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
- Birds routinely solve high-speed, three-dimensional collision-avoidance problems that
remain a central challenge for autonomous micro-aerial vehicles (MAVs). While pairwise
avoidance is well studied in budgerigars, comparatively little is known about how
avoidance kinematics change when more than two birds must simultaneously resolve a
potential collision-the regime in which distributed control becomes attractive for MAV
swarms. Using an openly available stereo-camera dataset (n = 150 1v1, n = 80 2v2,
n = 30 3v3 trials), we extracted nine kinematic indices per encounter and tested for
group-size effects using dual statistical frameworks supplemented by stratified,
subsampling-robustness and noise-floor sensitivity analyses. The two most robust findings
are (i) that the optic-flow time-to-contact margin τ is qualitatively conserved across group
sizes (the time-course is preserved while the absolute margins compress with group size),
and (ii) that the minimum inter-bird separation does not shrink with group size and in
fact grows mildly. By contrast, evidence that birds in the 3v3 condition react later,
modulate forward speed less, or fly more curved paths is conditionally supported at best:
the reaction-distance effect replicates in only 19.5% of subsampled iterations, and the
path-complexity effects are significant only after trial-level aggregation. The agility
metrics (peak lateral acceleration and minimum turn radius) are heavily confounded with
tracking noise; a majority of 3v3 encounters fall below the empirical noise floor and these
values should not be used as an engineering target. These observations are consistent
with-but do not strongly mandate-a bioinspired design hypothesis in which a fixed
τ-based visual policy is paired with a group-size- adaptive reaction threshold. A
proof-of-concept multi-agent simulation of this controller resolves pairwise head-on
encounters reliably (100% collision-free) but degrades sharply with group size and density,
indicating that a purely reactive single-threat policy is insufficient for swarm-scale
operation and that an explicit multi-threat coordination mechanism is required. - Source: PubMed
Publication date: 2026/09/30
Tawhid S MMohim Abdul KaderAli Sk ShahedHaque Tanzil Kazi TanzizulBhowmik AbhijitKarmaker Debajyoti - Flying insects are agile and can withstand impacts and compression because of their low inertia and resilient wings, exoskeletons, and muscles. These capabilities inspire the development of micro aerial vehicles (MAVs) for surveillance, disaster response, and environmental monitoring in confined or hazardous spaces. However, MAVs, especially subgram flapping-wing platforms, remain fragile because they rely on rigid components in their wings, transmissions, or actuators. We report a resilient all-polymer flying robot weighing 185 milligrams, powered by an electrostrictive bending actuator that directly drives cone-shaped compliant wings without a transmission. The actuator achieves a power density of 1600 watts per kilogram and a bending angle of 136° at 110 hertz, enabling the flying robot to achieve a lift-to-weight ratio of 3.0 and a lift-to-power ratio of 8.3 millinewtons per watt at 30 hertz. The robot demonstrates unaided takeoff with an average ascending speed of 40 centimeters per second. Thanks to its compliant and transmission-free structure, the robot can resume flight after being hit by a flyswatter or flattened by heavy loads. The robot design features mechanical simplicity and resilience, promising a paradigm for subgram flight in harsh environments. - Source: PubMed
Publication date: 2026/09/30
Zhu YuanWu HanxiangSun DaweiBudiman WilliamLiu KedeChen YufengYan WenzhongPei Qibing - 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