RNAseq data comparing iKPC cells overexpressing WT-USP21 and ED-USP21
Ontology highlight
ABSTRACT: USP21 belongs to ubiquitin specific protease (USP) family. To dissect the molecular mechanisms that regulated by USP21 overexpression in PDAC cells, we conducted RNA-seq analysis of iKPC PDAC cells overexpressing wild-type USP21 (WT-USP21) and enzyme dead USP21 (ED-USP21).
Project description:USP21 promotes PDAC tumor cells to bypass KRAS* dependency. To dissect the molecular mechanism, we conducted RNA-seq analysis comparing iKPC cancer cells overexpressing GFP, wildtype USP21 and enzyme-dead USP21 at day 3 after KRAS* extinction. KRAS*-expressing iKPC cells with GFP overexpression are positive control.
Project description:KRAS* is required for PDAC tumor mantainence. To dissect the molecular mechanisms that regulated by KRAS* in PDAC tumors, we conducted RNA-seq analysis of KRAS*-expressing iKPC PDAC tumors and iKPC tumors after KRAS* extinction for 24 hours.
Project description:RNAseq data comparing GFP, wildtype USP21 and enzyme-dead USP21 overexpressing iKPC PDAC cells with KRAS* expression (on dox) and KRAS* extinction (off dox)
Project description:HDAC5 drives PDAC cells to bypass KRAS* dependency. To dissect the molecular mechanisms that regulated by overexpressed HDAC5 in the bypass of KRAS* dependency, we conducted RNA-seq analysis of HDAC5 escaper PDAC cells and KRAS*-expressing iKPC PDAC cells.
Project description:TGFbeta promotes the bypass of KRAS* dependency in PDAC. To dissect the molecular mechanisms that regulated by TGFbeta in PDAC cells, we conducted RNA-seq analysis of iKPC PDAC cells with or without TGFbeta treatment.
Project description:Skeletal muscle is the pivotal organ for energy homeostasis, but the regulatory mechanisms are largely unknown. Here, we report that ubiquitin specific protease 21 (USP21) is a regulator of skeletal muscle physiology. To elucidate features important for USP21, we performed RNA-sequencing analysis using the muscle tissue of muscle-specific USP21 knockout (USP21-MKO) mice or wild-type littermates with floxed genotype, screened and analyzed the differentially expressed genes. Transcriptomics assay enabled us to discover major signaling nodes persistently activated by USP21 ablation in close association with the genes linked to fuel oxidation. Consequently, USP21 ablation altered gross metabolic phenotypes.