ROTA-Adeno Card
- Known as:
- ROTA-Adeno Card
- Catalog number:
- ODZ-122
- Product Quantity:
- Tests in kit 20
- Category:
- -
- Supplier:
- Vidia
- Gene target:
- ROTA-Adeno Card
Related genes to: ROTA-Adeno 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: ROTA-Adeno Card
Related articles to: ROTA-Adeno Card
- Coronaviruses have persistently triggered global pandemics in the 21 century, featuring either high transmissibility or high pathogenicity. A hallmark of these infections is the delayed activation of innate immune responses, resulting in dysregulated antiviral signaling and uncontrolled viral replication. Multiple viral proteins and hijacked host proteins contribute to immune evasion, representing potential therapeutic targets. Here, we identify viral ORF9b as a conserved accessory protein across the Sarbecovirus subgenus that consistently suppresses innate immune responses by recruiting the protein phosphatase, Mg/Mn-dependent 1A (PPM1A). Mechanistically, PPM1A exerts dual roles by directly dephosphorylating ORF9b and indirectly downregulating STAT2 phosphorylation, thereby suppressing RIG-I/MAVS and JAK-STAT signaling pathways. The PPM1A inhibitor SMIP-031 inhibits coronavirus replication and restores the antiviral innate immune homeostasis. These findings reveal a conserved immune-evasion strategy in sarbecoviruses and highlight the ORF9b-PPM1A axis as a potential target for broad-spectrum sarbecovirus therapeutics to help prevent future pandemics. - Source: PubMed
Publication date: 2026/09/27
Xie LixiangHuang ZiyeZhang ZhiyuanZhu YiqiangLiu XiaoqingWang LeiBi TongyuLiang TaizhenLai JintaoHu MeilinQiu GuochangXiao ShiqiLiu SenLiu YaomingRao HaiyueChen TaoPeng HaojieZhang BinTang JiaLi QianyingLi YaxinHou YuxinYang WeiboJiang HeweiMa Xiancai - Endogenous double-stranded RNA (dsRNA) links disrupted RNA homoeostasis in cancer to innate immunity. Tumour-associated dsRNA arises from complementary repeat transcripts, mitochondrial transcriptional imbalance, defective RNA processing and cellular stress. Its immunogenicity depends on ligand structure, editing, persistence, localisation, sensor access and pathway competence. ADAR1 and RNA-binding or decay factors buffer self-dsRNA, allowing tumour cells to tolerate potentially immunogenic RNA. Disruption of this control engages RIG-I-MAVS, MDA5-MAVS, TLR3-TRIF, PKR-eIF2α, and OAS-RNase L pathways; Z-conformation RNA can activate ZBP1. Outputs include interferon responses, translational arrest, RNA degradation, and regulated cell death, which can promote antigen presentation and immune-cell recruitment or drive chronic interferon adaptation, suppressive inflammation and treatment resistance. This Review examines critical-target and cumulative-burden models, methods for ligand identification, biomarker-guided patient selection and therapeutic strategies based on viral mimicry, ADAR1 targeting, engineered dsRNA agonists, and delivery platforms. - Source: PubMed
Publication date: 2026/09/26
Li ShaopingHuo YanfeiFa HangweiHan LinyuLuan HuiwenHan PengxiaoLiu YiZheng LixinLiu ChangFan KaiyueZhang NashaYang Ming - Herpesviruses establish lifelong persistence through acute replication, immune evasion, latency, and reactivation. Nucleotide-binding oligomerization domain-like receptors (NLRs) are most commonly discussed in the context of inflammasome sensors, pyroptosis, and IL-1 family cytokines. Here, we depart from this canonical framework to focus on three regulatory NLRs-NLRC3, NLRC5, and NLRX1-that act outside inflammasome assembly. Using HSV-1 as the central model and other herpesviruses as comparators, we propose a conceptual framework in which these NLRs modulate three host-control layers: cGAS-STING-dependent DNA sensing, MHC class I antigen presentation, and MAVS-mediated mitochondrial antiviral signaling. We explicitly frame these NLRs as regulatory hypotheses for HSV-1 biology rather than established restriction factors, and we provide prioritized, falsifiable predictions to guide future experimentation. Current evidence is strongest at the pathway level; direct tests of NLRC3, NLRC5, and NLRX1 in acute infection, latency, and reactivation remain necessary. The evidence is asymmetric: NLRC3 has been functionally tested in HSV-1-infected cells and mice, whereas direct HSV-1 regulation by NLRC5 or NLRX1 remains unestablished. Comparative herpesvirus and pathway studies, therefore, support testable hypotheses for NLRC5 and NLRX1 in acute infection, latency and reactivation. - Source: PubMed
Publication date: 2026/08/28
Zhu MengtingZhao ShuaiSun XingWang ShuhanHou ShiyuanShen XingZhou JielinLiu ZiyuWu XinganLiu Rongrong - Atopic dermatitis (AD) and psoriasis (PsO) are chronic inflammatory skin diseases with distinct features, but clinical and molecular overlap exists. These ambiguous phenotypes complicate diagnosis and treatment, and their immunologic basis remains poorly defined. This study aimed to delineate compartment-specific immune profiles in AD-PsO overlap lesions and explore candidate markers associated with molecular stratification. - Source: PubMed
Publication date: 2026/09/25
Lee JongeunChun Yookyung SophieNam Hyo JeongHuh Yun JungKim JaehwanKrueger James GPaik Seung SamKim Hyun JeJin Seon-PilKim Jeong Eun - The DNA damage response (DDR) is increasingly recognized not only as a genome-maintenance network and source of synthetic-lethal vulnerabilities, but also as a regulator of tumor immunity. DDR defects and pharmacologic inhibition can increase neoantigen formation, generate micronuclei and cytosolic nucleic acids, activate cGAS-STING, DNA-PK-NF-κB, and ERV-driven RIG-I/MDA5-MAVS signaling, and alter antigen presentation and immune checkpoint expression. However, the same processes may also promote chronic interferon tolerance, PD-L1 induction, lymphocyte stress, myeloid suppression, extracellular cGAMP degradation, stromal exclusion, and treatment resistance. This review frames DDR targeting around damage-to-immunity conversion, asking when DNA damage becomes a productive antitumor immune signal and when it does not. We summarize targetable DDR modules across cancer types, examine tumor-intrinsic and host-cell sensing mechanisms, and discuss antigen-processing defects, STING regulation, and microenvironmental barriers that shape divergent outcomes. We further review PARP, ATR, WEE1, ATM, and DNA-PK inhibitor combinations with immunotherapy and other treatment modalities, emphasizing clinical evidence, scheduling, and host-cell toxicity. Finally, we propose a modular biomarker framework integrating genomic, functional, immune-context, spatial and dynamic readouts to guide patient selection, treatment adaptation, and precision therapeutic decision-making. - Source: PubMed
Publication date: 2026/09/23
Qiao YihuanKang BoyuZhang JianZhang RuiLi Jipeng