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Nuclear adenine activation of hnRNPA2B1 promotes IL-1 transcription in antibacterial innate immunity [Cut&Tag-seq]

ABSTRACT: Nuclear adenine activation of hnRNPA2B1 promotes IL-1 transcription in antibacterial innate immunity [Cut&Tag-seq]

PROVIDER: PRJNA1096986 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28576490_1.fastq.gz	Fastqsanger.gz
	SRR28576490_2.fastq.gz	Fastqsanger.gz
	SRR28576491_1.fastq.gz	Fastqsanger.gz
	SRR28576491_2.fastq.gz	Fastqsanger.gz
	SRR28576492_1.fastq.gz	Fastqsanger.gz

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Nuclear adenine activation of hnRNPA2B1 promotes IL-1 transcription in antibacterial innate immunity [Cut&Tag-seq]

Project description:Deciphering the rapid expression and the underlying mechanisms of antibacterial effectors is critical to host defense against bacterial infection. Bacterial infection can reprogram cellular metabolism, however, the immunometabolism and its cross-talk with epigenetics in the regulation of antibacterial innate immunity remain to be fully understood. Here we report that nuclear hnRNPA2B1 is required to antibacterial innate response by promoting Il1b transcription. Myeloid-specific Hnrnpa2b1-deficient mice are susceptible to bacterial infection, resulting from IL-1β production insufficiency. The screenings identify the metabolite adenine in the nucleus to be able to bind and activate hnRNPA2B1. Adenine directly recruits hnRNPA2B1 to Il1b enhancers for increasing chromatin accessibility to promote Il1b transcription through NCL and FTO-mediated DNA 6mA demethylation of Il1b gene enhancers. Furthermore, bacterial infection elevates nuclear adenine levels, and in vivo administration of adenine protects mice from bacterial infection through hnRNPA2B1-IL1 circuit. Our findings provide an undiscovered paradigm of cross-regulation between epigenetic and metabolic pathways in antibacterial innate immunity, adding insight and proposing new approach to the treatment of bacterial infections.

2025-04-28 | GSE263374 | GEO

Nuclear adenine activation of hnRNPA2B1 promotes IL-1 transcription in antibacterial innate immunity [ATAC-seq]

2025-04-28 | GSE263373 | GEO

Nuclear adenine activation of hnRNPA2B1 promotes IL-1 transcription in antibacterial innate immunity [ATAC-seq]

Project description:Nuclear adenine activation of hnRNPA2B1 promotes IL-1 transcription in antibacterial innate immunity [ATAC-seq]

| PRJNA1096984 | ENA

Itaconate uptake via SLC13A3 improves hepatic antibacterial innate immunity

Project description:Itaconate is an immunoregulatory metabolite produced by the mitochondrial enzyme immune-responsive gene 1 (IRG1) in inflammatory macrophages. We recently identified an important mechanism by which itaconate is released from inflammatory macrophages. However, it remains unknown whether extracellular itaconate is taken up by non-myeloid cells to exert immunoregulatory functions. Here, we used a custom-designed CRISPR screen to identify the dicarboxylate transporter solute carrier family 13 member 3 (SLC13A3) as an itaconate importer and to characterize the role of SLC13A3 in itaconate-improved hepatic antibacterial innate immunity. Functionally, liver-specific deletion of Slc13a3 impairs hepatic antibacterial innate immunity in vivo and in vitro. Mechanistically, itaconate uptake via SLC13A3 induces transcription factor EB (TFEB)-dependent lysosomal biogenesis and subsequently improves antibacterial innate immunity in murine hepatocytes. These findings identify SLC13A3 as a key itaconate importer in murine hepatocytes and will aid in the development of potent itaconate-based antibacterial therapeutics.

2024-07-08 | GSE230735 | GEO

Nuclear HNRNPA2B1 HITS-CLIP and RNA-seq

Project description:To identify HNRNPA2B1 binding sites on endogenous nuclear RNAs, we performed HITS-CLIP for endogenous HNRNPA2B1 and RNA-seq to analyze the nuclear RNA under either METTL3 or HNRNPA2B1 depletion. Wild type MDA-MB-231 cells were subjected to the HITS-CLIP procedure on immunoprecipitated HNRNPA2B1 associated RNA obtained from the nuclear fraction (Licatalosi D, et al. 2008, Nature 456:464-U22). For RNA-seq, nuclear RNA was extracted from MDA-MB-231 or Hela cells knocked down for METTL3 or HNRNPA2B1.

2015-06-20 | E-GEOD-70061 | biostudies-arrayexpress

Itaconate uptake via SLC13A3 improves hepatic antibacterial innate immunity

Project description:Itaconate uptake via SLC13A3 improves hepatic antibacterial innate immunity

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The RNA binding protein HNRNPA2B1 regulates IFNG signaling in macrophages

Project description:Heterogeneous nuclear ribonucleoprotein A2B1 (HNRNPA2B1) is a well known RNA binding protein but the mechanisms by which it contributes to innate immune gene regulation is poorly understood. Here we report that HNRNPA2B1 functions in macrophages to regulate IFNG signaling through alternative splicing of the IFNG receptor. Specific deletion of HNRNPA2B1 in macrophages using our newly developed conditional mice crossed to LysMCre resulted in altered cytokine responses in both an endotoxic shock model and following Salmonella infection. Interestingly, while HNRNPA2B1 can function as a viability gene, we observed increased macrophage and neutrophil numbers in the KO mice following LPS induced endotoxic shock. HNRNPA2B1 KO mice were more susceptible to Salmonella and Mycobacterium Tuberculosis infections and failed to effectively clear the pathogens. Mechanistically, loss of HNRNPA2B1 resulted in an increase in No-GO transcripts of the IFNG receptor (Ifngr) leading to lower expression of the receptor at the cell surface impacting the downstream IFNG signaling cascade. Collectively, our data highlights an important role for HNRNPA2B1 in regulating IFNG signaling in macrophages.

2024-09-30 | GSE243269 | GEO

Nuclear HNRNPA2B1 HITS-CLIP and RNA-seq

2015-06-20 | GSE70061 | GEO

An essential role for the antiviral endoribonuclease, RNase-L, in antibacterial immunity.

Project description:Type I interferons were discovered as the primary antiviral cytokines and are now known to serve critical functions in host defense against bacterial pathogens. Accordingly, established mediators of interferon antiviral activity may mediate previously unrecognized antibacterial functions. RNase-L is the terminal component of an RNA decay pathway that is an important mediator of interferon-induced antiviral activity. Here we identify a novel role for RNase-L in the host antibacterial response. RNase-L-/- mice exhibited a dramatic increase in mortality following challenge with Bacillus anthracis and Escherichia coli; this increased susceptibility was due to a compromised immune response resulting in increased bacterial load. Investigation of the mechanisms of RNase-L antibacterial activity indicated that RNase-L is required for the optimal induction of proinflammatory cytokines that play essential roles in host defense from bacterial pathogens. RNase-L also regulated the expression of the endolysosomal protease, cathepsin-E, and endosome-associated activities, that function to eliminate internalized bacteria and may contribute to RNase-L antimicrobial action. Our results reveal a unique role for RNase-L in the antibacterial response that is mediated through multiple mechanisms. As a regulator of fundamental components of the innate immune response, RNase-L represents a viable therapeutic target to augment host defense against diverse microbial pathogens. two strains: wildtype and knockout, three time points: untreated, 2hours, and 8hours. three replication for each group. Totally 18 samples.

2008-12-19 | E-GEOD-13530 | biostudies-arrayexpress

Transcriptome sequencing of the hnRNPA2B1 knockout Huh7 cell line

Project description:To investigate the role of hnRNPA2B1 in the progression of hepatocellular carcinogenesis, we established a Huh7 cell line in which the hnRNPA2B1 gene was knocked out by crisper/cas9.

2023-09-01 | GSE226544 | GEO

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