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UBR5 mediates chemoresistance in colorectal cancer by attenuating ferroptosis via Lys11 ubiquitin-dependent stabilization of Smad3-SLC7A11 signaling

ABSTRACT: UBR5 mediates chemoresistance in colorectal cancer by attenuating ferroptosis via Lys11 ubiquitin-dependent stabilization of Smad3-SLC7A11 signaling

PROVIDER: PRJNA988323 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25055624_1.fastq.gz	Fastqsanger.gz
	SRR25055624_2.fastq.gz	Fastqsanger.gz
	SRR25055625_1.fastq.gz	Fastqsanger.gz
	SRR25055625_2.fastq.gz	Fastqsanger.gz
	SRR25055626_1.fastq.gz	Fastqsanger.gz

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UBR5 mediates chemoresistance in colorectal cancer by attenuating ferroptosis via Lys11 ubiquitin-dependent stabilization of Smad3-SLC7A11 signaling

Project description:To elucidate the mechanisms underlying UBR5 deficiency-enhanced cytotoxic effects of Oxaliplatin, we performed transcriptome profiling by RNA-seq to explore the signaling pathways affected by UBR5.

2024-01-22 | GSE236003 | GEO

UBR5 promotes antiviral immunity by disengaging the transcriptional brake on RIG-I like receptors

Project description:RIG-I like receptors (RLRs) are the major viral RNA sensors essential for the initiation of antiviral immune responses to numerous RNA viruses. RLRs are subjected to stringent transcriptional and posttranslational regulations, of which ubiquitination is one of the most important. However, the role of ubiquitination in RLR transcription is unknown. Here, we generated, screened 375 definite ubiquitin ligase knockout cell lines and identified UBR5 as a positive regulator of RLR transcription. UBR5 deficiency (UBR5-/-) reduced antiviral immune responses to RNA viruses, while increased viral replication in primary cells and mice. Ubr5-/- mice were more susceptible to lethal RNA virus infection than Ubr5+/+ littermates. Mechanistically, UBR5 mediated the Lysine 63-linked ubiquitination of TRIM28, an epigenetic repressor of RLRs. This modification prevented intramolecular SUMOylation of TRIM28, thus disengaged the TRIM28-imposed brake on RLR transcription. In sum, UBR5 enables rapid upregulation of RLR expression to boost antiviral immune responses by ubiquitinating and de-SUMOylating TRIM28.

2023-12-13 | GSE245604 | GEO

UBR5 promotes antiviral immunity by disengaging the transcriptional brake on RIG-I like receptors (RNA-Seq)

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UBR5 promotes antiviral immunity by disengaging the transcriptional brake on RIG-I like receptors (ChIP-Seq)

2023-12-13 | GSE245602 | GEO

RNA-seq for UBR5 and Cdc73-regulated genes in 4T1 cells treated with Dovitinib

Project description:In order to understand the molecular mechanisms underlying the regulatory activities of UBR5 and CDC73 in dovitinib-induced apoptosis in 4T1 tumor cells that were Dox-silenced for the expression of Ubr5, Cdc73, or both and treated with dovitinib.

2023-01-27 | GSE222787 | GEO

Quantitative Analysis of Transcriptomes between Negative control, UBR5 depleted and MYC depleted HeLa cells

Project description:Purpose: The goal of this study is to compare the transcriptome changes between Negative control, UBR5 depleted and MYC depleted HeLa cells Methods: Gene expression profiles of Negative control, UBR5 depleted and MYC depleted HeLa cells were generated by deep sequencing, in triplicate. Results:The data were analyzed, and we sucessfully detected global differences in the gene expression between the given groups. Conclusions: UBR5 depletion induces gene expression changes that are partly overlapping with gene expression changes induced by MYC depletion

2020-01-15 | GSE143517 | GEO

UBR5 in B cell development TMT

Project description:Coordination of a number of molecular mechanisms including transcription, alternative splicing, and class switch recombination are required to facilitate development, activation, and survival of B cells. Disruption of these pathways can result in malignant transformation. Recently, next generation sequencing has identified a number of novel mutations in mantle cell lymphoma (MCL) patients including the ubiquitin E3 ligase UBR5. Approximately 18% of MCL patients were found to have mutations in UBR5 with the majority of mutations within the HECT domain of the protein which can accept and transfer ubiquitin molecules to the substrate. Determining if UBR5 controls the maturation of B cells is important to fully understand malignant transformation to MCL. To elucidate the role of UBR5 in B cell maturation and activation we generated a conditional mutant disrupting UBR5’s C-terminal HECT domain. Loss of the UBR5 HECT domain leads to a block in maturation of B cells in the spleen and up-regulation of proteins associated with mRNA splicing via the spliceosome. Our studies reveal a novel role of UBR5 in B cell maturation by regulating alternative splicing of key transcripts during B cell development and suggests UBR5 mutations may promote mantle cell lymphoma initiation.

2020-11-19 | PXD014307 | Pride

RNA-seq for UBR5-regulated genes in tumor associated macrophages

Project description:RNA-seq analysis of peritoneal macrophages derived from non-tumor bearing, WT ID8 tumor-bearing, and Ubr5 KO ID8 tumor bearing C57BL/6 mice.

2020-11-10 | GSE158911 | GEO

LncRNA SLC7A11-AS1 suppresses ferroptosis in hepatocellular carcinoma to promote tumorigenesis

Project description:LncRNAs are playing essential roles in epigenetic regulation, mRNA translation, and protein modification. However, the function of SLC7A11-AS1, an antisense lncRNA derived from the solute carrier family 7 member 11 (SLC7A11) gene, remains incompletely known. In this study, we utilized shRNA technology to knock down SLC7A11-AS1 in HepG2 cells, aiming to investigate the role of SLC7A11-AS1 in hepatocellular carcinoma. RNA-seq results revealed that there were 2536 differentially expressed genes upon SLC7A11-AS1 knockdown.

2024-07-17 | GSE244762 | GEO

ChIPseq Smad3-JMJD3

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