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
- 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 Netherton syndrome/NS, 6 congenital ichthyosiform erythroderma/CIE, 7 lamellar ichthyosis/LI, 5 epidermolytic ichthyosis/EI) and 18 demographically matched healthy controls were analyzed with RNA-seq. Differential expression was defined as fold change>2 and false-discovery rate<0.05. All subtypes shared significant Th17/Th22 upregulation (e.g. S100A7/8/9, PI3, CCL20), and Th2 products (e.g. TNFRSF4, IL13, CCR4) were particularly increased in NS. Tape strips additionally captured common increases in Th1 (IL1B, OASL), and IL4R upregulation in NS, LI, and EI. While modulation of lipid markers was variable across subtypes, several epidermal differentiation complex/cornified envelope (EDC-CE) 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 EDC-CE tape-strip markers correlated significantly and positively with those measured in biopsies. Our findings highlight tape-stripping as a minimally invasive approach to profile 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 - We constructed a gene coexpression network to uncover central key genes related to Sjögren's disease (SjD), and investigated the clinical significance of bone marrow stromal antigen 2 (BST2) in SjD. - Source: PubMed
Publication date: 2026/04/09
Ren TianZhou XinZhou EryeLiu CuipingWu JianChang XinChen Weichang - Helicobacter pylori (H. pylori) has been identified as a pathogenic factor in gastric cancer (GC). Building on our previous findings that VacA upregulates TRAF1, which in turn transcriptionally activates OASL, we explored the role of this TRAF1-OASL-PANoptosis axis in GC using clinical samples, cell lines, and mouse models. Functional assays (CCK-8, colony formation, migration, invasion, TUNEL) demonstrated that TRAF1 promotes GC cell proliferation, migration, and invasion via OASL, while suppressing apoptosis. RNA-seq revealed that upregulation of TRAF1 and OASL, combined with H. pylori infection in gastric epithelial cells, enriched pathways associated with PANoptosis. Rescue experiments showed that TRAF1 knockdown increased PANoptosis, and this increase was attenuated by the pan-caspase inhibitor Z-VAD-FMK, whereas subsequent OASL overexpression reversed the suppression of PANoptosis caused by TRAF1 knockdown, whereas LPS further induced PANoptosis. Both in vitro and in vivo models confirmed that H. pylori infection triggers PANoptosis. Co-Immunoprecipitation assays uncovered a protein interaction between OASL and the ZBP1-PANoptosome. Critically, under H. pylori infection conditions, OASL overexpression rescued the PANoptosis suppressed by TRAF1 knockdown in gastric epithelial cells. This study demonstrates that H. pylori infection induces PANoptosis, and defines a pathway wherein TRAF1 promotes PANoptosis by regulating OASL-mediated activation of the ZBP1-PANoptosome. Our findings reveal a novel, context-dependent duality of the TRAF1/OASL axis: it promotes PANoptosis, contributing to mucosal damage during the precancerous inflammatory stage, yet in established GC, this axis appears to suppress PANoptosis, facilitating tumor progression. These insights provide a theoretical foundation for targeting this pathway in treating H. pylori-associated gastritis-cancer progression. - Source: PubMed
Publication date: 2026/04/06
Zhang MinglinYang XueerXie JieCai TingZhao XuelinLiu XiaomingWang Fen