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RNA sequencing results of wild type and knockout USP11 in E13.5 or E18.5 of cortex based on IlluminaNovaSeq 6000 platform

ABSTRACT: RNA sequencing results of wild type and knockout USP11 in E13.5 or E18.5 of cortex based on IlluminaNovaSeq 6000 platform

PROVIDER: PRJNA602406 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10918481_1.fastq.gz	Fastqsanger.gz
	SRR10918481_2.fastq.gz	Fastqsanger.gz
	SRR10918482_1.fastq.gz	Fastqsanger.gz
	SRR10918482_2.fastq.gz	Fastqsanger.gz
	SRR10918483_1.fastq.gz	Fastqsanger.gz

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RNA sequencing results of wild type and knockout USP11 in E13.5 or E18.5 of cortex based on IlluminaNovaSeq 6000 platform

Project description:We found that USP11 expression perturbed neurogenesis.

2023-01-01 | GSE143976 | GEO

USP11 promotes prostate cancer progression by upregulating AR and c-Myc activity [CUT&RUN]

Project description:Androgen receptor (AR) is a main driver for castration-resistant prostate cancer (CRPC). c-Myc is an oncogene underlying prostate tumorigenesis. Here we find that the deubiquitinase USP11 targets both AR and c-Myc in prostate cancer. USP11 expression was upregulated in metastatic prostate cancer and CRPC. USP11 knockdown significantly inhibited prostate cancer cell growth. Our RNA-seq studies revealed AR and c-Myc as the top transcription factors altered after USP11 knockdown. ChIP-seq analysis showed that either USP11 knockdown or replacement of endogenous USP11 with a catalytic-inactive USP11 mutant significantly decreased chromatin binding by AR and c-Myc. We find that USP11 employs two mechanisms to upregulate AR and c-Myc levels: namely, deubiquitination of AR and c-Myc proteins to increase their stability; deubiquitination of H2A-K119Ub, a repressive histone mark, on promoters of AR and c-Myc genes to increase their transcription. AR and c-Myc re-expression in USP11-knockdown prostate cancer cells partly rescued cell growth defects. Thus, our studies reveal a tumor-promoting role for USP11 in aggressive prostate cancer through upregulation of AR and c-Myc activities and support USP11 as a potential target against prostate cancer.

2024-07-13 | GSE268252 | GEO

USP11 promotes prostate cancer progression by upregulating AR and c-Myc activity [RNA-seq]

2024-07-13 | GSE268124 | GEO

RNA-seq of KYSE410 cells expressing control, USP11 or ARID1A-targeting shRNAs

Project description:We examined gene expression level in KYSE410 cells expressing control, USP11 or ARID1A-targeting shRNAs to study the mechanism underlying the tumor suppressive effect of ARID1A and USP11.

2019-11-30 | GSE132359 | GEO

Proteome for Usp11 knockout E17.5 cortex

Project description:Since Usp11 encodes a DUB, we reasoned that Usp11 deficiency may lead to increased ubiquitination and destabilization of a protein that functions in neuronal differentiation and migration.To define the molecular mechanism of Usp11 deficiency on cortical development, we performed a label-free quantitative liquid chromatography-tandem Mass Spectrometry (LC-MS/MS) analysis to detect the protein expression profiles in E17.5 WT and Usp11 KO cortices in four biological repeats.

2021-01-29 | PXD021587 | Pride

USP11/LSH/CYP24A1 axis activation underlies calcium homeostasis and potentiates the resistance of colorectal cancer cells to ferroptosis

Project description:To explore the key downstream factors for USP11 stable LSH regulation, we performed transcriptome analysis using controls, USP11 knockdown, and LSH knockdown HCT116 cells We then performed gene expression profiling analysis using data obtained from RNA-seq of 3 different cells.

2023-07-12 | GSE211866 | GEO

Versatile regulation of autophagy by the deubiquitinase USP11

Project description:Ubiquitination is a versatile post-translational modification known to regulate autophagy. Here, we show that loss of the deubiquitinase USP11 leads to an increase in the autophagic flux. To investigate the molecular details of how USP11 impacts autophagy, we determined interaction partners of USP11 using an affinity purification-mass spectrometry approach. GFP-tagged, catalytically inactive USP11(C318S) was overexpressed in 293 cells. After 4 hour treatment with Torin 1, an inhibitor of mTOR that induces autophagy, cells were lysed and samples further processed for analysis. Catalytically inactive USP11 was used to increase the chances of capturing both interaction partners and potential substrates. We identified many autophagy-related proteins that co-precipitated with USP11, suggesting that USP11 does not regulate autophagy via a single substrate, but that the observed phenotype is the sum of many interactions, each of which should be independently investigated in more detail. Our work focused on elucidating the regulation of autophagy via the lipid kinase complex PI3KC3 complex I, as one of its components (VPS15) was identified in our USP11 interactome data. PI3KC3 complex I is crucial for initiation of autophagosome formation at the endoplasmatic reticulum. USP11 knockout caused an increase in complex activity, which could explain enhanced autophagy in these cells.

2022-02-16 | PXD022143 | Pride

Transcriptome analysis of lung epithelial cells from various developmental stages (E13.5, E15.5, E18.5, P14, and P56)

Project description:Transcriptome analysis of lung epithelial cells from various developmental stages (E13.5, E15.5, E18.5, P14, and P56)

| PRJNA432185 | ENA

USP11 deubiquitinates monoubiquitinated SPRTN to repair DNA-protein crosslinks

Project description:DNA-protein crosslinks (DPCs) are toxic DNA lesions that interfere with DNA metabolic processes such as replication, transcription, and recombination. SPRTN is a replication-coupled DNA-dependent metalloprotease that degrades proteins crosslinked to DNA to promote DPC repair. SPRTN function is tightly regulated by a monoubiquitin switch that controls SPRTN chromatin accessibility during DPC repair. The deubiquitinase regulating SPRTN function in DPC repair is unknown. To identify SPRTN modifiers, we performed tandem-affinity purification and mass spectrometry (TAP-MS) analysis of SFB (S-FLAG-streptavidin binding peptide)-tagged SPRTN expressed in HEK 293T cells. We screened the MS list for proteins that are known to function as a deubiquitinase and identified only one potential SPRTN modifier, USP11 deubiquitinase. A reciprocal TAP-MS analysis of SFB-USP11 expressed in HEK 293T cells treated with camptothecin (CPT) immunoprecipitated SPRTN. USP11 interacts with SPRTN and cleaves monoubiquitinated SPRTN in cells and in vitro. USP11 depletion impaired SPRTN deubiquitination in response to formaldehyde-induced DPCs. Loss of USP11 causes an accumulation of unrepaired DPCs and cellular hypersensitivity to treatment with DPC-inducing agents. Our findings elucidates the function of USP11 in the regulation of SPRTN monoubiquitination and SPRTN-mediated DPC repair.

2021-04-01 | PXD019923 | Pride

Transfer RNA (tRNA) processing profiles of mouse embryonic frontal lobes at E13.5/E18.5

Project description:Purpose: High-throughput RNA sequencing has accelerated discovery of the complex regulatory roles of small RNAs, such those derived from tRNAs. Also recent advances in high-throughput RNA sequencing has revealed the complex RNA modification landscape and the complex role these nucleosides modifactions have in cell signalling, stem cell biology and development. The goal of this study is to establish how tRNA-derived small RNAs can affect stem cell function. Methods: four replicates of tRNAs sequencing of wild-type (WT) and NSun2 -/- mouse embryonic frontal lobes at E18.5 were generated by deep sequencing, using Illumina HiSeq platform. Results: Our analyses reveal that deletion of the cytosine-5 tRNA methylase NSUN2 increases tRNA cleaveage of NSUN2 tRNA substrates.

2017-01-02 | GSE82162 | GEO

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