to the different treatments), which suggests that the ABX464 molecule did not induce a major difference in CD4 T cell gene expression.

2018-06-22 | GSE116073 | GEO

miR-124 transfection time course

Project description:This time course analysis is to study the targets and functions of miR-124. MiR-124 was overexpressed and the effect of miR-124 overexpression was compared to negative controls to identify downregulated genes and potential miRNA targets. Keywords: time course

2006-11-03 | GSE6207 | GEO

An Imaging Agent (I-124 M5A) in Detecting CEA-Positive Liver Metastases in Patients With Colorectal Cancer

Project description:This phase I trial studies how well an imaging agent called I-124 M5A works in detecting CEA-positive colorectal cancer that has spread to the liver. I-124 M5A is a monoclonal antibody, called M5A, linked to a radioactive substance called I-124. M5A binds to CEA-positive cancer cells and may, through imaging scans, be able to detect liver metastases by picking up signals from I-124.

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miR-124 acts through coREST to control the onset of Sema3A sensitivity in navigating retinal growth cones

Project description:During axon pathfinding, growth cones commonly exhibit changes in sensitivity to guidance cues that follow a strict timetable, even in the absence of pathway feedback, implicating cell-intrinsic regulation. Cellular timer mechanisms, however, are poorly understood. Here we have investigated microRNAs in the timing control of Sema3A sensitivity in retinal ganglion cell (RGC) growth cones. A developmental profiling screen identified miR-124 as a candidate timer. Loss of miR-124 delayed the onset of Sema3A sensitivity and concomitant Neuropilin-1 (NRP-1) receptor expression, and caused cell autonomous pathfinding errors. CoREST, a cofactor of a NRP1 repressor, was identified as a novel target and mediator of miR-124 for this highly specific temporal aspect of RGC growth cone responsiveness. Our findings indicate that miR-124 plays an important role in regulating the intrinsic temporal changes in RGC growth cone sensitivity and suggest that microRNAs may play a broad role as linear timers in vertebrate neuronal development.

2011-12-12 | GSE33444 | GEO

Transcription profiling of human HepG2 cell line overexpressing miR-124 sampled at multiple times points to study the targets and functions of miR-124

2007-11-01 | E-GEOD-6207 | biostudies-arrayexpress

Proteomic profile of human CHME3 microglia in response to the miR-124-3p modulation in Swedish neuronal cells

Project description:We aim to evaluate how the levels of miR-124 in APPSwedish neuronal change the signature of interferon-gamma-stimulated human microglia, in a co-culture system. We want to fing possible pathways involved in cell-to-cell signaling and traficking, as well as inflammation-associated and miRNA targets in microglia, with potential interest to be further explored in Alzheimer's disease field.

2022-06-02 | PXD030315 | Pride

miR-124 acts through coREST to control the onset of Sema3A sensitivity in navigating retinal growth cones

2011-12-12 | E-GEOD-33444 | biostudies-arrayexpress

miR-124 coordinates metabolic regulators acting at early stages of human neurogenesis

Project description:Metabolic dysregulation of neurons is associated with diverse human brain disorders. Metabolic reprogramming occurs during neuronal differentiation, but it is not fully understood which molecules regulate metabolic changes at the early stages of neurogenesis. In this study, we report that miR-124 is a driver of metabolic change at the initiating stage of human neurogenesis. Proteome analysis has shown the oxidative phosphorylation pathway to be the most significantly altered among the differentially expressed proteins (DEPs) in the immature neurons after the knockdown of miR-124. In agreement with these proteomics results, miR-124-depleted neurons display mitochondrial dysfunctions, such as decreased mitochondrial membrane potential and cellular respiration. Moreover, morphological analyses of mitochondria in early differentiated neurons after miR-124 knockdown result in smaller and less mature shapes. Lastly, we show the potential of identified DEPs as novel metabolic regulators in early neuronal development by validating the effects of GSTK1 on cellular respiration. GSTK1, which is upregulated most significantly in miR-124 knockdown neurons, reduces the oxygen consumption rate of neural cells. Collectively, our data highlight the roles of miR-124 in coordinating metabolic maturation at the early stages of neurogenesis and provide insights into potential metabolic regulators associated with human brain disorders characterised by metabolic dysfunctions.

2024-10-13 | PXD042371 | Pride

The microRNA miR-124 controls gene expression in the sensory nervous system of Caenorhabditis elegans

Project description:We generated animals carrying a genomically integrated mir-124 promoter::gfp transgene and identified mir-124 promoter::GFP labelled cells as a subset of the C. elegans sensory neurons. We used fluorescence activated cell sorting (FACS) to isolate four distinct cell populations: mir-124 expressing (GFP+) and non-expressing (GFP-) cells from both wild-type and mutant animals. RNA samples obtained from the four cell populations were used for Affymetrix gene expression analysis to study the effect of mir-124 deletion on the transcriptome of mir-124 expressing (GFP+) and non-expressing (GFP-) cells.

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The microRNA miR-124 controls gene expression in the sensory nervous system of Caenorhabditis elegans

2010-03-22 | E-GEOD-16050 | biostudies-arrayexpress