Expression data from transgenic mice overexpressing TFEB specifically in liver
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ABSTRACT: In order to identify the effects of TFEB overexpression on liver transcriptome, we performed Affymetrix Gene-Chip hybridization experiments for transgenic mice at P9 Transcriptome analysis of transgenic mice overexpressing TFEB specifically in liver
Project description:In order to identify the effects of transcription factor EB (TFEB) overexpression on the liver transcriptome, we performed Affymetrix GeneChip hybridization experiments on injected mice overexpressing TFEB specifically in the liver. For the analysis of the injected mice overexpressing TFEB, total RNA was extracted from the liver of three mice. RNA extracted from the liver of 3 not-injected mice was used as a control.
Project description:In order to identify the effects of TFEB overexpression on the liver transcriptome, we performed Affymetrix Gene-Chip hybridization experiments for the injected mice For the analysis on the injected mice overexpressing TFEB, total RNA was extracted from the liver of three mice; RNA extracted from the liver of not-injected mice was used as control.
Project description:Expression data from Ppara (peroxisome proliferator activated receptor alpha) KO mice injected with TFEB specifically in liver. In order to identify the effects of TFEB overexpression together with Ppara absence on the liver transcriptome, we performed Affymetrix Gene-Chip hybridization experiments for the injected mice For the analysis on the injected Ppara-KO mice overexpressing TFEB, total RNA was extracted from the liver of three mice; RNA extracted from the liver of not-injected mice was used as control.
Project description:In order to identify the effects of transcription factor EB (TFEB) overexpression on the liver transcriptome, we performed Affymetrix GeneChip hybridization experiments on injected mice overexpressing TFEB specifically in the liver.
Project description:Expression data from Ppara (peroxisome proliferator activated receptor alpha) KO mice injected with TFEB specifically in liver. In order to identify the effects of TFEB overexpression together with Ppara absence on the liver transcriptome, we performed Affymetrix Gene-Chip hybridization experiments for the injected mice
Project description:In order to identify the effects of TFEB overexpression on the liver transcriptome, we performed Affymetrix Gene-Chip hybridization experiments for the injected mice
Project description:Birt-Hogg-Dubè (BHD) syndrome is an inherited condition caused by loss-of-function mutations in the gene encoding the tumor-suppressor protein folliculin (FLCN) and frequently associated with kidney cysts and cancer. FLCN acts as a negative regulator of TFEB and TFE3 transcription factors, master controllers of lysosomal biogenesis and autophagy, by enabling their phosphorylation by the mechanistic Target Of Rapamycin Complex 1 (mTORC1). We previously showed that deletion of TFEB rescued the renal cystic phenotype of kidney-specific Flcn KO mice. Using Flcn/TFEB/TFE3 double and triple KO mice we now show that both TFEB and TFE3 contribute, in a differential and cooperative manner, to kidney cystogenesis. Importantly, silencing of either TFEB or TFE3 rescued tumorigenesis in patient-derived xenografts (PDXs) generated from a kidney tumor of a BHD patient. Furthermore, transcriptome analyses performed in transgenic mice, PDXs and patient tumor samples revealed TFEB/TFE3 downstream targets that may contribute to their tumorigenic activity. Our findings demonstrate in disease-relevant models that TFEB and TFE3 are key drivers of kidney tumorigenesis and suggest novel therapeutic strategies based on the inhibition of these transcription factors.
Project description:In order to identify the effects of TFEB overexpression on the hela cells transcriptome, we performed Affymetrix Gene-Chip hybridization experiments for the hela TFEB stable clones Transcriptome analysis of hela stable clones overexpressing TFEB-GFP
Project description:In order to identify the effects of TFEB overexpression on the hela cells transcriptome, we performed Affymetrix Gene-Chip hybridization experiments for the hela TFEB stable clones Transcriptome analysis of hela stable clones overexpressing TFEB-3xFLAG
Project description:To determine whether endothelial TFEB is critical for glucose metabolism in vivo, we utilized EC-selective TFEB knockout mice and EC selective TFEB transgenic mice fed a high fat diet (HFD). EC-TFEB knockout mice exhibited significantly impaired glucose tolerance compared with control mice. Consistently, EC-TFEB transgenic mice showed improved glucose intolerance. In primary human ECs, small interfering RNA-mediated TFEB knockdown blunts the Akt signaling. adenovirus-mediated overexpression of TFEB consistently activates Akt signaling and significantly increases glucose uptake in ECs. Mechanically, TFEB upregulates insulin receptor substrate 1 and 2 (IRS1 and IRS2). TFEB increases IRS2 transcription measured by reporter gene and chromatin immunoprecipitation assays. Furthermore, we found that TFEB increases IRS1 protein via downregulation of microRNAs (miR-335, miR-495 and miR548o). In vivo, Akt signaling in the skeletal muscle and adipose tissue was significantly impaired in EC-TFEB knockout mice and consistently improved in EC-TFEB transgenic mice on HFD