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Usp22 controls multiple signaling pathways that are essential for vasculature formation in the mouse placenta

ABSTRACT: Usp22 controls multiple signaling pathways that are essential for vasculature formation in the mouse placenta

PROVIDER: PRJNA520911 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8528313_1.fastq.gz	Fastqsanger.gz
	SRR8528313_2.fastq.gz	Fastqsanger.gz
	SRR8528314_1.fastq.gz	Fastqsanger.gz
	SRR8528314_2.fastq.gz	Fastqsanger.gz
	SRR8528315_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Usp22 controls multiple signaling pathways that are essential for vasculature formation in the mouse placenta

Project description:Usp22, a component of the SAGA complex, is over expressed in highly aggressive cancers, but the normal functions of this deubiquitinase are not well defined. We determined that loss of Usp22 in mice results in embryonic lethality due to defects in extra-embryonic placental tissues and failure to establish proper vascular interactions with the maternal circulatory system. These phenotypes arise from abnormal gene expression patterns that reflect defective kinase signaling, including TGFβ and several receptor tyrosine kinase (RTK) pathways. Usp22 deletion in endothelial cells and pericytes induced from embryonic stem cells also hinders these signaling cascades with detrimental effects on cell survival and differentiation as well as ability to form vessels. Our findings provide new insights to Usp22 functions during development that may offer clues to its role in disease states.

2019-02-04 | GSE126069 | GEO

USP22 controls multiple signaling pathways that are essential for vasculature formation in the mouse placenta.

Project description:USP22, a component of the SAGA complex, is overexpressed in highly aggressive cancers, but the normal functions of this deubiquitinase are not well defined. We determined that loss of USP22 in mice results in embryonic lethality due to defects in extra-embryonic placental tissues and failure to establish proper vascular interactions with the maternal circulatory system. These phenotypes arise from abnormal gene expression patterns that reflect defective kinase signaling, including TGF? and several receptor tyrosine kinase pathways. USP22 deletion in endothelial cells and pericytes that are induced from embryonic stem cells also hinders these signaling cascades, with detrimental effects on cell survival and differentiation as well as on the ability to form vessels. Our findings provide new insights into the functions of USP22 during development that may offer clues to its role in disease states.

| S-EPMC6398448 | biostudies-literature

USP22 controls necroptosis by regulating receptor interacting protein kinase 3 ubiquitination

Project description:Dynamic control of ubiquitination by deubiquitinating enzymes is essential for almost all biological processes. Ubiquitin-specific peptidase 22 (USP22) is part of the SAGA complex and catalyzes the removal of monoubiquitination from histone H2B, thereby regulating gene transcription. However, novel roles for USP22 have recently emerged, such as tumor development and cell death. Apart from apoptosis, the relevance of USP22 in other programmed cell death pathways still remains unclear. Here, we describe a novel role for USP22 in controlling necroptotic cell death in a variety of tumor cell lines. Loss of USP22 expression significantly delays TNF/Smac mimetic/zVAD.fmk (TBZ)-induced necroptosis, without affecting TNF-mediated NF-B activation or extrinsic apoptosis. Mass-spectrometric ubiquitin remnant profiling identified lysine 518 of Receptor-interacting protein kinase 3 (RIPK3) as USP22-dependent ubiquitination target during necroptosis induction. Mutation of K518 in RIPK3 reduced necroptosisassociated RIPK3 ubiquitination and amplified necrosome formation and necroptotic cell death. In conclusion, we identify a novel role of USP22 in necroptosis and further elucidate the relevance of ubiquitination as crucial regulator of necroptotic cell death.

2021-05-03 | PXD020909 | Pride

Transcriptional profiling of Usp22-WT and Usp22-KO pancreatic tumor cells

Project description:RNA-seq analysis of sorted Usp22-WT and Usp22-KO tumor cells from subcutaneously implanted mouse pancreatic tumors

2019-11-08 | GSE140088 | GEO

USP22 overexpression leads to aberrant signal transduction but is not sufficient to drive tumor formation in mice

Project description:USP22 overexpression is observed in several human cancers and is correlated with poor patient outcomes. The molecular basis underlying this correlation is not clear. USP22 is the catalytic subunit of the deubiquitylation module in the SAGA histone modifying complex, which regulates gene transcription. Our previous work demonstrated that loss of USP22 in mice leads to decreased expression of several components of receptor tyrosine kinase and TGFβ signaling pathways. To determine whether these pathways are upregulated when USP22 is overexpressed, we created a mouse model that expresses high levels of USP22 in all tissues. Phenotypic characterization of these mice revealed over branching of the mammary glands in females. Transcriptomic analyses indicate upregulation of key pathways involved in mammary gland branching in mammary epithelial cells derived from the USP22 overexpressing mice, including estrogen receptor, ERK/MAPK and TGFβ signaling. However, USP22 overexpression did not lead to increased tumorigenesis in any tissue. Our findings indicate that elevated levels of USP22 are not sufficient to induce tumors but it may enhance signaling abnormalities associated with oncogenesis.

2021-08-13 | GSE180005 | GEO

ACC-MESO1 cells: Control shRNA vs USP22 shRNA

Project description:USP22 plays oncogenic role and in order to study molecular mechanism of USP22 to promote tumorigenesis, microarray analysis was performed on USP22 knockdowned cells.

2018-10-01 | GSE104929 | GEO

The SAGA complex regulates early steps in transcription via its deubiquitylase module subunit USP22

Project description:SAGA is a modular cofactor complex that is essential for eukaryotic transcription. SAGA’s complement of ~20 proteins exist within four structurally and functionally distinct modules, two of which are catalytic. Within the KAT module, GCN5 acetylates histone tails, leading to increased chromatin accessibility and bromodomain protein recruitment. The DUB module contains the ubiquitin hydrolase USP22. In yeast, the USP22 ortholog deubiquitylates H2B, resulting in Pol II S2 phosphorylation and subsequent transcriptional elongation. We report here that metazoan SAGA, and USP22 specifically, are required at a more proximal stage in activator-driven transcription, i.e. pre-initiation complex (PIC) assembly. A combination of genome-wide and proteomic analyses revealed that H2B deubiquitylation is not linked to USP22-dependent transcription. Instead, USP22 controls Mediator tail subunit ubiquitylation. Mechanistically, USP22 controls loading of Mediator tail and GTFs onto promoters, with Mediator core recruitment being USP22-independent. These findings place human SAGA function at the earliest steps in activator-driven transcription.

2021-04-12 | GSE158108 | GEO

The SAGA complex regulates early steps in transcription via its deubiquitylase module subunit USP22

2019-10-24 | GSE121798 | GEO

Isl1 identifies the extraembryonic mesodermal / allantois progenitors and required for placenta morphogenesis and vasculature formation

Project description:Isl1 identifies the extraembryonic mesodermal / allantois progenitors and required for placenta morphogenesis and vasculature formation

| PRJNA1036585 | ENA

Usp22 depletion in E14 mouse ESCs

Project description:Mouse ESCs depleted of the epigenetic modifying enzyme Usp22 fail to differentiate properly. Ectopic expresison of Usp22 results in spontaneous differnetiation. In order to understand the transcriptional program underlying this biological defect, whole genome expression analysis was performed. E14 mESCs were infected with lentivirus containing shRNA targeting Usp22 or control (Luc). RNA was extracted from both samples and subjected to expression analysis by affymetrix array.

2013-05-15 | E-GEOD-42934 | biostudies-arrayexpress

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