GGCX antibody
- Known as:
- GGCX (anti-)
- Catalog number:
- orb29075
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- GGCX antibody
Related genes to: GGCX antibody
- Gene:
- GGCX NIH gene
- Name:
- gamma-glutamyl carboxylase
- Previous symbol:
- -
- Synonyms:
- VKCFD1
- Chromosome:
- 2p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-04
- Date modifiied:
- 2019-04-23
Related products to: GGCX antibody
Related articles to: GGCX antibody
- Mitochondria function not only as metabolic and bioenergetic centers but also as critical signaling hubs that integrate cellular context with innate immune response. The mitochondrial antiviral-signaling protein (MAVS), anchored to the outer mitochondrial membrane, is a central adaptor in the RIG-I-like receptor (RLR) pathway, orchestrating type I interferon (IFN) production and apoptosis. Although long regarded as a docking platform for RLR-derived signals, recent advances, particularly concerning its diverse post-translational modifications (PTMs), reveal MAVS as a dynamic integrator that decodes cellular stress and metabolic cues to fine-tune antiviral immunity. Canonical PTMs such as ubiquitination and phosphorylation highlight the importance of precisely controlling both the initiation and downregulation of MAVS signaling, but recent discoveries substantially broaden this regulatory landscape. Stress-responsive phosphorylation mediated via the ASK1-p38 MAPK pathway enhances MAVS signaling capacity under oxidative and ER stress, linking cellular damage to amplified interferon production. In parallel, a newly identified vitamin K-dependent carboxylation of MAVS reshapes downstream signaling by promoting interferon induction while restraining apoptosis, introducing a regulatory layer that may reflect the metabolic context surrounding GGCX activity, including vitamin K availability. Understanding this multilayered regulatory network not only redefines MAVS as a stress-sensitive mitochondrial signaling hub responsive to cellular context but also highlights new avenues for therapeutic modulation of innate immunity and cell fate during viral infection. This review summarizes emerging insights into PTM-mediated regulation of MAVS and outlines their broader implications for mitochondrial antiviral signaling. - Source: PubMed
Publication date: 2026/08/27
Morimoto NaoOkazaki Tomohiko - The maturation of key coagulation factors requires γ-carboxylation catalyzed by γ-glutamyl carboxylase (GGCX), in which vitamin K hydroquinone (VKH) is oxidized to vitamin K epoxide (VKO) and recycled by vitamin K epoxide reductase (VKORC1). Clinically, vitamin K antagonists (VKAs) inhibit VKORC1 but are thought not to target GGCX. Here, we demonstrate that a member of VKA, anisindione and its analogs can dock within the VK-binding pocket of GGCX. Importantly, both in vitro and cell-based γ-carboxylation assays showed that anisindione inhibits GGCX activity. Furthermore, our cryo-electron microscopy structure of the GGCX-BGP (bone Gla protein or osteocalcin)-anisindione complex reveals that anisindione directly occupies the VK-binding pocket of GGCX, consistent with competitive inhibition with VK. These results establish anisindione as a structural prototype for direct GGCX inhibition and provide a structural framework for developing anticoagulants beyond VKORC1. - Source: PubMed
Publication date: 2026/08/27
Zhou NingWang RongChen BaozhiLi JieTie Jian-KeLiu FangyuQi Xiaofeng - - Source: PubMed
Publication date: 2026/08/03
Zou JiahuiJiang MeijunXiao RongSun HuiminLiu HailongPeacock ThomasTu ShaoyuChen TongGuo JinliZhao YaxinBarclay WendyXie ShengsongZhou Hongbo - Pulmonary arterial hypertension (PAH) is a progressive, fatal disease of the pulmonary vasculature characterized by obliterative remodeling of small pulmonary arteries, leading to sustained elevation of pulmonary vascular resistance, right ventricular failure, and premature death. The diagnostic gold standard remains right heart catheterization, requiring a mean pulmonary artery pressure greater than 20 mmHg at rest, a pulmonary arterial wedge pressure of 15 mmHg or below, and a pulmonary vascular resistance exceeding 2 Wood units. PAH is an autosomal dominant disorder with markedly incomplete penetrance of approximately 20-30%, indicating that germline mutations alone are insufficient to cause disease. Disease manifestation requires additional "second hits", including chronic hypoxia, systemic inflammation, hemodynamic stress, hormonal influences, and common genetic modifiers such as single-nucleotide polymorphisms (SNPs). This genetic and environmental complexity underpins the broad clinical heterogeneity observed across PAH subtypes, which include idiopathic PAH, heritable PAH, and disease associated with connective tissue disorders, HIV infection, portal hypertension, congenital heart disease, schistosomiasis, and drug or toxin exposure. This review provides a comprehensive and critical appraisal of the molecular-genetic architecture of PAH. Thirty genes have now been implicated in disease pathogenesis, spanning seven functional categories: receptors of the TGF-β/BMP signaling family (, , , ); circulating BMP ligands (, ); transcription factors (, , , , , , ); membrane and polyamine transporters (, ); potassium channel regulators (, , ); metabolic and mitochondrial genes (, , ); signaling receptors and structural proteins (, , , ); vasoactive and extracellular matrix regulators (, , ); and epigenetic regulators (, ). Among these, is the dominant contributor, accounting for 53-86% of heritable PAH and 14-35% of idiopathic cases. The remaining genes each account for fewer than 5% of cases individually, collectively reflecting a broad landscape of rare and ultra-rare genetic contributions. For each gene, we critically evaluate the strength of genetic evidence, pathogenic mechanisms, degree of mechanistic resolution, and clinical relevance. We further discuss the contribution of emerging technologies, including whole-genome sequencing, single-cell and spatial transcriptomics, multi-omics integration, iPSC-derived vascular models, and artificial intelligence, to expanding the PAH genetic architecture beyond single-gene discovery. A key theme across this landscape is convergence: despite mechanistic diversity at the gene level, most PAH-associated variants ultimately impair endothelial quiescence, promote smooth muscle proliferation, and drive apoptosis resistance through disruption of BMP signaling amplitude, transcriptional stability, ion channel homeostasis, metabolic integrity, or epigenetic regulation. This convergence supports both a unified therapeutic rationale and a precision medicine framework for genotype-stratified intervention in PAH. - Source: PubMed
Publication date: 2026/05/29
Okot MarkAhmed AneesaWright Colin WNasim Md Talat - Stroke is a severe cerebrovascular disease characterized by narrow time windows and complications. This study aimed to identify novel drug targets and repurposed drugs for stroke. - Source: PubMed
Publication date: 2026/06/23
Zhang XiaZhang Yi-MingLi Ji-LaiWang WeiTu Wen-JunWang Hong-Qi