GGCX antibody (FITC)
- Known as:
- GGCX (anti-) (fluorecein)
- Catalog number:
- orb102658
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- GGCX antibody (FITC)
Related genes to: GGCX antibody (FITC)
- 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 (FITC)
Related articles to: GGCX antibody (FITC)
- - 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 - Studies in humans suggest that vitamin K is involved in the regulation of bone remodeling, but the precise mechanism at play remains unknown. In cells, vitamin K functions as a co-factor for the γ-glutamyl carboxylase (GGCX), an enzyme responsible for the conversion of glutamic acid residues (Glu) into γ-carboxyglutamic acid (Gla) residues in secreted proteins. We aim here at determining the role of γ-carboxylation in bone remodeling and at identifying the Gla protein(s) involved. We show that male mice lacking γ-carboxylation specifically in osteoblasts (Ggcx;OCN-Cre) have increased bone mass at 6 months of age due to a reduced number of multinucleated bone resorbing osteoclasts. In co-culture experiments, Ggcx-deficient osteoblasts were less effective than control osteoblasts at supporting osteoclast formation. Among known Gla proteins, we identify GAS6 as an osteoblast-secreted γ-carboxylated factor which signals to differentiating osteoclasts. The GAS6 receptors MerTK and AXL are expressed in pre-osteoclasts and pharmacological inhibitors of AXL and MerTK block osteoclast generation in co-culture. Conversely, recombinant γ-carboxylated GAS6 dose-dependently increases the size of osteoclasts and the number of nuclei per osteoclast in culture. GAS6 marginally affected the induction of osteoclast-specific genes during osteoclast differentiation but significantly increased pre-osteoclast fusion. Finally, increasing bone marrow GAS6 level in transgenic male mice was sufficient to increase the number and size of osteoclasts and to decrease bone mass. This work identifies GAS6 as a novel osteoblast-derived vitamin K-dependent protein regulating osteoclast maturation. - Source: PubMed
Publication date: 2026/04/28
Pata MonicaPham Diep Ngoc ThiLacombe JulieReddy B AshokKim Young WoongAhmed Abeer Gamal AliMurshed MonzurFerron Mathieu
- Source: PubMed