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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

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RNA sequencing of WT and Uhrf1 KO iNKT cells

Project description:Deletion of Uhrf1 resulted in stage 1-specific defects during iNKT cell development. To investigate the molecular mechanism, we sorted WT and Uhrf1-KO stage 1 iNKT cells and performed RNA-seq. By comparing gene expression profile, we found metabolic defects in Uhrf1-KO stage 1 iNKT cells. The expression of CD71 (Tfrc), two subunits of CD98 (Slc3a2 and Slc7a5) and Glut3 (Slc2a3) was reduced in stage 1 iNKT cells. Besides, the downstream pathways of AKT-mTOR axis were significantly reduced. Collectively, our results suggest that Uhrf1 is required for iNKT cell development by regulating the Akt-mTOR signaling pathway. We first sorted WT and Uhrf1-KO stage 1 iNKT cells, extracted the mRNA and performed RNA-seq. We then analyzed the differentially expressed genes and performed KEGG pathway analysis. We used RT-PCR to verify the expression of the key nutrient related genes (Tfrc, Slc3a2, Slc7a5 and Slc2a3) and used flow cytometry to test the protein level of metabolic related molecules. Besides, we also analyzed the expression of genes of mTOR downstream pathways to demonstrate that Uhrf1 mediated AKt-mTOR axis regulates iNKT cell development.

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