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Neurofibromin (Nf1) controls metabolic balance and Notch-dependent quiescence of murine juvenile myogenic progenitors [ChIP-seq]

ABSTRACT: Neurofibromin (Nf1) controls metabolic balance and Notch-dependent quiescence of murine juvenile myogenic progenitors [ChIP-seq]

PROVIDER: PRJNA667437 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12773618_1.fastq.gz	Fastqsanger.gz
	SRR12773618_2.fastq.gz	Fastqsanger.gz
	SRR12773619_1.fastq.gz	Fastqsanger.gz
	SRR12773619_2.fastq.gz	Fastqsanger.gz
	SRR12773620_1.fastq.gz	Fastqsanger.gz

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Neurofibromin (Nf1) controls metabolic balance and Notch-dependent quiescence of murine juvenile myogenic progenitors [RNA-seq]

Project description:Purpose: To study Nf1 regulated pathways in controlling juvenile satellite cells quiescence induction. Methods: We sequenced total mRNAs isolated from juvenile satellite cells FACS sorted from postnatal day 7 Control (Nf1flox/+ Myf5Cre+) and KO (Nf1flox/flox Myf5Cre+) mouse hindlimb skeletal muscle. Results: Our study suggests that Nf1 is required for maintaining the balance between quiescence induction and amplification / differentiation in the postnatal MP pool. Conclusions: The tumor suppressor Nf1 maintains the myogenic progenitor (MP) pool during postnatal muscle development.

2021-09-25 | GSE159021 | GEO

Neurofibromin (Nf1) controls metabolic balance and Notch-dependent quiescence of murine juvenile myogenic progenitors

Project description:Neurofibromin (Nf1) controls metabolic balance and Notch-dependent quiescence of murine juvenile myogenic progenitors

| PRJNA667433 | ENA

Neurofibromin (Nf1) controls metabolic balance and Notch-dependent quiescence of murine juvenile myogenic progenitors [RNA-seq]

Project description:Neurofibromin (Nf1) controls metabolic balance and Notch-dependent quiescence of murine juvenile myogenic progenitors [RNA-seq]

| PRJNA667436 | ENA

Neurofibromin (Nf1) controls metabolic balance and Notch-dependent quiescence of murine juvenile myogenic progenitors [MeDIP-Seq]

Project description:Neurofibromin (Nf1) controls metabolic balance and Notch-dependent quiescence of murine juvenile myogenic progenitors [MeDIP-Seq]

| PRJNA667435 | ENA

Neurofibromin (Nf1) controls metabolic balance and Notch-dependent quiescence of murine juvenile myogenic progenitors [ChIP-seq]

Project description:We conclude that Nf1Myf5 MPs are driven towards quiescence and show metabolic reprogramming with severely inhibited glycolytic metabolism that, in turn impinges on H4K16ac decoration and expression of myogenic differentiation-related genes. ChIP-Seq analysis of freshly isolated p7 MPs showed apparently unaltered H3K4me3 levels between controls and Nf1Myf5 MPs, while H3K27me3 levels were globally reduced in Nf1Myf5 MPs. A reduction of H3K27me3 decoration was observed at genes associated with quiescence as Pax7, or with cell cycle repression as Cdkn2a. The assumption of a quiescent state in Nf1Myf5 MPs is concomitant to decreased repressive H3K27me3 modification at quiescence-associated genes.

2021-09-25 | GSE159022 | GEO

Neurofibromin (Nf1) controls metabolic balance and Notch-dependent quiescence of murine juvenile myogenic progenitors [MeDIP-Seq]

Project description:We conclude that the epigenetic alterations we observed in Nf1Myf5 MPs are in line with a shift towards a quiescent state, and that these alterations could contribute to impaired myogenic differentiation. Furthermore, hypermethylation and transcriptional downregulation of metabolic genes points towards changes in cellular energy metabolism in Nf1Myf5 MPs.

2021-09-25 | GSE159025 | GEO

Neurofibromin (Nf1) is required for skeletal muscle development

Project description:Neurofibromatosis type 1 (NF1) is a multi-system disease caused by mutations in the NF1 gene encoding a Ras-GAP protein, neurofibromin, which negatively regulates Ras signalling. Besides neuroectodermal malformations and tumours, the skeletal system is often affected (e.g. scoliosis and long bone dysplasia), demonstrating the importance of neurofibromin for development and maintenance of the musculoskeletal system. Here we focus on the role of neurofibromin in skeletal muscle development. Nf1 gene inactivation in the early limb bud mesenchyme using Prx1-cre (Nf1Prx1) resulted in muscle dystrophy characterised by fibrosis, reduced number of muscle fibres, and reduced muscle force. To gain insight into the molecular changes of the observed muscle dystrophy and fibrosis and to compare these with other known muscle dystrophies, we performed transcriptional profiling of the entire triceps muscles of threemonth-old wild type (wt) and mutant animals using Affymetrix high-density microrrays. We analyzed triceps muscles from 4 three-month-old wt controls and 4 three-month-old Nf1Prx1 mice using the Affymetrix Mouse Gene 1.0 ST platform. Array data was processed by the Affymetrix Exon Array Computational Tool. RNA isolated from each animal was hybridized to a separate microarray.

2011-05-18 | E-GEOD-29343 | biostudies-arrayexpress

Neurofibromin (Nf1) is required for skeletal muscle development

2011-05-18 | GSE29343 | GEO

Neurofibromin (Nf1) controls metabolic balance and Notch-dependent quiescence of murine juvenile myogenic progenitors

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

2021-09-25 | GSE159026 | GEO

Gene profiles of pathway interference downstream neurofibromin signaling

Project description:Malignant peripheral nerve sheath tumor (MPNST) is a type of soft tissue sarcoma that occurs in carriers of mutations in the neurofibromatosis type I gene (Nf1) as well as sporadically.　Plexiform neurofibromas in NF1 patients have a significant risk of developing into MPNSTs leading to increased morbidity and mortality from this syndrome.　Surgery is the primary intervention but it is not always effective due to the tendency of MPNSTs to infiltrate the surrounding tissue or grow in an inoperable location. Neurofibromin, the protein coded by the Nf1 gene, functions as a GTPase activating protein (GAP) whose mutation leads to constitutive activation of RAS and mitogen-activated protein kinase (MAPK) signaling in NF1 patients’ tumors. However, therapeutic targeting of RAS and MAPK have had limited success (Kalamarides, et al., 2012). 　In this study, we modulated NRAS, MEK1/2 and neurofibromin levels in MPNST cell lines and determined the global gene expression changes that were associated with each experimental condition. Furthermore, gene expression changes due to neurofibromin deficiency but independent of NRAS and MEK1/2 regulation were characterized for the first time in MPNST cell lines.

2013-03-15 | GSE39764 | GEO

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