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Mus musculus

ABSTRACT: Proteogenomic characterization of developmental defects in the forebrain resulting from hyperactivated mTOR signaling

OTHER RELATED OMICS DATASETS IN: PXD005768

PROVIDER: PRJNA360611 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5163400_1.fastq.gz	Fastqsanger.gz
	SRR5163400_2.fastq.gz	Fastqsanger.gz
	SRR5163401_1.fastq.gz	Fastqsanger.gz
	SRR5163401_2.fastq.gz	Fastqsanger.gz
	SRR5163402_1.fastq.gz	Fastqsanger.gz

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Proteogenomic characterization of developmental defects in the forebrain resulting from hyperactivated mTOR signaling

Project description:Hyperactivated mTOR signaling in the developing brain by mutation of TSC1 genes has multiple forms of pathology including tuberous sclerosis complex (TSC). To examine the downstream networks affected in the developing brain by hyperactivated mTOR signaling, we performed an integrated analysis of transcriptomic and proteomic analysis of forebrain of wild-type and TSC1/Emx1-Cre mouse. Our results provide novel and fundamental molecular bases for understanding hyperactivaed mTOR signaling-induced brain defects which can in turn facilitate identification of potential diagnostic markers and therapeutic targets for mTOR signaling-related neurological disorders.

2018-08-16 | PXD005768 | Pride

Proteogenomic characterization of developmental defects in the forebrain resulting from hyperactivated mTOR signaling

Project description:Hyperactivated mTOR signaling in the developing brain has been implicated in multiple forms of pathology including tuberous sclerosis complex (TSC). Here, we present an integrated analysis of transcriptomes and proteomes generated from wild-type and TSC1/Emx1-Cre forebrains. This led to comprehensive lists of genes and proteins whose expression levels were altered by hyperactivated mTOR signaling.

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Tumor Suppressor TSC1 Negatively Regulates Polo-like Kinase Expression and Controls the Balance of Schwann Cell Proliferation and Differentiation

Project description:Activation of mTOR signaling by Tsc1 ablation during early developmental stages increases SC proliferation and delays radial sorting, while causing hypomyelination in the PNS. However, knockout Tsc1 in myelinating SCs at postnatal stages promotes myelin overgrowth and outfoldings. Sustained mTOR pathway leads to activation of the PLK signaling pathway. mTOR attenuation or pharmacological inhibition of PLK1 could partially rescue myelination defects in Tsc1 mutant sciatic nerves. Our data suggest that TSC1-mTOR maintains the homeostasis of SC proliferation and differentiation in a stage-specific manner.

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Proteogenomic characterization and comprehensive integrative genomic analysis of human colorectal cancer liver metastasis

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A Cellular and Molecular Basis of Leptin Resistance

Project description:Humans with obesity and diet-induced obese mice (DIO) have high leptin levels and fail to respond to the exogenous hormone suggesting that obesity is caused by leptin resistance, the pathogenesis of which is unknown. We found that leptin treatment reduced plasma levels of leucine and methionine, mTOR-activating ligands, leading us to hypothesize that chronic mTOR activation might inhibit leptin signaling. Rapamycin, an mTOR inhibitor, reduced fat mass and increased leptin sensitivity in DIO mice but not in mice with defects in leptin signaling. Rapamycin restored leptin’s actions on POMC neurons and failed to reduce the weight of mice with defects in melanocortin signaling. mTOR activation in POMC neurons caused leptin resistance while POMC specific mutations in mTOR activators decreased weight gain of DIO mice. Thus, increased mTOR activity in POMC neurons is necessary and sufficient for the development of leptin resistance in DIO mice establishing a key pathogenic mechanism leading to obesity.

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