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 [scRNA-Seq]

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

PROVIDER: PRJNA448160 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR6919911.fastq.gz	Fastqsanger.gz
	SRR6919912.fastq.gz	Fastqsanger.gz
	SRR6919913.fastq.gz	Fastqsanger.gz

Items per page:

1 - 3 of 3

Similar Datasets

Spop restrains inflammation-induced emergency hematopoiesis by targeting MyD88

Project description:Spop restrains inflammation-induced emergency hematopoiesis by targeting MyD88

| PRJNA448157 | 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:Bone marrow adipocytes fuel emergency hematopoiesis

| PRJNA716047 | ENA

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

Usp22 is an intracellular regulator of systemic emergency hematopoiesis

Project description:Usp22 is an intracellular regulator of systemic emergency hematopoiesis

| PRJNA877206 | ENA