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Mecp2 fine-tunes quiescence exit by targeting nuclear receptors [RNA-Seq]

ABSTRACT: Mecp2 fine-tunes quiescence exit by targeting nuclear receptors [RNA-Seq]

PROVIDER: PRJNA946719 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23920360_1.fastq.gz	Fastqsanger.gz
	SRR23920360_2.fastq.gz	Fastqsanger.gz
	SRR23920361_1.fastq.gz	Fastqsanger.gz
	SRR23920361_2.fastq.gz	Fastqsanger.gz
	SRR23920362_1.fastq.gz	Fastqsanger.gz

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Mecp2 fine-tunes quiescence exit by targeting nuclear receptors

Project description:Mecp2 fine-tunes quiescence exit by targeting nuclear receptors

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Mecp2 fine-tunes quiescence exit by targeting nuclear receptors [ChIP-Seq]

Project description:Mecp2 fine-tunes quiescence exit by targeting nuclear receptors [ChIP-Seq]

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Mecp2 fine-tunes quiescence exit by targeting nuclear receptors [ChIP-Seq]

Project description:To identify the Mecp2-dependent transcriptome genome-wide during the very early stage of liver regeneration, we mapped the binding landscape of Mecp2 in control and MeCP2-KO livers before and after PHx using ChIP-seq. we mapped the binding landscape of Mecp2 in control livers before and after PHx by filtering out peaks identified in Mecp2-cKO livers. we identified a total of 14640 and 15350 Mecp2-binding genes before and after PHx in the Mecp2 control liver, respectively.

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Mecp2 fine-tunes quiescence exit by targeting nuclear receptors [RNA-Seq]

Project description:To identify the MeCP2 targets gene during the very early stage of liver regeneration，ChIP-seq analyses in control and Mecp2-cKO mice livers before and 6 h after PHx were performed. We found 3048 Mecp2-dependent genes that were differentially expressed in a Mecp2-dependent manner.

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Mecp2 fine-tunes quiescence exit by targeting nuclear receptors

Project description:This SuperSeries is composed of the SubSeries listed below.

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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

Riboproteome remodelling during quiescence exit in Saccharomyces cerevisiae

Project description:Characterization of the riboproteome composition in quiescent cells and post-translational reactivation. To characterize ribosome heterogeneity during the exit from quiescence, the protein composition of ribosomal particles from stationary phase and nutrient-stimulated cells was assessed. A label-free quantitative mass spectrometry strategy was taken to compare quiescent yeast cells with cells that had been nutrient stimulated for 30 and 60 min. To this end, crude extracts from these cells were subjected to sucrose gradient centrifugation and three fractions free (F); monosome (M=80S + 60S + 40S) and polysome (P) were analyzed by nano-HPLC-MS/MS. A total of 528 proteins were identified.

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p110α of PI3K is Indispensable for Quiescence Exit in Adult Muscle Satellite Cells

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LRIG1 is a gatekeeper to exit from quiescence in adult neural stem cells

Project description:Adult neural stem cells (NSCs) must tightly regulate quiescence and proliferation. Single cell analysis has suggested a continuum of cell states as NSCs exit quiescence. Here we capture and characterize in vitro primed quiescent NSCs and identify LRIG1 as an important regulator. We show that BMP-4 signaling induces a dormant non-cycling quiescent state (d-qNSCs), whereas combined BMP-4/FGF-2 signalling induces a distinct primed quiescent state poised for cell cycle re-entry. Primed quiescent NSCs (p-qNSCs) are defined by high levels of LRIG1 and CD9, as well as an interferon response signature, and can efficiently engraft into the adult subventricular zone (SVZ) niche. Genetic disruption of Lrig1 in vivo within the SVZ NSCs leads an enhanced proliferation. Mechanistically, LRIG1 primes quiescent NSCs for cell cycle re-entry and EGFR responsiveness by enabling EGFR protein levels to increase but limiting signaling activation. LRIG1 is therefore an important functional regulator of NSC exit from quiescence.

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

2014-01-27 | GSE51668 | GEO