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
- Takayasu arteritis (TAK) is a refractory chronic vasculitis of the aorta and its major branches, characterized by unsatisfactory treatment responses and high relapse rates. This review synthesizes current evidence to propose and elaborate a novel pathogenic paradigm: a self-reinforcing "metabolism-epigenetics-inflammation" feedback loop that sustains chronic vascular inflammation in TAK. We detail how immunometabolic reprogramming in immune and vascular wall cells not only meets bioenergetic demands but also generates metabolites (e.g., acetyl-CoA, lactate) that serve as substrates or cofactors for epigenetic modifications. These modifications, in turn, lock in a persistent pro-inflammatory gene expression profile. A central focus is the dissection of the ANK2-MAVS-IL-8 axis, a critical link connecting genetic susceptibility (via ANK2 variants) through mitochondrial dysfunction to sustained, IL-8-driven vascular injury. Building on this mechanistic framework, the review explores the translational potential of emerging biomarker candidates (e.g., IL-8, specific methylation marks) and proposes stratified therapeutic strategies that target distinct nodes within this interactive network, including metabolic drivers, epigenetic stabilizers, and inflammatory effectors. Ultimately, this work provides an integrated conceptual and translational roadmap for advancing precision medicine in TAK. - Source: PubMed
Publication date: 2026/04/03
Xie TianjianZhang LeyuLi ShurongXu BenmoZhang XinyuWang YajunShang ZixiangXi HongxuanShi HanNi XinLi PingLi Hengxi - Human cytomegalovirus (HCMV) encodes the viral mitochondria-localized inhibitor of apoptosis (vMIA) protein which blocks host cell apoptosis. vMIA also inhibits innate immune signaling through the DNA sensing cGAS-STING pathway and the RNA sensing RLR pathway which interacts with the mitochondrial adapter protein MAVS. We demonstrate stable expression and mitochondrial localization of vMIA in a human Mueller cell line (MIO-M1). In a real time apoptosis assay, vMIA significantly reduced staurosporine (STS)-induced apoptosis in MIO-M1 cells. In addition, immunoblots indicated that vMIA blocked apoptotic cleavage of the nuclear enzyme PARP1. vMIA also reduced STS mediated necrosis at later time points in MIO-M1 cells. The steady state level of cGAS protein was increased in vMIA expressing MIO-M1 cells. In contrast, vMIA decreased the amount STING protein in MIO-M1 cells. A decrease in the percentage of aggregated mitochondrial antiviral-signaling protein (MAVS), and alteration of the classic mitochondrial localization of MAVS, in the presence of vMIA suggested that vMIA induced changes in mitochondrial morphology in MIO-M1 cells. Activation of NF-κB by stimulators including LPS, poly I:C, hrTNFα, and zymosan was significantly reduced in MIO-M1 cells expressing vMIA. The transduction efficiency of a lentiviral gene delivery vector was not reduced in the presence of vMIA. These results represent the first demonstration of the anti-apoptotic and anti-innate immune signaling capabilities of vMIA in a human retinal cell line. The dual functions of vMIA could provide an effective strategy to treat multiple neurodegenerative diseases and also reduce gene therapy induced ocular inflammation. - Source: PubMed
Publication date: 2026/04/10
Sauter Monica MNoel Hongyu RBrandt Curtis R - The DNA sensing signaling pathway mediated by cGAS-STING has achieved significant progress in cancer therapy. However, the role of the RNA sensing signaling pathway mediated by RLRs-MAVS in cancer has been relatively underexplored. In this review, we first elaborate on the structural basis, activation, and regulatory mechanisms of MAVS, and examine its functional interplay with other innate immune pathways. We then comprehensively review its functions in cancer. Finally, we summarize its potential clinical applications, existing challenges, and proposed solutions. Moreover, we compare MAVS with STING across these three dimensions and find that they exhibit similarities in signaling pathways, perform analogous functions in cancer, and share comparable potential for clinical applications. Therefore, we propose that MAVS could emerge as the next STING in cancer therapy. - Source: PubMed
Publication date: 2026/04/08
Li SiyingBai JunqiangWang XinmiaoGuo ShutianGuo XiaomengShang ZhengjunShao Zhe - Long interspersed nuclear element 1 (LINE-1 or L1) retrotransposons pose a significant threat to somatic genomic integrity and are a source of sterile inflammation. Consequently, L1 activity is stringently controlled by multiple regulatory layers to ensure silencing, while its transcriptional derepression is linked to aging and age-related diseases. Recent studies have revealed complex interrelationships between L1 and cGAS, but whether cGAS regulates L1 transcription and its biological significance remains unclear. Here, we demonstrate that human cGAS activates L1 transcription by upregulating the transcriptional regulators CTCF and RUNX3. This cGAS-mediated promotion of L1 transcription is absent in mice due to functional divergence in CTCF and RUNX3. Furthermore, cGAS-mediated elevation of L1 mRNA promotes cellular senescence via MAVS, a key RNA-sensing pathway component. Together, our findings reveal a novel role of cGAS in activating L1 transcription and define a cGAS-L1-MAVS senescence pathway, thereby bridging the noncanonical function of cGAS and the RNA-sensing signaling. - Source: PubMed
Chen ZhixiChen LingjiangChen XinyuWang HaoTang HuanyinZhen ZhengyiJiang YingMao ZhiyongChen Yu - Ubiquitination is a pivotal post-translational mechanism regulating antiviral innate immunity. TRIM28, a member of the transcription intermediary factor 1 (TIF1) subfamily of the TRIM protein family, has been implicated in the modulation of retinoic acid-inducible gene I (RIG-I) signaling. However, the molecular basis and relevance remain unclear. - Source: PubMed
Publication date: 2026/03/24
Xin RuihuaZou WenshuQiu ZhengyingHuang LinaJing XiaohanHuang QilinZhu ZixiangLi JianxiGarigliany Mutien-Marie