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PTEN facilitates lysosome biogenesis and decreases exosome secretion by directly dephosphorylating TFEB

ABSTRACT: PTEN facilitates lysosome biogenesis and decreases exosome secretion by directly dephosphorylating TFEB

PROVIDER: PRJNA893213 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22013491_1.fastq.gz	Fastqsanger.gz
	SRR22013491_2.fastq.gz	Fastqsanger.gz
	SRR22013492_1.fastq.gz	Fastqsanger.gz
	SRR22013492_2.fastq.gz	Fastqsanger.gz
	SRR22013493_1.fastq.gz	Fastqsanger.gz

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PTEN facilitates lysosome biogenesis and decreases exosome secretion by directly dephosphorylating TFEB

Project description:To investigate the differentially expressed genes in the PTEN_x005f_x0002_intact CCA cells, compared with the PTEN-deficient CCA cells. group.cooperative function KDM4D/NFIB/MLL1 complex in the regulation of adipogenic differentiation, we established

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Molecular analysis of a case of renal cell carcinoma with t(6;11) (p21;q12) reveals a link to a lysosome-like structure

Project description:TFEB has been recently reported to be a key molecule for lysosomal regulation. Renal cell carcinoma (RCC) with t(6;11) (p21;q12) is known to be the only tumor in which TFEB is upregulated. Transcriptome analysis using a whole-genome expression array and pathway analysis using upregulated genes in tumor tissue revealed that the lysosome-associated pathways were significantly deregulated. Total RNA was extracted from non-tumor and tumor in patient of renal cell carcinoma with t(6;11) (p21;q12) and subjected to gene expression microarray analysis.

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Project description:Our studies in Salmonella Typhimurium (S. Typhimurium)-infected cells indicate that TFEB has a non-transcriptional, cytosolic function in addition to its well-characterized role as a transcription factor in regulating autophagy and lysosome biogenesis. An unbiased proteomics approach revealed that TFEB interacts with several mitochondrial proteins, which is lost when infected with S. Typhimurium. Microscopical and biochemical examinations further confirmed a novel localization of TFEB in mitochondria. We have also identified a TOMM20 binding motif within the protein sequence of TFEB which, facilitates the mitochondrial translocation in a mTOR-dependent manner. Our results further demonstrate that TFEB and the mitochondrial protease LonP1 co-regulate the assembly of complex I and its function. Moreover, during S. Typhimurium infection, lack of TFEB specifically in the mitochondria exacerbates the expression of pro-inflammatory cytokines.

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Project description:The transcription factor EB (TFEB) is a master regulator of lysosomal biogenesis and autophagy. We identify a distinct nuclear interactome of TFEB, with USP7 emerging as a key post-translational modulator of TFEB. Genetic depletion and inhibition of USP7 reveal its critical role in preserving TFEB stability within both nuclear and cytoplasmic compartments. Specifically, USP7 is identified as the deubiquitinase responsible for removing the K48-linked polyubiquitination signal from TFEB at lysine residues K116, K264, and K274, thereby preventing its proteasomal degradation. Functional assays demonstrate the involvement of USP7 in preserving TFEB-mediated transcriptional responses to nutrient deprivation, while also modulating autophagy flux and lysosome biogenesis. As USP7 is a deubiquitinase that protects TFEB from proteasomal degradation, these findings provide the foundation for therapeutic targeting of the USP7-TFEB axis in conditions characterized by TFEB dysregulation and metabolic abnormalities, particularly in certain cancers.

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