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Post-transcriptional control of homeostatic B- cell signalling by HuR is required for innate B cell maintenance and function. [RNA-Seq]

ABSTRACT: Post-transcriptional control of homeostatic B- cell signalling by HuR is required for innate B cell maintenance and function. [RNA-Seq]

PROVIDER: PRJNA1159118 | ENA |

REPOSITORIES: ENA

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Post-transcriptional control of homeostatic B- cell signalling by HuR is required for innate B cell maintenance and function.

Project description:Innate B-1 cells constitute a self-maintained layer of defence for early detection of bacteria, clearance of apoptotic cell debris and removal of autoantigens driving autoimmunity. B-1 cells are originated from foetal tissues but, as opposed to B-2 cells, the molecular mechanisms behind their development and homeostatic maintenance remain largely unknown. Here we demonstrate that post-transcriptional regulation by the RNA binding protein HuR is essential for the homeostatic self-replenishment of innate B-1 cells, the expansion of B-1 cell clones targeting self-antigens and the production of natural autoantibodies. HuR KO B-1 cells fail to express the high levels of surface BCR, TACI and BAFFR required for tonic signalling and cell survival. Mechanistically, HuR binds to the 3’UTRs of mRNAs encoding these surface receptors and of pro-survival molecules, like BCL-2 and MCL-1, promoting their translation into protein. In summary, we reveal the need of post-transcriptional regulation in BCR expression, tonic signalling and homeostatic maintenance of functional B-1 cells.

2025-08-28 | GSE276641 | GEO

Post-transcriptional control of homeostatic B- cell signalling by HuR is required for innate B cell maintenance and function. [RNA-Seq]

2025-08-28 | GSE276801 | GEO

Post-transcriptional control of homeostatic B- cell signalling by HuR is required for innate B cell maintenance and function.

Project description:Post-transcriptional control of homeostatic B- cell signalling by HuR is required for innate B cell maintenance and function.

| PRJNA1158261 | ENA

TRIF drives homeostatic signalling in IECs

Project description:TRIF signalling drives homeostatic intestinal epithelial antimicrobial peptide expression

| PRJEB6686 | ENA

COMMD10 is required for homeostatic maintenance of Kupffer cells

Project description:COMMD10 is required for homeostatic maintenance of Kupffer cells

| PRJNA761079 | ENA

Homeostatic maintenance and age-related functional decline in the Drosophila ear

Project description:Homeostatic maintenance and age-related functional decline in the Drosophila ear

| PRJNA622826 | ENA

HuR inhibition reduces post-ischemic cardiac remodeling by dampening inflammatory gene expression and the innate immune response

Project description:In this study, we applied a novel small molecule inhibitor of HuR to define the functional role of HuR in the acute response to I/R injury and gain a better understanding of the HuR-dependent mechanisms during post-ischemic myocardial remodeling. Our results show an early post-ischemic increase in HuR activity that is necessary for inflammatory gene expression in cardiomyocytes. Despite the early reductions inflammatory gene expression, HuR inhibition has no effect on initial infarct size at 24-hours post-I/R. However, in agreement with previously published work by our group using a pressure overload model, we do see a protection with regard to pathological remodeling and cardiac function at two weeks post-I/R upon HuR inhibition. RNA-sequencing analysis of neonatal rat ventricular myocytes (NRVMs) post-LPS treatment to model damage associated molecular pattern (DAMP)-mediated activation of toll like receptors (TLRs) demonstrates a broad HuR-dependent regulation of pro-inflammatory chemokine and cytokine gene expression in cardiomyocytes. Importantly, we show that conditioned media from NRVMs pre-treated with HuR inhibitor loses the ability to induce inflammatory gene expression in bone marrow derived macrophages (BMDMs) compared to NRVMs treated with LPS alone. Functionally, HuR inhibition in NRVMs also reduces their ability to induce endocrine migration of peripheral blood monocytes in vitro and reduces post-ischemic macrophage infiltration to the heart in vivo. In summary, these results suggest a HuR-dependent expression of pro-inflammatory gene expression by cardiomyocytes that leads to subsequent monocyte recruitment and macrophage activation in the post-ischemic myocardium.

2024-01-01 | GSE235081 | GEO

Homeostatic maintenance and age-related functional decline in the Drosophila ear

Project description:Age-related hearing loss (ARHL) is a threat to future human wellbeing. Multiple factors contributing to the terminal auditory decline have been identified; but a unified understanding of ARHL - or the homeostatic maintenance of hearing before its breakdown - is missing. We here present an in-depth analysis of homeostasis and ageing in the antennal ears of the fruit fly Drosophila melanogaster. We show that Drosophila, just like humans, display ARHL. By focusing on the phase of dynamic stability prior to the eventual hearing loss we discovered a set of evolutionarily conserved homeostasis genes. The transcription factors Onecut (closest human orthologues: ONECUT2, ONECUT3), Optix (SIX3, SIX6), Worniu (SNAI2) and Amos (ATOH1, ATOH7, ATOH8, NEUROD1) emerged as key regulators, acting upstream of core components of the fly’s molecular machinery for auditory transduction and amplification. Adult-specific manipulation of homeostatic regulators in the fly’s auditory neurons accelerated - or protected against - ARHL.

2020-04-03 | GSE148023 | GEO

Targeting the HuR oncogenic role with a new class of inhibitors of HuR dimerization

Project description:Comprehensive meta-analysis and target screening confirmed that the mRNA-binding protein of ELAV-family HuR is oncogenic and universally upregulated in brain tumors, which highlight HuR as an universal chemotherapeutic target. HuR functionality in cancer cells is strictly dependent on HuR nuclear/cytoplasmic shuttling and dimerization; therefore, we developed a new class of inhibitors of HuR protein dimerization by utilizing medicinal chemistry techniques and reporter cell-based assay of HuR dimerization. The therapeutic potentials of lead compound (SRI-42127) were evaluated in five primary patient-derived glioma xenolines of classic, proneural, and mesenchymal subtypes, in vitro, and in mouse glioma model, in vivo. The Illumina global RNA-Sequencing was performed on PDGx-derived glioma neurospheres of different subtypes after treatment with DMSO (control) or SRI-42127 (3 uM) for 12 h to analysis transcripts and cell-signaling pathways affected by new inhibitor of HuR dimerization.

2020-11-05 | GSE158271 | GEO

HuR (ELAVL1) RIP-chip and knockdown exon array

Project description:Integrative regulatory mapping indicates that the RNA-binding protein HuR (ELAVL1) couples pre-mRNA processing and mRNA stability In this dataset, we employed two distinct experiments. 1) HuR RIP-chip to identify mRNA targets of HuR. 2) HuR knockdown to identify mRNAs whose expression are dependent on HuR. All 12 samples were normalized with PLIER using Affymetrix power tools. To identify RNA targets of HuR, HuR RIP samples were compared to Mock RIP samples. To identify RNA regulated by HuR, HuR knockdown samples were compared to mock knockdown samples.

2011-08-18 | E-GEOD-29778 | biostudies-arrayexpress

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