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RNA Seq profiling of transcriptional response in IFNg-primed C57BL6 mouse primary bone marrow derived macrophages exposed to vehicle, compound 2062 and an inactive control analog at 0, 1, 2 and 6 hours post treatment

ABSTRACT: RNA Seq profiling of transcriptional response in IFNg-primed C57BL6 mouse primary bone marrow derived macrophages exposed to vehicle, compound 2062 and an inactive control analog at 0, 1, 2 and 6 hours post treatment

PROVIDER: PRJNA631363 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11743903.fastq.gz	Fastqsanger.gz
	SRR11743904.fastq.gz	Fastqsanger.gz
	SRR11743905.fastq.gz	Fastqsanger.gz
	SRR11743906.fastq.gz	Fastqsanger.gz
	SRR11743907.fastq.gz	Fastqsanger.gz

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RNA Seq profiling of transcriptional response in IFNg-primed C57BL6 mouse primary bone marrow derived macrophages exposed to vehicle, compound 2062 and an inactive control analog at 0, 1, 2 and 6 hours post treatment

Project description:The goals of this study were to probe cellular networks that became engaged upon small molecule 2062 exposure in primary mouse bone marrow macrophages and compare them with the control inactive compound. Compound 2062 activated BMDM to enhance the production of nitric oxide and TNFa and potentiated rifampin activity in a mouse model of tuberculosis. We used biochemical, pharmacologic, transcriptomic and genetic approaches to identify the targets of 2062. RNASeq demonstrated that early changes in the BMDM transcriptome in response to 2062 exposure were consistent with an extensive stress response. INFg-primed BMDM were exposed to vehicle, compound 2062, a TFEB activator, or a close structural analog for 1, 2 or 6 hours. Cells were collected, mRNA isolated and subjected to NGS. Transcriptional response was compared between the timepoints for the vehicle vs active 2062 compound and vehicle vs inactive compound.

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