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RNA-seq analysis of the effect of loss of Tp53, NF1 or CBS in telomerase-reverse transcriptase (TERT)-immortalized human BJ fibroblasts (BJ-TERT) overexpressing myristoylated AKT1

ABSTRACT: RNA-seq analysis of the effect of loss of Tp53, NF1 or CBS in telomerase-reverse transcriptase (TERT)-immortalized human BJ fibroblasts (BJ-TERT) overexpressing myristoylated AKT1

PROVIDER: PRJNA824798 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18685611.fastq.gz	Fastqsanger.gz
	SRR18685612.fastq.gz	Fastqsanger.gz
	SRR18685613.fastq.gz	Fastqsanger.gz
	SRR18685614.fastq.gz	Fastqsanger.gz
	SRR18685615.fastq.gz	Fastqsanger.gz

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RNA-seq analysis of the effect of loss of Tp53, NF1 or CBS in telomerase-reverse transcriptase (TERT)-immortalized human BJ fibroblasts (BJ-TERT) overexpressing myristoylated AKT1

Project description:Overexpression myristoylated AKT1 in human BJ-TERT fibroblasts induces senescence (AIS). We depleted CBS, Tp53 or NF1 gene by shRNA in AIS cells and performed RNA-seq analysis to investigate the regulatory effect of these genes in AIS maintenance.

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Comparative gene expression profiling of telomerase-reverse transcriptase (TERT)-immortalised BJ fibroblasts and those with overexpression of myristoylated AKT1 (myrAKT1)

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Evolutionarily conserved role of Telomerase reverse transcriptase (TERT) in programming the microenvironment via regulation of cGAS/STING pathway

Project description:Telomerase holoenzyme plays a critical role in maintaining telomere length, and thus in regulating inflammation caused by telomeric DNA damage. However, beyond its role in telomere maintenance, the molecular function of telomerase in directly regulating inflammation remains unclear. Here, we show that the reverse transcriptase component of telomerase, TERT, has a cell-type-specific role in directly regulating inflammation via the cytoplasmic cGAS-STING nucleic acid-sensing pathway. Analyses of murine and zebrafish models of gut inflammation and human colitis/Crohn’s patients document that this function of TERT is evolutionarily conserved. Using our novel knock-in TERTVAA mouse model where reverse-transcriptase-inactive TERT is driven by its endogenous loci, and molecular, pharmacological and single-cell approaches we identify the myeloid subpopulation, termed T-MAC, wherein TERT enhances STING activation and initiates type-1 interferon responses independent of reverse transcriptase activity or telomere length. We highlight a hitherto unappreciated role of TERT in directly regulating inflammation and provide a therapeutic rationale for targeting TERT beyond cancers.

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