Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

CD38 enzymatic activity promotes hematopoietic stem cell dormancy [bulk RNA-Seq]

ABSTRACT: CD38 enzymatic activity promotes hematopoietic stem cell dormancy [bulk RNA-Seq]

PROVIDER: PRJNA807274 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR18034805.fastq.gz	Fastqsanger.gz
	SRR18034806.fastq.gz	Fastqsanger.gz
	SRR18034807.fastq.gz	Fastqsanger.gz
	SRR18034808.fastq.gz	Fastqsanger.gz
	SRR18034809.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

CD38 enzymatic activity promotes hematopoietic stem cell dormancy

Project description:CD38 enzymatic activity promotes hematopoietic stem cell dormancy

| PRJNA807170 | ENA

CD38 enzymatic activity promotes hematopoietic stem cell dormancy [bulk RNA-Seq]

Project description:Quiescence is a fundamental property that protects hematopoietic stem cells’ (HSCs) function throughout life. A subpopulation of deeply quiescent, so-called dormant HSCs (dHSCs) harbors the highest long-term blood repopulation capacity and resides at the top of the hematopoietic hierarchy. However, the mechanisms of HSC dormancy remain elusive, mainly due to the absence of surface markers for dHSCs’ prompt isolation. We identified CD38 nicotinamide adenine dinucleotide (NAD+) catabolic ecto-enzyme as a novel surface marker for murine dHSCs. The product of CD38 cyclase activity – cyclic adenosine diphosphate ribose (cADPR), regulates the expression of the transcription factor and cell cycle regulator c-Fos via an increase of cytoplasmic Ca2+ concentration. Strikingly, we uncovered that c-Fos drives HSCs quiescence through the induction of the cell cycle inhibitor p57Kip2 expression. Moreover, we found a similar CD38-dependent mechanism of quiescence regulation for human HSCs, which are CD38 negative. Specifically, we found that CD38 ecto-enzymatic activity at the neighboring CD38-positive cells promote human HSCs’ dormancy. Together, our work reveals how extracellular metabolic cues trigger a signaling cascade blocking HSC cell cycle entrance. Pharmacological manipulations of defined pathway will provide new strategies to modulate HSCs activation upon infections, blood loss or transplantation in clinical practice.

2022-02-18 | GSE196758 | GEO

CD38 enzymatic activity promotes hematopoietic stem cell dormancy [scRNA-Seq]

2022-02-18 | GSE196759 | GEO

CD38 enzymatic activity promotes hematopoietic stem cell dormancy [scRNA-Seq]

Project description:CD38 enzymatic activity promotes hematopoietic stem cell dormancy [scRNA-Seq]

| PRJNA807273 | ENA

The enzymatic activities of CD38 enhance CLL growth and trafficking: implications for therapeutic targeting

Project description:The ecto-enzyme CD38 is a marker of unfavorable prognosis for chronic lymphocytic leukemia (CLL) patients and an indicator of activation and proliferation of leukemic cells. Here we show that CD38 is enzymatically active in primary CLL cells and that its forced expression increases disease aggressiveness in a xenograft model. The effect is completely lost when using an enzyme deficient version of CD38 with a single amino-acid mutation. Through the enzymatic conversion of NAD, CD38 increases cytoplasmic Ca2+ concentrations, positively influencing proliferation, chemotaxis, adhesion and matrix digestion. Inhibition of the enzymatic activities of CD38 using the flavonoid kuromanin blocks CLL homing. In a short-term xenograft model using primary cells, kuromanin treatment traps CLL cells in the blood, increasing responses to chemotherapy. Microarrays were performed comparing genetic signature derived from Mec-1 cell line variants, generated infecting cells by lentiviruses carrying the genetic material for a wild-type (CD38WT ) or an enzymatically-inactive form of CD38 (CD38M), grown in vitro and in vivo in NSG mice. GFP+ Mec-1 clones (Mec-1/GFP) were generated with the same protocol and used as control.

2014-04-01 | E-GEOD-56369 | biostudies-arrayexpress

The enzymatic activities of CD38 enhance CLL growth and trafficking: implications for therapeutic targeting

2014-04-01 | GSE56369 | GEO

Lin-, CD38-, CD34+ Hematopoietic Stem Cells.

Project description:Lin-, CD38-, CD34+ hematopoietic stem cells. Keywords: other

2005-12-09 | GSE3788 | GEO

CD38 enzymatic activity promotes hematopoietic stem cell dormancy

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

2022-02-18 | GSE196760 | GEO

Transcription profiling of human Lin-, CD38-, CD34+ Hematopoietic Stem Cells.

Project description:Lin-, CD38-, CD34+ hematopoietic stem cells. Experiment Overall Design: this experiment include 1 samples and 6 replicates

2008-06-12 | E-GEOD-3788 | biostudies-arrayexpress

CD38 promotes hematopoietic stem cell dormancy.

Project description:A subpopulation of deeply quiescent, so-called dormant hematopoietic stem cells (dHSCs) resides at the top of the hematopoietic hierarchy and serves as a reserve pool for HSCs. The state of dormancy protects the HSC pool from exhaustion throughout life; however, excessive dormancy may prevent an efficient response to hematological stresses. Despite the significance of dHSCs, the mechanisms maintaining their dormancy remain elusive. Here, we identify CD38 as a novel and broadly applicable surface marker for the enrichment of murine dHSCs. We demonstrate that cyclic adenosine diphosphate ribose (cADPR), the product of CD38 cyclase activity, regulates the expression of the transcription factor c-Fos by increasing the release of Ca2+ from the endoplasmic reticulum (ER). Subsequently, we uncover that c-Fos induces the expression of the cell cycle inhibitor p57Kip2 to drive HSC dormancy. Moreover, we found that CD38 ecto-enzymatic activity at the neighboring CD38-positive cells can promote human HSC quiescence. Together, CD38/cADPR/Ca2+/c-Fos/p57Kip2 axis maintains HSC dormancy. Pharmacological manipulations of this pathway can provide new strategies to improve the success of stem cell transplantation and blood regeneration after injury or disease.

| S-EPMC10931502 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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