Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-Seq of in vitro generated purified cDC1 from c-Jun/JunB fl/fl and c-Jun/JunB Δ/Δ Itgax-Cre mice

ABSTRACT: We used RNA-Seq to define genes that control cDC1 indentity in the absence of the transcription factors c-Jun and JunB.

ORGANISM(S): Mus musculus

PROVIDER: GSE156484 | GEO | 2021/02/16

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RNA-Seq of in vitro generated purified cDC1 from c-Jun/JunB fl/fl and c-Jun/JunB Δ/Δ Itgax-Cre mice

Project description:RNA-Seq of in vitro generated purified cDC1 from c-Jun/JunB fl/fl and c-Jun/JunB Δ/Δ Itgax-Cre mice

| PRJNA658102 | ENA

Microarray analysis of c-Jun/JunB knockout mice treated with dithranol

Project description:Ears of c-Jun/JunB knockout mice were topically treated with dithranol

2020-05-28 | GSE145126 | GEO

RNA-seq of Zbtb10 Knockdown and Control cDC1 dendritic cells (Cd8+)

Project description:RNA-seq of the immune-suppressed cDC1 was done to look into the mechanism underlying TLR9. It was then compared with the inflammatory cDC1 DCs.

2021-09-03 | E-MTAB-9495 | biostudies-arrayexpress

ZEB1 ChIP-seq Data from Control CD8+cDC1

Project description:To identify the direct targets of Zeb1 we performed ChIP-seq of wild type cDC1 cell line in unstimulated condition. cDC1 cell line was used for Chromatin Immunoprecipitation, it was then fixed and crosslinked and then fragmented and the fragmented DNA-protein was immunoprecipated using Zeb1 antibody. The chromatin sample was then used to prepare library using NEB kit following the manufacturer's protocol

2018-11-13 | E-MTAB-6917 | biostudies-arrayexpress

JUNB ChIP-seq

Project description:JUNB ChIP-seq

| PRJNA802851 | ENA

Identification of sites bound by c-Jun and JunB transcription factors in the Karpas 299 ALK+ ALCL cell line

Project description:In order to identify sites bound by c-Jun/JunB in ALK+ ALCL, we performed ChIP-Seq on the Karpas 299 ALK+ ALCL cell line.

2020-09-01 | GSE151413 | GEO

JunB ChIP of human keratinocytes [ChIP-seq]

Project description:This study is designed to determine the direct target genes of JunB transcription factor in human keratinocytes Mice with epidermal deletion of JunB transcription factor displayed a psoriasis-like inflammation. The relevance of these findings to humans and the mechanisms mediating JunB function are not fully understood. Here, we demonstrate that impaired JunB function via gene silencing or overexpression of a dominant negative mutant increased human keratinocyte cell proliferation but decreased cell barrier function. RNA-seq revealed over 500 genes affected by JunB loss-of-function which included an upregulation of an array of proinflammatory molecules relevant to psoriasis. Among these were TNFa, CCL2, CXCL10, IL6R and SQSTM1, an adaptor protein involved in NF-kB activation. ChIP-Seq and gene reporter analyses showed that JunB directly suppressed SQSTM1 through binding to a consensus AP-1 cis-element located around 2 Kb upstream of SQSTM1-trasncription start site. Similar to JunB loss-of-function, SQSTM1-overexpression induced TNFa, CCL2 and CXCL10. Conversely, NF-kB-inhibition genetically with a mutant IkBa or pharmacologically with PDTC prevented cytokine, but not IL6R, induction by JunB-deficiency. Taken together, our findings indicate that JunB controls epidermal growth, barrier formation and proinflammatory responses through direct and indirect mechanisms, pinpointing SQSTM1 as a key mediator of JunB-suppression of NF-kB-dependent inflammation.

2015-10-05 | GSE63080 | GEO

JUNB ChIP-seq

Project description:Genome-wide mapping of JUNB binding sites in U2OS cell line by ChIP-seq.

2022-09-29 | GSE195991 | GEO

JunB control of keratinocyte-mediated inflammation [RNA-seq]

Project description:To determne JunB target gene in human keratincoytes Mice with epidermal deletion of JunB transcription factor displayed a psoriasis-like inflammation. The relevance of these findings to humans and the mechanisms mediating JunB function are not fully understood. Here, we demonstrate that impaired JunB function via gene silencing or overexpression of a dominant negative mutant increased human keratinocyte cell proliferation but decreased cell barrier function. RNA-seq revealed over 500 genes affected by JunB loss-of-function which included an upregulation of an array of proinflammatory molecules relevant to psoriasis. Among these were TNFa, CCL2, CXCL10, IL6R and SQSTM1, an adaptor protein involved in NF-kB activation. ChIP-Seq and gene reporter analyses showed that JunB directly suppressed SQSTM1 through binding to a consensus AP-1 cis-element located around 2 Kb upstream of SQSTM1-trasncription start site. Similar to JunB loss-of-function, SQSTM1-overexpression induced TNFa, CCL2 and CXCL10. Conversely, NF-kB-inhibition genetically with a mutant IkBa or pharmacologically with PDTC prevented cytokine, but not IL6R, induction by JunB-deficiency. Taken together, our findings indicate that JunB controls epidermal growth, barrier formation and proinflammatory responses through direct and indirect mechanisms, pinpointing SQSTM1 as a key mediator of JunB-suppression of NF-kB-dependent inflammation.

2015-10-05 | GSE63079 | GEO

Global miRNA expression profiling of Junb-deficient murine embryonic fibroblasts

Project description:The AP-1 transcription factor subunit Junb acts as a context-dependent transcriptional regulator. While positive regulatory functions of Junb are widely studied, the mechanism by which Junb exerts negative regulatory functions remains unclear. miRNAs could translate repressor functions of Junb. Therefore, the aim of this study was to identify Junb-dependent miRNAs in immortalized fibroblasts (MEFs) derived from murine Junb knock-out and wildtype embryos. Cells were published previously in Licht et al. (2010) J Clin Invest. 120(7):2307-18.

2015-10-13 | GSE43380 | GEO

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