TCA Tricyclic Antidepresants Test Card
- Known as:
- TCA Tricyclic Antidepresants Test Card
- Catalog number:
- 4s00259
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Good Biotech Corp - GBC
- Gene target:
- TCA Tricyclic Antidepresants Test Card
Related genes to: TCA Tricyclic Antidepresants Test 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: TCA Tricyclic Antidepresants Test Card
Related articles to: TCA Tricyclic Antidepresants Test Card
- Intrinsic, cell-autonomous antiviral defenses can restrict infection without involving paracrine interferon (IFN) programs. Previous studies have demonstrated the importance of intact mitochondrial homeostasis in antiviral immunity. Mitochondrial antiviral signaling (MAVS) protein is a critical adaptor molecule in the RLR pathway that regulates IFN production in response to RNA viral infections. Here, we identify a potent intrinsic antiviral immunity that is orchestrated through stable mitochondria. We further identify MAVS as a regulator of mitochondrial import machinery whose activity is required for an IFN-independent antiviral state. Loss of MAVS leads to severe mitochondrial fragmentation, depolarization, and mitophagy, accompanied by diminished mitochondrial bioenergetics and protein import. Mechanistically, MAVS maintains mitochondrial integrity by maintaining the expression and assembly of the translocase of the outer membrane complex and sustaining the abundance of its core components. Restoration of MAVS expression reverses these defects and reinstates a robust antiviral state. Remarkably, this mitochondrial-driven immunity efficiently restricts SARS-CoV-2 replication even under IFN-deficient conditions and operates alongside the IFN pathways during infection by RNA viruses, such as the Japanese encephalitis virus. Our findings reveal a mitochondrial maintenance function of MAVS that operates in parallel to, and independently of, canonical interferon signaling during RNA virus infection. These findings highlight mitochondrial integrity as a common determinant behind a broad, collective antiviral immunity that involves both intrinsic and IFN-dependent mechanisms.IMPORTANCEHow do mitochondria contribute to the intrinsic cellular antiviral defense even when the primary immune arsenal is silenced? This work reveals that MAVS, long known for triggering interferon, acts as a vital bridge that stabilizes mitochondria to impart a potent intrinsic antiviral state against RNA viruses. We show that MAVS serves as a structural guardian of the organelle, a function it orchestrates by stabilizing the translocase of the outer membrane complex, the essential gateway for mitochondrial protein import. When MAVS is lost or targeted by viruses like SARS-CoV-2 and Japanese encephalitis virus (JEV), this gateway collapses, leading to organelle failure that viruses exploit. Crucially, we demonstrate that MAVS can restrict viral replication entirely independently of traditional interferon signaling. This discovery shifts our understanding of MAVS from a simple signal transducer to a multidimensional protector. By safeguarding the cell's "powerhouse," MAVS provides a fundamental layer of intrinsic immunity that remains active even when other immune responses are evaded. - Source: PubMed
Publication date: 2026/09/29
Sah VishalPotharaju Poojitha SaiNair Karthika SSahoo Prangya ParamitaPooja Ravicanti AbhiramBasu DebasmitaTandel DixitVaradarajan K SChauhan SantoshPatel Anant BahadurHarshan Krishnan Harinivas - 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