MOP (OPIATES) Card
- Known as:
- MOP (OPIATES) Card
- Catalog number:
- ODZ-223
- Product Quantity:
- Tests in kit 20
- Category:
- -
- Supplier:
- Vidia
- Gene target:
- MOP (OPIATES) Card
Related genes to: MOP (OPIATES) Card
- Gene:
- MAVS NIH gene
- Name:
- mitochondrial antiviral signaling protein
- Previous symbol:
- -
- Synonyms:
- VISA, KIAA1271, IPS-1, Cardif
- Chromosome:
- 20p13
- Locus Type:
- gene with protein product
- Date approved:
- 2009-04-01
- Date modifiied:
- 2017-09-22
Related products to: MOP (OPIATES) Card
Related articles to: MOP (OPIATES) Card
- While mutations in tricarboxylic acid (TCA) cycle enzyme succinate dehydrogenase B (SDHB) are well-established drivers of renal cell carcinoma via the accumulation of the oncometabolite succinate, its precise role in renal fibrosis remains entirely unexplored. In this study, we demonstrate that SDHB is down-regulated in fibrotic kidneys. Tubule-specific knockdown of Sdhb exacerbated fibrosis, mitochondrial dysfunction, and inflammation in unilateral ureteral obstruction (UUO) mice, while its overexpression exerted protective effects. Mechanistically, SDHB deficiency induced succinate accumulation, which directly bound to residue Leu150 (L150) of voltage-dependent anion channel 1 (VDAC1), promoting VDAC1 oligomerization and triggering mitochondrial RNA (mtRNA) leakage. Cytosolic mtRNA activated the retinoic acid-inducible gene I (RIG-I)-mitochondrial antiviral signaling protein (MAVS) pathway, driving proinflammatory responses. Pharmacological inhibition of VDAC1 oligomerization by VBIT-4 attenuated mtRNA release. Furthermore, we identified E2F transcription factor 4 (E2F4) as an upstream transcriptional activator of SDHB, and overexpression of E2f4 restored SDHB expression and ameliorated renal pathology. These findings provide mechanistic insights into how TCA cycle disruptions and mtRNA leakage interactions drive renal inflammation, suggesting SDHB as a potential therapeutic target for renal fibrosis. - Source: PubMed
Publication date: 2026/09/18
Zhu ZijingChen PingShu HongxinZeng QinglinLuo QinghuaZhu WenpingYang LiYan TengFengZhu Xingen - Ring finger protein 5 (RNF5), a membrane-associated RING-type E3 ubiquitin ligase, serves as a critical regulator of cellular homeostasis by controlling protein stability, metabolic adaptation, and immune signaling. This review provides a comprehensive overview of the multifaceted functions of RNF5, with particular emphasis on its context-dependent roles in cancer progression, antiviral immunity, and non-neoplastic diseases. In cancer, RNF5 exhibits highly context-dependent and sometimes paradoxical functions that are influenced by cellular environments, disease stages, and substrate availability. RNF5 regulates tumor-associated metabolic reprogramming by targeting glutamine transporters and key regulators of lipid metabolism. Moreover, through interactions with autophagy-related proteins and Ephrin receptors, RNF5 modulates tumor growth, therapeutic resistance, and antitumor immune responses. These findings highlight RNF5 as a complex regulator of tumor biology with both oncogenic and tumor-suppressive potential. During viral infections, RNF5 demonstrates dual regulatory activities in host-pathogen interactions. On one hand, RNF5 can suppress antiviral innate immune signaling by promoting the ubiquitination and degradation of key immune adaptors, including STING and MAVS. On the other hand, RNF5 may restrict viral replication by directly targeting viral components, such as the SARS-CoV-2 envelope protein and foot-and-mouth disease virus VP1, for ubiquitination and degradation. Thus, RNF5 functions as a versatile modulator of antiviral defense, with effects determined by the specific viral context and host signaling landscape. Beyond cancer and viral infection, emerging evidence implicates RNF5 in a variety of non-neoplastic disorders. RNF5 contributes to protein quality control in neurodegenerative diseases by facilitating the clearance of pathological tau through the ERAD pathway. In addition, genetic inhibition of RNF5 ameliorates intestinal pathological phenotypes in a mouse model of cystic fibrosis, while RNF5 has also been associated with hepatic and cardiovascular injury responses through regulation of cellular stress pathways. From a therapeutic perspective, RNF5-targeting strategies, including small-molecule inhibitors and pathway modulators, have emerged as potential approaches for manipulating RNF5-associated biological processes. However, substantial challenges remain, including achieving target specificity, understanding the context-dependent consequences of RNF5 modulation, minimizing potential disruptions to proteostasis and innate immune regulation, and developing clinically feasible therapeutic interventions. This review summarizes the complex regulatory network governed by RNF5 and discusses future opportunities and challenges in translating mechanistic insights into therapeutic applications while carefully considering potential risks associated with RNF5 targeting. - Source: PubMed
Publication date: 2026/09/16
He RuobingWang JiaoLin MengjiaSu YuxinLi ZhuoranDong WeiZhang DanFengYu Xiaowen - 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 - Berberine is an isoquinoline alkaloid derived from various medicinal plants, including Coptis chinensis. Berberine exhibits multiple biological activities, including immune modulation, antibacterial activity, and antioxidant properties. Wenchang chicken is a local breed from Hainan Province, China, which is still primarily raised under free-range conditions. In this study, we compared the effects of dietary berberine supplementation on body measurements, weight, meat quality, serum immunoglobulin levels, antioxidant indices, liver transcriptome, proteome, and phosphoproteome in Wenchang chickens. Berberine had no significant effect on the body measurements and weights of Wenchang chickens. However, it significantly altered the color of the breast muscles and significantly reduced the shear force of the breast and leg muscles. Berberine also significantly increased serum Immunoglobulin A(IgA) and Immunoglobulin M(IgM) concentrations and glutathione (GSH) activity in Wenchang chickens, while significantly decreasing malondialdehyde (MDA) concentration. RNA-seq identified 764 differentially expressed genes (DEGs) in the liver. The significantly enriched GO terms were related to immune and inflammatory processes, such as cell chemotaxis, granulocyte migration, and chemotaxis. GSEA identified 50 gene sets, many of which were associated with immune regulation and inflammatory responses, such as Hedgehog signaling, interferon alpha response, and IL-6 JAK-STAT3 signaling. Liver proteomics identified 530 differentially abundant proteins (DAPs), some of which were associated with innate immune responses, such as mitochondrial antiviral signaling protein (MAVS), TNF receptor-associated factor 3 (TRAF3), and BH3-interacting domain death agonist (BID) in the Herpes simplex virus 1 infection pathway. Joint analysis of transcriptome and proteome revealed a highly significant positive correlation between mRNA expression and protein abundance in the liver. A total of 3,482 phosphorylated proteins containing 39,142 phosphorylation sites were identified in Wenchang chicken livers. Among these, 2,086 phosphorylation sites in 714 phosphorylated proteins were significantly upregulated, whereas 2,426 phosphorylation sites in 659 phosphorylated proteins were significantly downregulated in the livers of berberine-treated Wenchang chickens. These phosphoproteins were significantly enriched in KEGG pathways associated with defense, immune signaling regulation, and apoptosis, such as the mTOR signaling pathway, Salmonella infection, and autophagy. This study provided foundational data for the application of berberine in broiler production. - Source: PubMed
Publication date: 2026/06/25
Zhang XiaohuiQi YanxiaXu TieshanGu LihongWu LehuanPeng YihuiWang ShuyangLiang WuZheng Xinli - Mitochondria function not only as metabolic and bioenergetic centers but also as critical signaling hubs that integrate cellular context with innate immune response. The mitochondrial antiviral-signaling protein (MAVS), anchored to the outer mitochondrial membrane, is a central adaptor in the RIG-I-like receptor (RLR) pathway, orchestrating type I interferon (IFN) production and apoptosis. Although long regarded as a docking platform for RLR-derived signals, recent advances, particularly concerning its diverse post-translational modifications (PTMs), reveal MAVS as a dynamic integrator that decodes cellular stress and metabolic cues to fine-tune antiviral immunity. Canonical PTMs such as ubiquitination and phosphorylation highlight the importance of precisely controlling both the initiation and downregulation of MAVS signaling, but recent discoveries substantially broaden this regulatory landscape. Stress-responsive phosphorylation mediated via the ASK1-p38 MAPK pathway enhances MAVS signaling capacity under oxidative and ER stress, linking cellular damage to amplified interferon production. In parallel, a newly identified vitamin K-dependent carboxylation of MAVS reshapes downstream signaling by promoting interferon induction while restraining apoptosis, introducing a regulatory layer that may reflect the metabolic context surrounding GGCX activity, including vitamin K availability. Understanding this multilayered regulatory network not only redefines MAVS as a stress-sensitive mitochondrial signaling hub responsive to cellular context but also highlights new avenues for therapeutic modulation of innate immunity and cell fate during viral infection. This review summarizes emerging insights into PTM-mediated regulation of MAVS and outlines their broader implications for mitochondrial antiviral signaling. - Source: PubMed
Publication date: 2026/08/27
Morimoto NaoOkazaki Tomohiko