Role of USP39 in HeLa and HEK293T cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA954021 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24120317.fastq.gz | Fastqsanger.gz | |||
| SRR24120318.fastq.gz | Fastqsanger.gz | |||
| SRR24120319.fastq.gz | Fastqsanger.gz | |||
| SRR24120320.fastq.gz | Fastqsanger.gz | |||
| SRR24120321.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 6 |
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Project description:We performed USP39 iCLIP2 in HEK293T WT cells
2024-09-25 | GSE229330 | GEO
Project description:RNA splicing and protein degradation systems allow the functional adaptation of the proteome in response to changing cellular contexts. However, the regulatory mechanisms connecting these processes remain poorly understood. Here, we show that impaired spliceosome assembly caused by USP39 deficiency leads to a pathogenic splicing profile characterized by the use of cryptic 5′ splice sites. To explore the interactions of USP39 and the effect of its depletion in HeLa cells, we performed complexome profiling of nuclear lysates. We observed most USP39 stably integrated into the tri-snRNP complex and there is almost no free nuclear protein. More importantly, the relative abundance of tri-snRNP spliceosome complex was impaired in USP39-depleted cells. As previous reports indicated, USP39 is a regulator of tri-snRNP stability and its depletion decreased the levels of assembled U4/U6.U5 complexes.
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Project description:Transcriptome-wide mapping of RNA:protein interactions of USP39 in HEK293T cells
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2024-09-30 | GSE229332 | GEO
Project description:Regulation of alternative splicing (AS) is crucial for gene expression and enables a single transcript to yield multiple isoforms that increase transcriptome and proteome diversity. Dysregulated AS has been linked to the development of non-alcoholic fatty liver diseases (NAFLD). However, the splicing factors involved in hepatic homeostasis and their functional mechanisms remain to be further characterized. Here, we report that spliceosome component Usp39 plays a critical role in the regulation of hepatocyte lipid homeostasis. We found that Usp39 expression is downregulated in hepatic tissues of NAFLD and non-alcoholic steatohepatitis (NASH) subjects. We observed increased lipid accumulation, spontaneous steatosis and impaired autophagy, lipophagy in particular, in mice with hepatocyte-specific Usp39 deletion. Combined analysis of RIP-seq and RNA-seq data revealed that Usp39 regulates AS of several autophagy-related genes including Hsf1. More specifically, deletion of Usp39 resulted in alternative 5’ splice site selection of exon 6 in Hsf1 and consequently reduced expression. Hsf1 was also found to be downregulated in NAFLD/NASH mice and patients. Importantly, overexpression of Hsf1 restored lipophagy, attenuated lipid accumulation and alleviated NASH caused by Usp39 deficiency. Taken together, our findings indicate that Usp39-mediated AS is crucial for sustaining lipophagy and lipid homeostasis in the liver.
2023-09-24 | GSE213633 | GEO
Project description:High-grade serous ovarian carcinoma is the most lethal type of gynecologic malignancy.Emerging evidences have suggested the vital roles of splicing factor in the human cancers. RNA splicing pathways was found excessive activated in HGSOC. USP39 was one of overexpressed splicing factor in HGSOC. However, the biological function and concrete regulatory mechanism of USP39 in ovarian cancer remain unclear. In this study, we investigate the oncogenic roles of the splicing factor USP39 in HGSOC through facilitated the growth speed and invasion of ovarian cancer cells.Elevated USP39 expression levels, based on immunohistochemistry staining, were associated with poor survival in HGSOC patients. In order to investigate the binding peaks of USP39 in ovarian cancer,we performed RIP-seq in A2780 cells with Flag-USP39 overexpression.
2021-04-20 | GSE157401 | GEO
Project description:KRAS is the most frequently mutated oncogene in human cancer, but its therapeutic targeting remains challenging. Here, we report a synthetic lethal screen with a library of deubiquitinases and identify USP39, which encodes an essential splicing factor, as a critical gene for the viability of KRAS-dependent cells. We show that the essentiality of USP39 for these cells is based on its critical role in splicing regulation, as splicing fidelity inhibitors also decrease preferentially the proliferation rate of KRAS-active cells. Moreover, depletion of DHX38, an USP39-interacting splicing factor, also reduces the viability of these cells. Furthermore, we show that USP39 is upregulated in lung and colon carcinomas and its expression correlates with KRAS levels and poor clinical outcome, supporting the oncogenic role of this deubiquitinase. Accordingly, our work provides critical information for the development of splicing-directed antitumor treatments and supports the potential of USP39-targeting strategies for the development of anticancer therapies.
2020-09-01 | GSE72794 | GEO
Project description:High-grade serous ovarian carcinoma is the most lethal type of gynecologic malignancy.Emerging evidences have suggested the vital roles of splicing factor in the human cancers. RNA splicing pathways was found excessive activated in HGSOC. USP39 was one of overexpressed splicing factor in HGSOC. However, the biological function and concrete regulatory mechanism of USP39 in ovarian cancer remain unclear. In this study, we investigate the oncogenic roles of the splicing factor USP39 in HGSOC through facilitated the growth speed and invasion of ovarian cancer cells.Elevated USP39 expression levels, based on immunohistochemistry staining, were associated with poor survival in HGSOC patients. Since many RNA-binding proteins showed DNA-binding ability , we performed ChIP-seq in A2780 cells with Flag-USP39 overexpression in order to detect the bindng of USP39 to DNA and POLR2A was used as a positive control.
2021-09-05 | GSE157543 | GEO
Project description:High-grade serous ovarian carcinoma is the most lethal type of gynecologic malignancy.Emerging evidences have suggested the vital roles of splicing factor in the human cancers. RNA splicing pathways was found excessive activated in HGSOC. USP39 was one of overexpressed splicing factor in HGSOC. However, the biological function and concrete regulatory mechanism of USP39 in ovarian cancer remain unclear. In this study, we investigate the oncogenic roles of the splicing factor USP39 in HGSOC through facilitated the growth speed and invasion of ovarian cancer cells.Elevated USP39 expression levels, based on immunohistochemistry staining, were associated with poor survival in HGSOC patients. In order to investigate the regulatory mechanism of USP39 in ovarian cancer,we performed RNA-seq in A2780 cells with USP39 knock down compared with control in three repeat. HMGA2 was identified as USP39 target gene because of different expression and downregulated splicing efficiency.
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