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Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and Otud1-/- distal colonic tumor Transcriptomes

ABSTRACT: Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and Otud1-/- distal colonic tumor Transcriptomes

PROVIDER: PRJNA588154 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10416347_1.fastq.gz	Fastqsanger.gz
	SRR10416347_2.fastq.gz	Fastqsanger.gz
	SRR10416348_1.fastq.gz	Fastqsanger.gz
	SRR10416348_2.fastq.gz	Fastqsanger.gz
	SRR10416349_1.fastq.gz	Fastqsanger.gz

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Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and Otud1-/- distal colonic Transcriptomes

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Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and Otud1-/- distal colonic tumor Transcriptomes

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Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and Otud1-/- distal colonic tissue Transcriptomes adjacent to tumors

Project description:Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and Otud1-/- distal colonic tissue Transcriptomes adjacent to tumors

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Next Generation Sequencing Facilitates Quantitative Analysis of Transcriptomes of aGVHD mice tranferred Wild Type or OTUD1-/- cells.

Project description:Donor OTUD1 deficiency significanltly ameliorates the severity of aGVHD mice. We used single cell RNA sequencing (scRNA-seq) to analyze the immune cells in aGVHD mice transferred wild type or OTUD1-deficient cells.

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Endothelial OTUD1 promotes Ang II-induced vascular remodeling by deubiquitinating SMAD3

Project description:Understanding the molecular mechanisms of pathological vascular remodeling is important for treating cardiovascular diseases and complications. Recent studies have highlighted a role of deubiquitinases in vascular pathophysiology. In this study, we investigated the role of a deubiquitinase, OTUD1, in angiotensin II (Ang II)-induced vascular remodeling. We identified upregulated OTUD1 in the vascular endothelium of Ang II-challenged mice and showed OTUD1 deletion attenuated vascular remodeling, collagen deposition, and EndMT. Conversely, OTUD1 overexpression aggravated these pathological changes both in vivo and in vitro. Mechanistically, SMAD3 was identified as a substrate of OTUD1 using co-immunoprecipitation followed with LC-MS/MS. We found OTUD1 stabilizes SMAD3 and facilitates SMAD3/SMAD4 complex formation and subsequent nuclear translocation through both K48- and K63-linked deubiquitination. OTUD1-mediated SMAD3 activation regulate the transcription of genes involved in vascular EndMT and remodeling in HUVECs. Finally, SMAD3 inhibition reversed OTUD1-promoted vascular remodeling. Our findings demonstrate endothelial OTUD1 promoted Ang II-induced vascular remodeling by deubiquitinating SMAD3. This study identified SMAD3 as a target of OTUD1 and indicates OTUD1 as a potential therapeutic target for the diseases related to vascular remodeling.

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Endothelial OTUD1 promotes Ang II-induced vascular remodeling by deubiquitinating SMAD3

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Azoxymethane induced changes in Rat proximal and distal colonic epithelium.

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Next Generation Sequencing Facilitates Quantitative Analysis of Transcriptomes of aGVHD mice tranferred Wild Type or OTUD1-/- cells.

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Project description:We have confirmed that OTUD1 interacted directly with Akt and inhibited Akt phosphorylation. To investigate the exact mechanism of OTUD1 in the regulation of Akt signaling pathway, we established T24 cells with stable OTUD1 depletion by using sgRNA.

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