Ask about this productRelated genes to: OASL Blocking Peptide
- Gene:
- OASL NIH gene
- Name:
- 2'-5'-oligoadenylate synthetase like
- Previous symbol:
- -
- Synonyms:
- TRIP14, p59OASL, OASL1
- Chromosome:
- 12q24.31
- Locus Type:
- gene with protein product
- Date approved:
- 1998-10-12
- Date modifiied:
- 2017-09-22
Related products to: OASL Blocking Peptide
Related articles to: OASL Blocking Peptide
- Microglia are key regulators of neuroinflammation and neuronal survival after ischemic stroke. Emerging single-cell, transcriptomic, and metabolic studies show that ischemia induces rapid microglial reprogramming toward pro-inflammatory states that exacerbate neuronal death, oxidative stress, blood-brain barrier (BBB) disruption, and white-matter injury. Multiple pathways, including TLR4/NF-κB, NLRP3 inflammasome activation, Notch1-JAK/STAT signaling, epigenetic modulators such as HDAC3 and METTL14, and metabolic shifts involving AMPK/mTOR/HIF1α, collectively shape post-stroke microglial polarization. High-altitude hypoxia elicits similar inflammatory responses, activating microglia through RAGE-MAPK/NFκB signaling, CX3CL1/CX3CR1-dependent synaptic pruning, mitochondrial dysfunction, and lactate-mediated chromatin changes, highlighting hypoxia as a convergent driver of neuroinflammation. Modulating microglial activity, therefore, represents a promising therapeutic strategy. A wide range of natural compounds (e.g., curcumin, acteoside, astagaloside IV, artemisinin), synthetic agents (e.g., DBZ, resolvin D1), and cellular/molecular cellular interventions (e.g., rhFGF21, S100A9 inhibition, RBM3 induction) have shown efficacy in reducing inflammation, preserving BBB integrity, improving mitochondrial function, and promoting M2-like reparative phenotypes in preclinical models. Advances in understanding microglial subtypes, including CH25H, OASL, CD11c, and antioxidant Prdx1-enriched populations, further highlight their dynamic roles across injury and repair. This review presents current insights into microglial signalling, epigenetic and metabolic regulation, and therapeutic targeting in ischemic stroke, integrating parallel insights from high-altitude hypoxia. Together, these prospectives illuminate microglia as crucial mediators of neurovascular injury and recovery, and highlight opportunities for translating microglia-directed therapies into clinical interventions. - Source: PubMed
Publication date: 2026/05/06
Khan ShafaSultan ArmiyaSadik MohdAshraf Mohammad Zahid - OASL, a distinctive member of the 2'-5'-oligoadenylate synthetase (OAS) family, is a well-characterized interferon-stimulated gene (ISG). In mammals and certain avian species, OASL exhibits dual functions in antiviral defense and innate immune regulation. However, the biological role of chicken OASL (chOASL) remains poorly understood, largely due to the natural absence of RIG-I in chickens. Infectious bronchitis virus (IBV) belongs to Gammacoronavirus genus and causes substantial economic losses in the global poultry industry. To explore whether chOASL is involved in the host defense against IBV, this study aimed to comprehensively characterize its expression dynamics and antiviral function. Firstly, the anti-chOASL polyclonal antibody was generated using prokaryotically expressed recombinant protein. Using this validated tool, we demonstrated that endogenous chOASL was significantly induced by Poly(I:C) and QX-IBV in various chicken cells. Furthermore, we mapped the baseline tissue distribution of chOASL protein for the first time and proved that chOASL was markedly upregulated, particularly in immune organs and IBV target tissues during IBV infection. Importantly, overexpression and knockdown assays verified that chOASL could suppress IBV replication. In conclusion, this study not only provides a reliable tool for detecting chOASL but also establishes its specific expression profile and direct antiviral activity against IBV, laying a solid foundation for further elucidating antiviral mechanisms of chOASL. - Source: PubMed
Publication date: 2026/04/27
Chen YangHu QiqiBo ZongyiGuo MengjiaoZhang ChengchengCao YongzhongWu YantaoZhang Xiaorong - Vitamin D is one of the most popular supplements worldwide, yet its appropriate dosage and full impact on health of humans and animals are still debatable. In this study, 30 pigs were divided into three groups, differing in the amount of vitamin D in the diet (Group A - no supplementation, group B-5000 IU/Kg of vitamin D, and group C 10000 IU/Kg). After 3 months of fattening, animals were slaughtered, and samples of jejunum (the longest part of the small intestine in pigs) and colon were collected for transcriptome analysis. Comparison of the transcriptomes between jejunum and colon identified 3872 Differentially Expressed Genes (DEGs). In contrast, transcriptomic changes under the influence of vitamin D were subtle in both parts of the intestine. RNA-seq results showed that vitamin D supplementation with 5000 IU/Kg enhanced the expression of 7 genes in the jejunum and one gene (MEP1B) in the colon (FDR < 0.05, base mean > 10, and log2fold change>0.6), while supplementation with 10,000 IU/Kg increased the expression of one gene (OASL) in the jejunum. No DEGs with FDR < 0.05 were identified after supplementation with 10,000 IU/kg of vitamin D in the colon, however qPCR analysis showed that genes connected to cell cycle control (PLK1, PLK3, KIF4A, KIFC1, AURKB) are upregulated in this group. Gene Set enrichment analysis of the whole RNA-seq dataset revealed that among the most affected by vitamin D processes are that connected to immunity, especially antiviral response in the jejunum, and that connected to cell cycle control in the colon. Despite the use of very high dietary vitamin D doses, no evidence of overt intestinal toxicity was observed at the transcriptomic level. Nevertheless, the activation of molecular pathways involved in calcium handling and cell cycle regulation suggests that prolonged exposure to supraphysiological vitamin D levels may trigger adaptive responses whose long-term consequences remain unknown. - Source: PubMed
Publication date: 2026/04/19
Oczkowicz MariaWierzbicka AlicjaŚwiątkiewicz MałgorzataSzmatoła TomaszSteg AnnaSmołucha Grzegorz - Copy number variants (CNVs) are large-scale genomic alterations that contribute substantially to genetic diversity and may influence phenotypic variation in livestock. This study investigated the genome-wide CNV landscape of three Vietnamese indigenous chicken breeds. Whole-genome sequencing on the Illumina platform (3-5× coverage) was performed on 24 individuals from Dong Tao (DT), Cay Cum (CC), and Ri (RI) breeds. A total of 1743 CNVs were detected, clustering into 315 copy number variation regions (CNVRs). Most CNVRs were rare, with 31.7% present in only one animal among breeds. Across the genome, 122 unique CNVRs were distributed over 28 chromosomes, predominantly the first five. Losses were the most frequent type (45.9%), followed by gains (39.3%), and mixed events (14.8%). Within these CNVRs, 3633 genes were identified. In DT and RI, CNVR-embedded genes included several candidates, potentially related to adaptability, development, and phenotypic diversification. Notably, DT harbored genes such as , , , (adaptation, stress/immune response) and , , , , , , , and (developmental and skeletal traits), whereas in RI they included genes such as , , , and , which may contribute to muscle, bone, and physiological regulation. Functional enrichment analysis revealed numerous genes and Quantitative Trait Loci (QTLs) associated with metabolic, developmental, and immune-related pathways. This study provides the first comprehensive genome-wide CNV profile of Vietnamese indigenous chickens and offers a valuable genomic resource for investigating the genetic basis of breed-specific and adaptive phenotypes. - Source: PubMed
Publication date: 2026/04/01
Nguyen Thuy Thi-DieuTzvetkova AnaBui Mai Thi-DieuDo Vo-Anh-KhoaDinh Thuy Thi-NgocNguyen Phuong ThanhKuss Andreas WalterPenasa MauroCendron Filippo - Prior studies in ichthyosis have demonstrated cutaneous and/or systemic immune abnormalities with barrier defects; however, the transcriptomes of the major orphan forms of ichthyosis have yet to be characterized through tape stripping, a minimally invasive sampling method validated in other inflammatory skin diseases. Skin tape strips from 27 patients with ichthyosis (9 with Netherton syndrome, 6 with congenital ichthyosiform erythroderma, 7 with lamellar ichthyosis, and 5 with epidermolytic ichthyosis) and 18 demographically matched healthy controls were analyzed with RNA sequencing. Differential expression was defined as fold change >2 and false discovery rate <0.05. All subtypes shared significant T helper (Th)17/Th22 upregulation (eg, S100A7/8/9, PI3, CCL20), and Th2 products (eg, TNFRSF4, IL13, CCR4) were particularly increased in Netherton syndrome. Tape strips additionally captured common increases in Th1 (IL1B, OASL) and IL4R upregulation in Netherton syndrome, lamellar ichthyosis, and epidermolytic ichthyosis. Although modulation of lipid markers was variable across subtypes, several epidermal differentiation complex/cornified envelope genes were increased in all or most subtypes. Disease-severity metrics were moderately correlated with increases in ceramide synthase CERS3 and Th17/Th22 and late cornified envelope markers. Changes in immune and epidermal differentiation complex/cornified envelope tape-strip markers correlated significantly and positively with those measured in biopsies. Our findings highlight tape stripping as a minimally invasive approach to profiling ichthyosis, which could provide future pathogenic and therapeutic insights. - Source: PubMed
Publication date: 2026/04/09
Kim MadelineManson MeredithLiu YingRangel StephanieKaplan NihalRabbaa LydiaChoate KeithBose SwaroopMetukuru RagasrutiLin XinyiLargen JosephShah ManaliEstrada Yeriel DPaller Amy SGuttman-Yassky Emma