Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Spop restrains inflammation-induced emergency hematopoiesis by targeting MyD88

ABSTRACT: Spop restrains inflammation-induced emergency hematopoiesis by targeting MyD88

PROVIDER: PRJNA448157 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Spop restrains inflammation-induced emergency hematopoiesis by targeting MyD88 [scRNA-Seq]

Project description:Spop restrains inflammation-induced emergency hematopoiesis by targeting MyD88 [scRNA-Seq]

| PRJNA448160 | ENA

Spop restrains inflammation-induced emergency hematopoiesis by targeting MyD88 [Bulk RNA-Seq]

Project description:Spop restrains inflammation-induced emergency hematopoiesis by targeting MyD88 [Bulk RNA-Seq]

| PRJNA448144 | ENA

Spop restrains inflammation-induced emergency hematopoiesis by targeting MyD88

Project description:Innate immune cells, and myeloid lineage cells in particular, constitute the first line ofdefense for the containment of invading pathogens. To meet the augmented demand of myeloidcells in response to systemic infections, inflammatory signals trigger a rapid transcriptional response inhematopoietic stem and progenitor cells (HSPCs), promoting their proliferation and preferential differentiation towards the granulocytic lineage

2019-07-12 | PXD009469 | Pride

Spop restrains inflammation-induced emergency hematopoiesis by targeting MyD88

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-08-12 | GSE112542 | GEO

Spop restrains inflammation-induced emergency hematopoiesis by targeting MyD88 [scRNA-Seq]

Project description:Examination of the single cell trasncriptional profile of bone marrow sorted LSK 10 days post Poly(I:C) challenge

2019-08-12 | GSE112541 | GEO

Spop restrains inflammation-induced emergency hematopoiesis by targeting MyD88 [Bulk RNA-Seq]

Project description:examination of the transcriptional profile of LSK and neutrophils (L6G+)

2019-08-12 | GSE112538 | GEO

Usp22 is an intracellular regulator of systemic emergency hematopoiesis

Project description:Emergency hematopoiesis is a concerted response geared towards enhanced protection from infection, involving multiple cell types and developmental stages across the immune system. Despite its importance, the underlying molecular regulation remains poorly understood. The deubiquitinase USP22 regulates the levels of monoubiquitinated histone H2B (H2Bub1), which is involved in intracellular interferon responses. Here we show that, in the absence of infection or inflammation, mice lacking Usp22 in blood and immune cells display profound systemic emergency hematopoiesis, evident by increased hematopoietic stem cell proliferation, myeloid bias, and extramedullary hematopoiesis. Functionally, loss of Usp22 results in elevated phagocytosis by neutrophilic granulocytes, and enhanced innate protection against Listeria monocytogenes infection. At the molecular level, we find this state of emergency hematopoiesis associated with transcriptional signatures of myeloid priming, enhanced mitochondrial respiration, as well as innate and adaptive immunity and inflammation. Augmented inflammatory gene expression was linked to elevated locus-specific H2Bub1 levels. Collectively, a tunable epigenetic state promotes systemic emergency hematopoiesis in a cell-autonomous manner and enhances innate protection, paving potential ways towards immune enhancement.

2022-11-02 | GSE212758 | GEO

Bone marrow adipocytes fuel emergency hematopoiesis

Project description:Hematopoiesis advances cardiovascular disease by generating inflammatory leukocytes that attack the arteries, heart and brain. While it is well documented that the bone marrow niche regulates hematopoietic stem cell proliferation and hence the systemic leukocyte pool, it is less clear how cardiovascular disease affects the vasculature forming this niche. Here we show that arterial hypertension, atherosclerosis and myocardial infarction alter the anatomy and function of bone marrow vasculature. Hypertension and atherosclerosis instigated vascular fibrosis, leakage and endothelial dysfunction in the bone marrow. Myocardial infarction induced vascular leakage and bone marrow angiogenesis via Vegf signaling. Endothelial cell-specific deletion of the Vegf receptor 2 limited emergency hematopoiesis after myocardial infarction, indicating that new vasculature supports higher blood cell production. RNA-sequencing of bone marrow endothelial cells revealed inflammatory gene expression in mice with cardiovascular disease. Endothelial cell-specific deletion of interleukin 6 or versican, which were highly expressed in mice with atherosclerosis or myocardial infarction, respectively, reduced hematopoiesis and systemic myeloid cells. Taken together, cardiovascular disease affects the vascular bone marrow niche, thus influencing hematopoietic stem cell behavior and expanding innate immune cell supply to atherosclerotic plaque and ischemic myocardium. Interrupting this feed back loop may constrain cardiovascular inflammation.

2023-11-04 | GSE169267 | GEO

Effects of SPOP on gene expression in prostate cancer

Project description:SPOP is a ubiquitin ligase adaptor frequently mutated in prostate cancer. It is involved in ubiquitination and degradation of substrate proteins. We examined the impact of wild-type and mutant SPOP on the transcriptional profile of prostate cancer cells. We cloned several naturally occurring (in human prostate cancer) SPOP mutants and expressed the corresponding constructs in prostate cancer cells. Our experimental conditions were: Human prostate cancer cells (LNCaP-Abl), transfected with control vector, SPOP-wt, and any of the following mutants: SPOP-F102C, SPOP-F133V, SPOP-F133L (2-4 biological replicates each). We analyzed their gene expression profiles for differences induced by SPOP-wt vs SPOP-mutant.

2014-10-10 | E-GEOD-59432 | biostudies-arrayexpress

SPOP mutation - SPOP Mutation Drives Prostate Tumorigenesis In Vivo through Coordinate Regulation of PI3K/mTOR and AR Signaling

Project description:Recurrent point mutations in SPOP define a distinct molecular subclass of prostate cancer. Here, we describe the first mouse model showing that mutant SPOP drives prostate tumorigenesis in vivo. Conditional expression of mutant SPOP in the prostate dramatically altered phenotypes in the setting of Pten loss, with early neoplastic lesions (high-grade prostatic intraepithelial neoplasia) with striking nuclear atypia, and invasive poorly differentiated carcinoma. In mouse prostate organoids, mutant SPOP drove increased proliferation and a transcriptional signature consistent with human prostate cancer. Using these models and human prostate cancer samples, we show that SPOP mutation activates both PI3K/mTOR and androgen receptor (AR) signaling, effectively uncoupling the normal negative feedback between these two pathways. Associated RNA-seq data deposited in GEO: GSE94839.

2017-03-20 | PXD005309 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data