Recombinant Human GP73 /GOLM1 Protein
- Known as:
- Recombinant Human GP73 /GOLM1 Protein
- Catalog number:
- gp-879
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Proxinobio
- Gene target:
- Recombinant Human GP73 /GOLM1 Protein
Related genes to: Recombinant Human GP73 /GOLM1 Protein
- Gene:
- GOLM1 NIH gene
- Name:
- golgi membrane protein 1
- Previous symbol:
- GOLPH2, C9orf155
- Synonyms:
- GP73, FLJ23608, bA379P1.3
- Chromosome:
- 9q21.33
- Locus Type:
- gene with protein product
- Date approved:
- 2001-04-27
- Date modifiied:
- 2015-08-25
Related products to: Recombinant Human GP73 /GOLM1 Protein
Related articles to: Recombinant Human GP73 /GOLM1 Protein
- Accurate early screening for hepatocellular carcinoma (HCC) requires multi-target detection methods with high sensitivity and strong anti-interference capability. In this study, we developed an aptamer-mediated SERS sensing method based on bimetallic magnetic nanotubes for the simultaneous detection of HCC markers alpha-fetoprotein (AFP) and Golgi protein 73 (GP73). Tubular FeO nanostructures were innovatively synthesized as magnetic carriers, onto which a gold-layer, an internal standard molecule (4-mercaptophenylboronic acid), and a silver-layer were sequentially deposited to construct a capture substrate integrating signal calibration and electromagnetic enhancement functions. Raman tags with non-overlapping spectra in the Raman-silent region (1800-2500 cm) were screened to establish a sandwich detection system. Using a portable Raman spectrometer and intelligent software, this method achieved rapid quantification of AFP and GP73, with detection limits of 0.433 pg/mL and 0.370 pg/mL, respectively, and recovery rates in spiked serum samples ranging from 95.62% to 106.2%. By simply replacing the aptamers, this method can be readily extended to other targets, demonstrating excellent versatility. This work provides a reliable analytical tool for early HCC diagnosis and establishes a foundation for developing on-site multi-target detection systems for complex samples. - Source: PubMed
Publication date: 2026/04/09
Wang YingDong XiaoyuLiu FaqiangLi YanLi HonghaoZhang YingGuan Ming - To identify oxidative stress (OS)-related genes involved in type 2 diabetes mellitus (T2DM) and screen potential Traditional Chinese Medicine (TCM) candidates for therapeutic use. - Source: PubMed
Jingnan H UMan LiaoZhongwen X IJing SongYining WangTao H E - Hepatic fibrosis, a hallmark of chronic liver diseases, arises from persistent activation of hepatic stellate cells (HSCs). Golgi protein 73 (GP73) is a recognized fibrosis biomarker, yet its active role in driving fibrogenesis and the underlying molecular mechanisms remain poorly defined. Using wild-type, GP73 knockout, and knock-in mouse models, we demonstrate that GP73 expression is not merely a marker but a key functional modulator of fibrotic progression, correlates strongly with fibrosis severity. While these genetic models do not develop spontaneous hepatic fibrosis under basal conditions-notwithstanding the potential metabolic roles of GP73-our results demonstrate that GP73 expression levels significantly dictate the severity of CCl-induced fibrotic progression. Mechanistically, endogenous co-immunoprecipitation (Co-IP) revealed that GP73 physically interacts with TGF-β receptor 1 (TGFBR1), mTOR, and the recycling endosome marker Rab11. GP73 enhances HSC activation by amplifying TGF-β and mTOR signaling through the inhibition of key fibrotic factors' degradation, such as TGFBR1 and mTOR. Protein half-life and rescue experiments confirmed that GP73 prevents the lysosomal degradation of TGFBR1 and mTOR; notably, re-introducing GP73 into knockdown cells successfully restored receptor stability and downstream signaling. Furthermore, pharmacological disruption of endocytic trafficking with Brefeldin A (BFA) abolished the protective effect of GP73, leading to accelerated receptor degradation. Suppressing GP73 reduced HSC activation and attenuated collagen deposition in vivo. Our findings identify GP73 as a molecular scaffold that reroutes fibrotic signaling complexes into the recycling pathway and away from degradation. Consequently, our results position GP73-mediated endocytic recycling as a potential therapeutic target and a viable adjunctive strategy for managing chronic liver diseases. - Source: PubMed
Publication date: 2026/04/17
Guo YueLiu Meng-YuanMo Yun-QiWan Lin-YanWang Ya-NanWang Sheng-YongNi Yi-RanLi Zhi-YingWang YingWang Xiao-LianMa LanZhang Rui-TaoZhang Yan-QiongLiu Chang-BaiZhang Hong-BingLi Bo-TaoWu Jiang-Feng - The microRNA (miR) cluster miR-143/145 represents a well-characterized tumor-suppressive regulatory system with a multifaceted role in prostate cancer. Both miRs are consistently downregulated during disease progression, and their loss is associated with enhanced proliferation, invasion, epithelial–mesenchymal transition, and metastatic competence. Mechanistically, the cluster modulates Rat Sarcoma Viral Oncogene Homolog (RAS)-Mitogen Activated Protein Kinase (MAPK) signaling via Kirsten Rat Sarcoma Viral Oncogene Homolog (KRAS) and Extracellular Signal-Regulated Kinase 5 (ERK5), Tumor Protein p53 (p53)-dependent growth control through MYC Proto-Oncogene, Basic Helix-Loop-Helix Transcription Factor (c-MYC) repression, apoptosis via B-Cell Lymphoma 2 Interacting Protein 3 (BNIP3), and cytoskeleton-associated motility factors including Fascin Actin-Bundling Protein 1 (FSCN1), Human Enhancer of Filamentation 1/ Neural Precursor Cell Expressed, Developmentally Down-Regulated Protein 9 (HEF1/NEDD9), Golgi Membrane Protein 1 (GOLM1), and Fibronectin Type III Domain Containing 3B (FNDC3B). Downregulation is mainly driven by p53 dysfunction, promoter methylation, and RAS-dependent transcriptional repression. A defining feature is pronounced cell-type specificity, with tumor-suppressive effects in epithelial cells and context-dependent pro-angiogenic functions in stromal compartments, with direct translational relevance. Clinically, miR-143/145 contribute to multimarker diagnostic signatures, while reduced miR-145 correlates with adverse pathology and biochemical recurrence. Preclinical replacement strategies reduce tumor growth and enhance docetaxel sensitivity, yet context-dependent effects necessitate cell type-specific delivery. Overall, the cluster represents a central regulator with diagnostic, prognostic, and therapeutic potential requiring prospective validation. - Source: PubMed
Publication date: 2026/04/11
Stope Matthias BErb Holger H H - To investigate the expression of Golgi membrane protein 1 (GOLM1) in oral squamous cell carcinoma (OSCC) and its effects on proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) in OSCC cells and the underlying mechanisms. - Source: PubMed
Li ShouchengWen CaiYu LiChen JunliangFeng Hao