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GEF-H1-IRF5 mediated gene expression changes in BMDM by MDP recognition

ABSTRACT: GEF-H1-IRF5 mediated gene expression changes in BMDM by MDP recognition

PROVIDER: PRJNA523187 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8591300_1.fastq.gz	Fastqsanger.gz
	SRR8591300_2.fastq.gz	Fastqsanger.gz
	SRR8591301_1.fastq.gz	Fastqsanger.gz
	SRR8591301_2.fastq.gz	Fastqsanger.gz
	SRR8591302_1.fastq.gz	Fastqsanger.gz

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GEF-H1-IRF5 mediated gene expression changes in BMDM by MDP recognition

Project description:The transcription factor IRF5 is essential for immune defense against pathogens. Here, the authors show that the microtubule-associated factor GEF-H1 plays a critical role in host defense against Listeria monocytogenes in macrophages via activation of the IRF5 kinase IKKe

2019-04-02 | GSE126749 | GEO

Microbial recognition by GEF-H1 controls IKK? mediated activation of IRF5.

Project description:During infection, transcription factor interferon regulatory factor 5 (IRF5) is essential for the control of host defense. Here we show that the microtubule-associated guanine nucleotide exchange factor (GEF)-H1, is required for the phosphorylation of IRF5 by microbial muramyl-dipeptides (MDP), the minimal structural motif of peptidoglycan of both Gram-positive and Gram-negative bacteria. Specifically, GEF-H1 functions in a microtubule based recognition system for microbial peptidoglycans that mediates the activation of IKK? which we identify as a new upstream IKK?/? and IRF5 kinase. The deletion of GEF-H1 or dominant-negative variants of GEF-H1 prevent activation of IKK? and phosphorylation of IRF5. The GEF-H1-IKK?-IRF5 signaling axis functions independent of NOD-like receptors and is critically required for the recognition of intracellular peptidoglycans and host defenses against Listeria monocytogenes.

| S-EPMC6430831 | biostudies-literature

Hypoxia inhibits HUNK-mediated phosphorylation of GEF-H1 for epithelial-to-mesenchymal transition

Project description:Hypoxia regulates epithelial to mesenchymal transition (EMT) of cancer cells. However, the mechanism underlying hypoxia-mediated EMT remains largely unknow. Here, utilizing colorectal cell carcinoma (CRC) as a model, we find that HUNK inhibits EMT and suppresses metastasis of CRC cells via its substrate GEF-H1 in a kinase-dependent manner. Mechanistically, HUNK directly phosphorylates GEF-H1 at ser645 site, which activates RhoA and consequently leads to a cascade of phosphorylation of LIMK1/CFL-1, thereby stabilizing F-actin and inhibiting EMT. Moreover, hypoxia suppresses HUNK activity and dephosphorylates GEF-H1 to promote EMT. Clinically, the expression levels of both HUNK and phosphorylation of GEH-H1 ser645 are not only downregulated in CRC tissues with metastasis compared to that without metastasis, but also positively correlated among these tissues. Our findings highlight the importance of hypoxia-regulated HUNK kinase activity and phosphorylation of GEF-H1 in regulation of EMT and metastasis of CRC.

2022-05-27 | GSE203440 | GEO

GEF-H1 mediated gene expression changes in BMDCs in response to microtubule destabilization

Project description:GEF-H1 controls transcriptional programs that mediate antitumor immuity upon microtubule destabilization.

2019-10-01 | GSE135264 | GEO

Genome-wide maps of chromatin state of IRF5+/+ and IRF5-/- CD4+ mouse T cells

Project description:Genetic variants in IRF5 are associated with multiple immune-mediated diseases. IRF5 has been predominantly focused on for its regulation of myeloid-derived cells. We found that IRF5 contributes to CD4+ T cell outcomes and that it regulates early T cell receptor-initiated signaling and subsequently translocates to the nucleus where it binds to promoters of various genes regulated with T cell activation. We report the chromatin state of freshly isolated and activated IRF5+/+ and IRF5-/- CD4+ T cells in vitro. While there are minimal differential peaks between freshly isolated IRF5+/+ and IRF5-/- CD4+ T cells, once activated multiple differential peaks are observed between IRF5+/+ and IRF5-/- CD4+ T cells.

2020-06-29 | GSE148672 | GEO

RNA-sequencing of IRF5+ and IRF5- circulating monocytes from patients with Type-2 Diabetes

Project description:Purpose: To characterise the transcriptomic landscape in monocytes associated with IRF5 expression Methods: RNA sequencing from FACS sorted IRF5+ and IRF5- CD14+ monocytes Results: Differential expression based on IRF5 postiivity provides insight into its roles in monocyte function and in type-2 diabetes Conclusions: This study represents the first analyses of IRF5-dependent transcriptome in circulating monocytes from patients with Type-2 diabetes

2022-07-22 | GSE176216 | GEO

MDP phosphorylation by NAGK is essential for NOD2 activation

Project description:Bacterial cell wall components provide various unique molecular structures that are detected by pattern recognition receptors (PRRs) of the innate immune system as non-self. Most bacterial species form a cell wall that consists of peptidoglycan, a polymeric structure comprising of alternating amino sugars. Muramyl dipeptide (MDP) is the minimal, biologically active molecular structure derived from peptidoglycan, and its immunogenicity is well documented in numerous studies. MDP is sensed by the cytosolic nucleotide-binding and nucleotide oligomerization domain-like receptor 2 (NOD2), which triggers a pro-inflammatory response upon engagement 1,2. Conducting a forward genetic screen to identify factors required for MDP detection, we discovered that N-acetylglucosamine kinase (NAGK) is essential for the immunostimulatory activity of MDP. NAGK, which has previously been identified to contribute to the hexosamine salvage pathway in humans, is broadly expressed and inducible in innate immune cells. Mechanistically, NAGK functions upstream of NOD2 in that it directly phosphorylates the N-acetylmuramic moiety of MDP at the hydroxyl group of its C6 position, yielding 6-O-phospho-MDP. NAGK-phosphorylated MDP constitutes an essential component of NOD2 dependent signal transduction. Altogether, these results unveil a previously unknown interconnection of amino sugar metabolism and innate immunity to bacterial cell walls.

2022-06-13 | PXD022384 | Pride

Expression analysis of murine splenic B-cells after retroviral transduction with a constitutively active variant of IRF5 (IRF5-4D)

Project description:Genome-wide gene expression analysis of murine splenic B-cells following retroviral transduction with a constitutively active IRF5 (IRF5-4D) Illumina WG-6 v2.0 arrays were hybridized to determine the gene expression profile of murine splenic B-cells following retroviral transduction with i) control virus (MSCV-IRES-CFP) or ii) IRF5-4D virus (MSCV-IRF5-4D-CFP). All hybridizations were done in biological triplicates.

2014-09-24 | E-GEOD-51719 | biostudies-arrayexpress

Gene expression profiling in wild-type, Irf5-KO, Lyn-KO and Lyn/Irf5-DKO BMDCs unstimulated or stimulated with CpG-B ODN

Project description:To characterize the relationship between IRF5 and Lyn in innate immune responses at a genome-wide scale, we performed gene expression microarray analysis for wild-type (WT), Irf5-KO, Lyn-KO and Lyn/Irf5-DKO bone marrow-derived dendritic cells (BMDCs) with or without 6 h-stimulation with 150 nM CpG-B ODN. We extracted the transcripts that were upregulated by CpG-B ODN in WT BMDCs, further upregulated in Lyn-KO BMDCs and then downregulated in Lyn/Irf5-DKO BMDCs (fold change â?¥ 2, false discovery rate < 0.05). When these 79 transcripts were sorted by their expression levels in Lyn-KO BMDCs, most of the top 20 genes (13 out of 20) were those encoding type I interferons (IFNs), indicating that Lyn particularly suppresses IRF5 induction of type I IFNs. BMDCs from WT, Irf5-KO, Lyn-KO and Lyn/Irf5-DKO mice in a C57BL/6 background were unstimulated or stimulated with CpG-B ODN. Biological triplicate for each genotype were analyzed (24 samples in total).

2016-07-25 | E-GEOD-63014 | biostudies-arrayexpress

Expression analysis of Reh cells after transfection with constitutively active variants of IRF5 (IRF5-4D) and/or constitutively active IKKÎ²(EE)

Project description:Genome-wide gene expression analysis of Reh cells following transfection with constitutively active IRF5-4D, constitutively active IKKÎ²(EE), or both in combination. Affymetrix U133 Plus 2.0 oligonucleotide arrays were hybridized to determine the gene expression profile of acute lymphoblastic leukemia-derived Reh cells following transfection with i) control constructs, ii), a constitutively active variant of IRF5 (IRF5-4D), iii) a constitutively active variant of the IkB kinase Î² (IKKÎ²(EE)), or iv) IRF5-4D in combination with IKKÎ²(EE). All hybridizations were done in biological duplicates.

2014-09-24 | E-GEOD-51717 | biostudies-arrayexpress

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