Tricyclic Antidepressant (TCA), Card
- Known as:
- Tricyclic Antidepressant (TCA), Card
- Catalog number:
- BQ 074-RTDA
- Product Quantity:
- 1/kit (x30)
- Category:
- Antibodies
- Supplier:
- Bioquant
- Gene target:
- Tricyclic Antidepressant (TCA) Card
Related genes to: Tricyclic Antidepressant (TCA), Card
- Gene:
- ASS1P11 NIH gene
- Name:
- argininosuccinate synthetase 1 pseudogene 11
- Previous symbol:
- ASSP11
- Synonyms:
- TCAG_1641141
- Chromosome:
- 7p15.3
- Locus Type:
- pseudogene
- Date approved:
- 1986-01-01
- Date modifiied:
- 2014-11-19
- Gene:
- CALM1P2 NIH gene
- Name:
- calmodulin 1 pseudogene 2
- Previous symbol:
- -
- Synonyms:
- TCAG_1643085
- Chromosome:
- 7p11.2
- Locus Type:
- pseudogene
- Date approved:
- 1995-11-02
- Date modifiied:
- 2016-06-27
- Gene:
- CCL1 NIH gene
- Name:
- C-C motif chemokine ligand 1
- Previous symbol:
- SCYA1
- Synonyms:
- I-309, TCA3, P500, SISe
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 1990-07-05
- Date modifiied:
- 2016-10-05
- Gene:
- CCL21 NIH gene
- Name:
- C-C motif chemokine ligand 21
- Previous symbol:
- SCYA21
- Synonyms:
- SLC, exodus-2, TCA4, CKb9, 6Ckine, ECL
- Chromosome:
- 9p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-04-10
- Date modifiied:
- 2016-10-05
- Gene:
- CDC26P1 NIH gene
- Name:
- cell division cycle 26 pseudogene 1
- Previous symbol:
- CDC26P
- Synonyms:
- TCAG_1970866
- Chromosome:
- 7q32.1
- Locus Type:
- pseudogene
- Date approved:
- 2003-11-24
- Date modifiied:
- 2013-01-17
Related products to: Tricyclic Antidepressant (TCA), Card
Related articles to: Tricyclic Antidepressant (TCA), Card
- The persistent threat of porcine epidemic diarrhea virus (PEDV) to the global swine industry is compounded by high neonatal piglet mortality and the absence of effective antiviral therapies. Host-directed strategies that reinforce immunity offer a promising avenue to counter viral immune evasion. Through screening of an FDA-approved compound library, we identify the small-molecule cyclocytidine hydrochloride (Cyclo-C) as a potent inhibitor of PEDV replication that acts by stabilizing the peroxisomal biogenesis factor PEX13, a previously unrecognized host restriction factor. The antiviral activity of Cyclo-C is strictly PEX13-dependent, as it is completely abrogated in PEX13 knockout cells. Mechanistically, Cyclo-C disrupts the interaction between PEX13 and the viral nonstructural protein 8 (NSP8), thereby preventing NSP8-mediated PEX13 degradation and the subsequent induction of PI3K/AKT/mTOR-driven pexophagy. Preservation of peroxisomal integrity stabilizes the peroxisome-localized pool of MAVS, leading to a robust enhancement of type III interferon (IFN-III) responses that suppress viral replication. Critically, this mechanism translates , where Cyclo-C treatment of PEDV-challenged piglets significantly reduces mortality, lowers viral loads, and protects intestinal villus architecture. Our findings establish Cyclo-C as a first-in-class host-directed therapeutic candidate and validate the concept that pharmacological preservation of peroxisome-mediated innate immunity represents an effective antiviral strategy against enteric coronaviruses. - Source: PubMed
Publication date: 2026/07/17
Lou JinxiuGuo ZhiweiChen KangTian YuanmingyueTang ZhenpengXin ZhendongJiang PingLiu GongguanWang Xianwei - Coordination between innate immune signaling and glucose metabolism is fundamental to organismal homeostasis, yet despite decades of study linking immunity and metabolism, the mechanisms by which metabolic cells restrain antiviral innate signaling while preserving glycolytic competence during overnutrition remain poorly defined. Here we identify Tetherin (BST2) as a unique cell-intrinsic immunometabolic checkpoint that couples restraint of type I interferon (IFN-I) signaling to preservation of glycolytic capacity in adipocytes. Tetherin localizes to endoplasmic reticulum and organizes an interactome enriched for antiviral sensing regulators and glycolytic control nodes in adipocytes. Mechanistically, Tetherin directly engages the ubiquitin-dependent degradation machinery NDFIP1 and RNF128 to terminate IRF3 activation, thereby limiting pro-inflammatory, anti-glycolytic signaling and protecting adipocytes from metabolic dysfunction. In parallel, multiomics integration reveals that Tetherin also acts as a scaffold that binds and spatially organizes and activates PFKFB3 to increase glycolytic capacity and restrain MAVS-IRF3 innate immune signalling. In vivo, adipocyte-specific loss of Tetherin amplifies high sucrose diet and high-fat-diet-induced glucose intolerance and liver steatosis, whereas overexpression of human Tetherin in adipocyte suppresses obesity-driven interferon signaling, restores glycolytic pathway, and improves metabolic homeostasis. Orthogonal perturbations in cancer and insulinoma cells further confirm an immunometabolic role for Tetherin. Together, these findings define Tetherin as a dual node immunometabolic checkpoint that couples restraint of antiviral innate inflammatory signaling to maintenance of glycolytic competence, thereby safeguarding adipocyte metabolic homeostasis. - Source: PubMed
Publication date: 2026/07/07
Cho Chung HwanJang YoungUkWarnock AidanYildiz RamazanJhang JingDavi KajalBrisnovali Niki FHuhn VictoriaWang PengBevaqua RominaGoedeke LeighSchotsaert Michael ABerisa MirelaPuleston DanielRajbhandari Prashant - Fowl adenovirus serotype 4 (FAdV-4) is the main pathogen causing hydropericardium‑hepatitis syndrome (HHS), which seriously endangers the poultry industry. Viperin, an interferon‑stimulated gene (ISG), possesses broad‑spectrum antiviral activity, but its role during FAdV‑4 infection remains unclear. In this study, the chicken viperin gene was cloned and expressed, and its sequence characteristics, protein structure and tissue distribution were systematically analyzed. By overexpressing or silencing viperin in chicken hepatocellular carcinoma (LMH) cells, the effect of viperin on FAdV‑4 replication was investigated; meanwhile, this study examined the expression levels of multiple factors associated with innate immune signaling pathways under different treatment conditions, to investigate the regulatory role of viperin in the innate immune response induced by FAdV‑4. The main results showed that chicken viperin is a ∼41 kDa protein predominantly composed of α‑helices and random coils, and is highly expressed in immune organs. Overexpression of viperin significantly reduced FAdV‑4 viral load and titer, whereas knockdown of viperin promoted viral replication. The expression levels of several innate immune factors, including LGP2, MDA5 and MAVS, varied under different conditions. This study preliminarily demonstrates that chicken viperin inhibits FAdV‑4 replication. By measuring the expression changes of multiple innate immune factors under different conditions, we analyzed and conjectured the innate immune regulatory mechanism of viperin against FAdV‑4. This research provides an important theoretical basis and potential molecular targets for the design of antiviral prevention and control strategies in poultry as well as for the development of next‑generation vaccine adjuvants. Moreover, it offers research directions and experimental ideas for further in‑depth dissection of the molecular mechanism by which viperin inhibits FAdV‑4. - Source: PubMed
Publication date: 2026/07/02
Wan LijunWang ShengZeng TingtingWang CanYa HouxunRen HongyuChen ZuoxinFan QingLi MengXie ZhixunLuo SisiYan MingXie Liji - In esophageal squamous cell carcinoma (ESCC), chemoradiotherapy potentiates the effects of immune checkpoint inhibitors (ICIs) by activating the tumor-intrinsic innate immune response. However, ESCC cells frequently suppress this activation, which contributes to the high rates of immunotherapy resistance (70-80%) observed clinically. Thus, identifying intracellular suppressors of this innate immune response remains an unmet critical need. Herein, through multi-omic analyses, we identify the chromatin assembly factor CHAF1A as a suppressor of the tumor-intrinsic innate immune response in ESCC. We found that CHAF1A was overexpressed in ESCC and negatively correlated with type I interferon production and CD8+ T-cell infiltration. Mechanistically, CHAF1A maintained heterochromatin silencing mediated by H3K9me3, thereby repressing endogenous retroviruses (ERVs). This suppression prevented the accumulation of double-stranded RNA (dsRNA) and the subsequent activation of the MAVS-IRF3 signaling pathway. Concurrently, CHAF1A preserved genomic stability, limiting the release of double-stranded DNA (dsDNA) and activation of the cGAS-STING pathway. Loss of CHAF1A potentiated the response to immunotherapy through the coordinated activation of these dual pathways. We then performed a small-molecule compound screen and identified a CHAF1A inhibitor, Baimaside, which enhanced the effect of anti-PD-1 therapy to augment antitumor immunity. Collectively, these data indicate that CHAF1A represents a potential therapeutic target for sensitizing ESCC to immunotherapy and provide a potential combination strategy for reversing immunotherapy resistance. - Source: PubMed
Publication date: 2026/07/16
Ma YueShi MengdeMa MingLi SiruCui NanaLi YingjueDang TianjiaoYang RuiBai YangWang BojunZhang ChunhuiLiu ChaoZhang Yanqiao - Chronic tissue inflammation causes progressive tissue damage, organ dysfunction, and increased susceptibility to inflammatory diseases. Viral infections are major drivers of this process, but the molecular mechanisms linking antiviral immune responses to persistent inflammation and tissue pathology remain poorly understood. - Source: PubMed
Publication date: 2026/07/15
Lu WentingXing JunjiWang JunyingMinze Laurie JLi Xian CZhang Zhiqiang