Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The miR-199-CDK2 axis modulates neutrophil migration and systemic inflammation

ABSTRACT: We performed RNAseq to identify miRNAs that were specifically down regulated in neutrophils, and RNAseq for identification of mRNA targets of miRNA-199 in neutrophils

ORGANISM(S): Danio rerio

PROVIDER: GSE127174 | GEO | 2019/10/08

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

The miR-199-CDK2 axis modulates neutrophil migration and systemic inflammation

Project description:The miR-199-CDK2 axis modulates neutrophil migration and systemic inflammation

| PRJNA524286 | ENA

miRNA overexpression modulates neutrophil migration

Project description:We performed RNAseq to identify miRNAs that were specifically down regulated in neutrophils, and RNAseq for identification of mRNA targets of miRNA-31, miRNA-190 and miRNA-375 in neutrophils

2022-02-25 | GSE167554 | GEO

miR-99 overexpression modulates neutrophil migration

Project description:We performed RNAseq to identify miRNAs that were specifically down regulated in neutrophils, and RNAseq for identification of mRNA targets of miRNA-99 in neutrophils

2021-02-06 | GSE144873 | GEO

RORa is required for neutrophil migration

Project description:We performed RNAseq to identify mRNAs that were specifically down regulated in neutrophils when RORa function is inhibited

2021-04-06 | GSE171501 | GEO

Epigenome analysis of parental and ABT-199 resistant AML cell lines

Project description:Genome wide DNA methylation profiling of parental, ABT-199 resistant population, and ABT-199 resistant clones from 3 acute myelogenous leukemia (AML) cell lines (MOLM-13, MV-4-11, OCI-AMLO2). The Illumina Infinium MethylationEPIC Human DNA methylation Beadchip was used to obtain DNA methylation profiles across approximately 850,000 CpGs from AML cell line samples. Samples include 4 ABT-199 sensitive parental MOLM-13 population samples, 4 ABT-199 resistant MOLM-13 population samples, 3 ABT-199 resistant MOLM-13 S2 clone samples, 3 ABT-199 resistant MOLM-13 S5 clone samples, 4 ABT-199 resistant MOLM-13 S6 clone samples, 3 ABT-199 sensitive parental MV-4-11 population samples, 3 ABT-199 resistant MV-4-11 population samples, 3 ABT-199 sensitive parental OCI-AML2 population samples, 3 ABT-199 resistant OCI-AML2 population samples, 3 ABT-199 resistant OCI-AML2 S1 clone samples, 3 ABT-199 resistant OCI-AML2 S2 clone samples, 3 ABT-199 resistant OCI-AML2 S8 clone samples.

2022-01-12 | GSE193254 | GEO

SRF is required for neutrophil migration in response to inflammation

Project description:RNA expression in Srf wildtype and knockout primary bone marrow derived mature neutrophils was determined via RNA sequencing Mature Gr1 high, 7/4 high, SSC high neutrophils were sorted from Srf WT and KO mouse bone marrow and submitted for RNA sequencing

2014-03-20 | E-GEOD-55090 | biostudies-arrayexpress

ATF3 is a novel regulator of mouse neutrophil migration.

Project description:Expression of the activating transcription factor 3 (ATF3) gene is induced by Toll-like receptor (TLR) signaling. In turn, ATF3 protein inhibits the expression of various TLR-driven pro-inflammatory genes. Given its counter-regulatory role in diverse innate immune responses, we defined the effects of ATF3 on neutrophilic airway inflammation in mice. ATF3 deletion was associated with increased lipopolysaccharide (LPS)-driven airway epithelia production of CXCL1, but not CXCL2, findings concordant with a consensus ATF3-binding site identified solely in the Cxcl1 promoter. Unexpectedly, ATF3-deficient mice did not exhibit increased airway neutrophilia after LPS challenge. Bone marrow chimeras revealed a specific reduction in ATF3-/- neutrophil recruitment to wild type lungs. In vitro, ATF3-/- neutrophils exhibited a profound chemotaxis defect. Global gene expression analysis identified ablated Tiam2 expression in ATF3-/- neutrophils. TIAM2 regulates cellular motility by activating Rac1-mediated focal adhesion disassembly. Notably, ATF3-/- and ATF3-sufficient TIAM2 knockdown neutrophils, both lacking TIAM2, exhibited increased focal complex area, along with excessive CD11b-mediated F-actin polymerization. Together, our data describe a dichotomous role for ATF3-mediated regulation of neutrophilic responses: inhibition of neutrophil chemokine production, but promotion of neutrophil chemotaxis. Ly6G+ neutrophils were purified by magnetic beads from WT or ATF3 KO bone marrow and RNA was immediately isolated for global gene expression using microarrays.

2014-04-05 | E-GEOD-53973 | biostudies-arrayexpress

Clavibacter sp. 199

Project description:Clavibacter sp. 199 Genome sequencing

| PRJNA463440 | ENA

Sinorhizobium meliloti strain:199

Project description:Sinorhizobium meliloti 199 Resequencing

| PRJNA501488 | ENA

Sinorhizobium fredii strain:USDA 199 | isolate:USDA 199

Project description:Sinorhizobium fredii USDA 199 genome sequencing

| PRJNA1115331 | ENA