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IyCamRapt

ABSTRACT: Campoletis raptor

PROVIDER: PRJEB56062 | ENA |

REPOSITORIES: ENA

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Dataset's files

Source:

			Action	DRS
		Other
	ERR10297824_1.fastq.gz	Fastqsanger.gz
	ERR10297824_2.fastq.gz	Fastqsanger.gz
	ERR10224930.fastq.gz	Fastqsanger.gz

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Campoletis raptor

Project description:Campoletis raptor overview

| PRJNA922296 | ENA

iyCamRapt1

Project description:Campoletis raptor genome assembly, iyCamRapt1

| PRJEB58800 | ENA

iyCamRapt

Project description:Campoletis raptor, genomic and transcriptomic data

| PRJEB56061 | ENA

iyCamRapt1 alternate haplotype

Project description:Campoletis raptor genome assembly, iyCamRapt1, alternate haplotype

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iyCamRapt1.Wolbachia_sp_1

Project description:Wolbachia endosymbiont (group A) of Campoletis raptor genome assembly, iyCamRapt1.Wolbachia_sp_1

| PRJEB74856 | ENA

Gene-expression changes resulting from loss of the mTORC1 component Raptor in murine hematopoietic stem and progenitor cell-enriched populations (HSPC)

Project description:We investigated the role of mTORC1 in murine hematopoiesis by conditionally deleting the Raptor gene in murine hematopoietic stem cells. We observed mutliple alterations evoked by Raptor loss in hematopoiesis and profiled gene-expression alterations induced by raptor loss in Flt3-Lin-Sca1+cKit+ hematopoietic stem and progenitor enriched cell populations, 5 weeks post Raptor deletion. Flt3-Lin-Sca1+cKit+ cells were flow sorted from mice containing homozygous floxed alleles for exon 6 of the Raptor gene in the presence (MT group) or absence (WT group) of the MxCre transgene, which was induced with injections of mice with pIpC 5 weeks before cell isolation.

2012-09-19 | E-GEOD-32265 | biostudies-arrayexpress

Raptor/mTORC1-dependent metabolic programming of exit from quiescence underlies T cell activation and fate decisions

Project description:Naïve T cells respond to antigen stimulation by exiting from quiescence into clonal expansion and functional differentiation, but the control mechanism is elusive. Here we describe that Raptor/mTORC1-dependent metabolic reprogramming is a central determinant of this transitional process. Loss of Raptor abrogates T cell priming and Th2 cell differentiation, although Raptor function is less important for continuous proliferation of actively cycling cells. mTORC1 coordinates multiple metabolic programs in T cells including glycolysis, lipid synthesis and oxidative phosphorylation to mediate antigen-triggered exit from quiescence. mTORC1 further links glucose metabolism to the initiation of Th2 differentiation by orchestrating cytokine receptor expression and cytokine responsiveness. Activation of Raptor/mTORC1 integrates T cell receptor (TCR) and CD28 co-stimulatory signals in antigen-stimulated T cells. Our studies identify a Raptor/mTORC1-dependent pathway linking signal-dependent metabolic reprogramming to quiescence exit, and this in turn coordinates lymphocyte activation and fate decisions in adaptive immunity. We used microarrays to explore the gene expression profiles differentially expressed in CD4+ T-cells from wild-type (WT) and CD4(cre) x Raptor(fl/fl) mice before and after stimulation with anti CD3/CD28 antibodies.

2014-01-27 | E-GEOD-51668 | biostudies-arrayexpress

Gene-expression changes resulting from loss of the mTORC1 component Raptor in murine hematopoietic stem and progenitor cell-enriched populations (HSPC)

2012-09-19 | GSE32265 | GEO

Raptor/mTORC1-dependent metabolic programming of exit from quiescence underlies T cell activation and fate decisions

2014-01-27 | GSE51668 | GEO

mTORC1 maintains renal tubular homeostasis and is essential in response to ischemic stress

Project description:The mechanistic target of rapamycin mTORC1 is a key regulator of cell metabolism and autophagy. Despite widespread clinical use of mTOR inhibitors, the role of mTORC1 in renal tubular function and kidney homeostasis remains elusive. By utilizing constitutive and inducible deletion of conditional Raptor alleles in renal tubular epithelial cells, we discovered that mTORC1 deficiency caused a marked concentrating defect, loss of tubular cells and slowly progressive renal fibrosis. Transcriptional profiling revealed that mTORC1 maintains renal tubular homeostasis by controlling mitochondrial metabolism and biogenesis as well as transcellular transport processes involved in counter-current multiplication and urine concentration. Although mTORC2 partially compensated the loss of mTORC1, exposure to ischemia and reperfusion injury exaggerated the tubular damage in mTORC1-deficient mice, and caused pronounced apoptosis, diminished proliferation rates and delayed recovery. These findings identify mTORC1 as an essential regulator of tubular energy metabolism and as a crucial component of ischemic stress responses. Pharmacological inhibition of mTORC1 likely affects tubular homeostasis, and may be particularly deleterious if the kidney is exposed to acute injury. Furthermore, the combined inhibition of mTORC1 and mTORC2 may increase the susceptibility to renal damage. Raptor fl/fl*KspCre and Raptor fl/fl animals were sacrificed at P14 before the development of an overt functional phenotype. Kidneys were split in half and immediately snap frozen in liquid nitrogen.

2014-06-09 | E-GEOD-54417 | biostudies-arrayexpress

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