DHX58 antibody - N-terminal region (ARP36500_P050)
- Known as:
- DHX58 (anti-) - N-terminal region (ARP36500_P050)
- Catalog number:
- arp36500_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- DHX58 antibody - N-terminal region (ARP36500_P050)
Ask about this productRelated genes to: DHX58 antibody - N-terminal region (ARP36500_P050)
- Gene:
- DHX58 NIH gene
- Name:
- DExH-box helicase 58
- Previous symbol:
- -
- Synonyms:
- LGP2, D11LGP2
- Chromosome:
- 17q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 2007-06-20
- Date modifiied:
- 2016-09-27
Related products to: DHX58 antibody - N-terminal region (ARP36500_P050)
Related articles to: DHX58 antibody - N-terminal region (ARP36500_P050)
- Vaccination (immune priming) against Ostreid herpesvirus 1 (OsHV-1) is a strategy for managing Pacific Oyster Mortality Syndrome (POMS), yet the transcriptional mechanisms underlying protection remain poorly defined. We evaluated the transcriptome in Pacific oysters (Magallana gigas) administered heat-treated (HT) and live OsHV-1 vaccines at 18 °C and 22 °C. All priming strategies improved survival after challenge with virulent OsHV-1 at 22 °C, with relative percent survival of 57.5% for HT OsHV-1 administered at 18 °C, 76.2% for HT OsHV-1 at 22 °C and 85.0% for live OsHV-1 at 18 °C. Primed surviving oysters exhibited significantly lower viral loads after challenge than controls, with distinct transcriptomic responses among live and HT OsHV-1 treatments. Live OsHV-1, which provided the highest protection, triggered a rapid antiviral response one day after priming, characterised by upregulation of predicted orthologs of viral RNA sensors and interferon-stimulated-like signalling components including RLR-family genes, DHX58, IFI44L and a MAVS-like adaptor. In contrast, HT OsHV-1 induced a delayed response on day four, enriched for protein quality control, endoplasmic reticulum-associated degradation and ribosome biogenesis pathways. By day 12, gene expression of primed oysters had returned to baseline. In live OsHV-1-primed oysters, post-challenge gene modules were enriched for predicted orthologs of antiviral and immune signalling components and DNA replication regulators, indicative of a coordinated antiviral response and increased haemocyte activity. Overall, these results highlight transcriptional signatures underlying OsHV-1-based vaccination, which is developing as a strategy in integrated POMS management. - Source: PubMed
Publication date: 2026/09/10
Hossain ArmanWhittington RichardCosta Vincenzo ACampbell Lee KPathirana ErandiSamsing Francisca - Duck Hepatitis A Virus type 3 (DHAV-3) causes high mortality in Pekin ducks, and the role of post-transcriptional regulation in disease resistance remains unclear. Here, we performed Oxford Nanopore full-length transcriptome sequencing on liver samples from resistant and susceptible ducks at 0 h and 24 h after DHAV-3 infection. Only one differentially expressed gene (DEG) and four differentially expressed transcripts (DETs) were identified pre-infection (0 h), whereas post-infection (24 h) we detected 2,539 DEGs and 2,909 DETs, indicating strong group-specific expression divergence. Functional enrichment revealed immune-related and metabolic pathway dysregulation in susceptible ducks, while resistant ducks maintained homeostasis. BulkSignalR identified an ECM-Integrin-JAK/Src module unique to the resistant group. Alternative splicing (AS) events increased from 16 pre-infection to 310 post-infection, enriched in immune and signaling pathways. Key immune genes showed isoform switching; in susceptible ducks, SELENOP transcripts lacked multiple selenocysteine sites, and a truncated PRPF8 isoform was highly expressed, while high DHX58 expression may suppress RIG-I activation. These findings highlight the critical role of post-transcriptional regulation in antiviral immunity and provide potential targets for improvement of disease resistance. - Source: PubMed
Publication date: 2026/08/17
Wang YingLi ShaofeiYang XueqinWang ShuaiqinLiang RuipingHou ShuishengWang XiaZhang Yunsheng - Interleukin-27 (IL-27) is an anti-HIV cytokine that induces 14 novel microRNAs (miRNAs) in primary CD4(+) T cells. We previously reported that transfection of two of these miRNA mimics, miRTC10 and miRTC14 into human primary macrophages, differentially induced interferon (IFN)-α2, -α8, -α13, and -λ1 expression. However, the mechanism underlying this activation remains unclear. Here, we demonstrate that miRTC14 does not directly target canonical IFN-regulatory genes but instead engages with pyruvate carboxylase (PC) and laboratory of genetics and physiology-2 (LGP2/DHX58) as direct binding partner proteins. Functional analysis revealed that miRTC14 transfection induces IFN expression by more than 100-fold (p<0.001), whereas PC or LGP2 depletion by siRNAs markedly attenuated this response (50-100-fold reduction, p<0.01). Reconstitution of PC and LGP2 in deficient HEK293 cells restored miRTC14-driven IFN induction. Notably, IFN activation depended on sequence features at the duplex termini. However, PC-miRTC14-LGP2 axis activates TBK1-dependent phosphorylation of IRF3/7, similarly to canonical RNA sensors (RIG-I/MDA5), but this process induced differential IFN subtype. These findings establish PC as a miRNA-binding protein and define a previously unrecognized RNA-sensing mechanism, linking metabolic enzymes to RNA sequence-dependent innate immunity. - Source: PubMed
Publication date: 2026/08/05
Kariyawasam UdeshikaGoswami SuranjanaHao MingWiscovitch-Russo RosanaChen QianYang JunQu JuMarquez MayraSui HongyanChang WeizhongImamichi Tomozumi - Immune and stress responses are closely interconnected, with glucocorticoids modulating neutrophil number and activity, and cytokines influencing stress response. Neutrophils, due to their role as primary responders to infection, high sensitivity to glucocorticoid fluctuations, and critical involvement in gut microbiota homeostasis, were selected as the central focus of this study. We examined how antibiotic-induced dysbiosis affects the hypothalamus-pituitary-interrenal (HPI) axis and stress-related neutrophil dynamics in common carp (Cyprinus carpio L.). We analyzed the expression of stress-related genes and characterized neutrophil maturation and function within the hematopoietic niche. Dysbiotic fish exposed to acute stress exhibited significantly elevated cortisol levels compared to stressed fish with intact microbiota. Notably, even non-stressed dysbiotic fish showed increased cortisol level, indicating that microbiota disruption alone impairs HPI axis regulation. Antibiotic-treated and stressed fish displayed upregulation of il1β, gcsfr, cxcl8_l2, and cxcr1, suggesting enhanced granulopoiesis and neutrophil mobilization. However, systemic neutrophilia was attenuated in dysbiotic fish regardless of stress exposure. Transcriptomic profiling of neutrophils from dysbiotic, stressed fish revealed downregulation of mpx and cxcr4, and upregulation of mmp9, mhc1, trb, nlrp12, dhx58, irf3, irf7 and stat1, indicating altered maturation, increased migratory potential, and possible neutrophil-T cell interactions. In contrast, stressed fish with intact microbiota exhibited anti-apoptotic signatures and suppression of antiviral pathways. Across all stressed and dysbiotic groups, neutrophil phagocytic activity was significantly reduced. These findings underscore the pivotal role of gut microbiota in modulating stress responses, neutrophil development and trafficking, and immune function in vertebrates. - Source: PubMed
Publication date: 2026/07/26
Klak KatarzynaMaciuszek MagdalenaKralka JakubPecio AnnaNowak Barbara FKonstantinidis IoannisGalindo-Villegas JorgeChadzinska Magdalena - Nervous necrosis virus (NNV) is a major viral pathogen that causes viral nervous necrosis in a wide range of fish species and poses a serious threat to global aquaculture. However, the antiviral responses of mandarin fish (Siniperca chuatsi) to NNV infection remain poorly understood. In this study, we investigated host antiviral responses using Chinese perch brain (CPB) cell line and in vivo infection models. Transcriptome sequencing of red-spotted grouper nervous necrosis virus (RGNNV)-infected CPB cells revealed extensive transcriptional reprogramming, with numerous interferon-stimulated genes (ISGs) significantly upregulated. Comparative transcriptomic analysis across multiple teleost species identified a conserved set of ISGs induced during RGNNV infection, including CMPK2, RSAD2, DHX58, IRF3, and EPSTI1. Among these genes, CMPK2 showed strong induction in both infected CPB cells and mandarin fish brain tissues. Functional assays further demonstrated that CMPK2 overexpression significantly inhibited RGNNV replication in CPB cells and was accompanied by increased expression of several interferon-related genes. These findings provide the first functional evidence that CMPK2 restricts RGNNV infection in S. chuatsi. Our study highlights a conserved interferon-responsive antiviral module in teleost fish and identifies CMPK2 as a potential antiviral effector involved in host defense against RGNNV infection. - Source: PubMed
Publication date: 2026/07/17
Qin ChanxiaHuang JinlongLi LinmiaoLiang YingFeng HaiqingJiang HaiyingChen JiarongChen JinpingOu WeihaoYu Yepin