Human Copine-1 CPNE1
- Known as:
- Human Copine-1 CPNE1
- Catalog number:
- C590
- Product Quantity:
- l0
- Category:
- -
- Supplier:
- Novoprotein
- Gene target:
- Human Copine-1 CPNE1
Ask about this productRelated genes to: Human Copine-1 CPNE1
- Gene:
- CPNE1 NIH gene
- Name:
- copine 1
- Previous symbol:
- -
- Synonyms:
- CPN1
- Chromosome:
- 20q11.22
- Locus Type:
- gene with protein product
- Date approved:
- 1999-02-09
- Date modifiied:
- 2016-01-26
Related products to: Human Copine-1 CPNE1
Related articles to: Human Copine-1 CPNE1
- Myopia, a complex condition influenced by genetic and environmental factors, is an increasing global health concern, and its underlying mechanisms remain unclear. Genome-wide association studies (GWAS) meta combined with summary-data-based Mendelian randomization (SMR) is a robust tool to identify novel regulatory genes associated with myopia. - Source: PubMed
Publication date: 2026/03/26
Jia LanboWei PinghuiWang YiningXia ZitianGao ShanWang YanHan Guoge - Patients with diabetes exhibit an increased susceptibility to vascular calcification, which is associated with significantly elevated risks of mortality and disability. As a new Glucagon-like peptide-1 receptor agonist, Semaglutide is primarily indicated for type 2 diabetes mellitus and obesity, while also demonstrating definitive cardiovascular protective effects. However, the effect of semaglutide on diabetic vascular calcification remains unknown. Our results demonstrated a dose-dependent reduction in calcium deposition with Semaglutide treatment, which was accompanied by downregulation of RUNX2 and BMP2 protein expression in aortic tissues. Additionally, Semaglutide also conferred protective effects in AGE-BSA stimulated mouse aortic smooth muscle cells (MOVAS). Autophagy, a lysosomal degradation pathway, is intimately involved in the pathological process of diabetic vascular calcification. During stimulation with AGEs-BSA, impaired lysosomal function and blocked autophagic flux were observed, as evidenced by increased protein levels of LC3-II and P62, alongside decreased expression of CTSD, CTSB, LAMP1 and LAMP2. These changes were accompanied by a decline in lysosomal pH, activity, and degradative capacity. Treatment with Semaglutide mitigated these abnormalities, restoring autophagic flux and lysosomal function, and consequently attenuating AGEs-BSA-induced calcification in MOVAS. Combined bioinformatics and Western blot analysis confirmed the significant downregulation of CPNE1 by Semaglutide in AGEs-BSA stimulated MOVAS. Copine-1 (CPNE1), a member of the copine protein family, is characterized as a calcium-dependent phospholipid-binding protein that primarily resides in the cytoplasm. These findings indicate that the attenuation of diabetic vascular calcification (DVC) by Semaglutide is associated with the inhibition of CPNE1-mediated autophagy, suggesting a potential novel therapeutic strategy for managing DVC. - Source: PubMed
Publication date: 2026/03/07
Xiao ShengjueLi WeiLiu Naifeng - Neuroblastoma (NB) is the most prevalent extracranial solid tumor in children. Therefore, urgent exploration of novel therapeutic targets and more effective approaches is imperative to enhance the prognosis of these children. - Source: PubMed
Publication date: 2025/11/01
Yang ZhengeZhang YunlongWang Shan - Vascular leakage is a major cause of multiple organ failure and mortality in sepsis, and factors that regulate endothelial integrity could serve as promising biomarkers of septic shock development. Copine family members (CPNEs) are well-characterized as soluble membrane-binding proteins, whether CPNEs play a critical role in maintaining vascular integrity during sepsis, however, remains unclear. - Source: PubMed
Publication date: 2025/11/19
Pan MingliangLi ZhixinWang XiaohongYang TianyuanLi JingqiHuang WeiFan HongkuanKesten Nebahat EcePeng TianqingZhan LiyingFan Guo-Chang - The causal relationship between gut microbiota (GM) and white matter injury and communication remains unclear. We aimed to scrutinize the plausible causal impact of GM on white matter hyperintensities (WMHs), white matter microstructure, white matter connectivity, and multiple neurological diseases via Mendelian randomization study. We identified four WMH-related bacterial taxa, including class , order , family , and genus In addition, three bacterial taxa were discovered that have consistent effect on multiple aspects of white matter microstructure. Furthermore, we found 12 strong associations between genetic liability in GM and white matter connectivity. Among these bacterial taxa, the family demonstrated a protective effect against ischemic stroke (IS). The genus showed protective effect on IS and small vessel stroke while posed a risk effect on neuromyelitis optica spectrum disorder (NMOSD), as well as on aquaporin-4 immunoglobulin G-positive neuromyelitis optica spectrum disorder (AQP4-IgG+ NMOSD). The order and family showed protective effect against cardioembolic stroke, and the genus showed a protective effect on amyotrophic lateral sclerosis. In terms of the mapped genes of statistically significant bacterial taxa, genes such as , , , , , and exhibited a significant causal correlation with the corresponding white matter connectivity. This study demonstrated a genetically predicted causal relationship between GM and WMH, white matter microstructure, white matter connectivity, and multiple neurological diseases, based on GWAS data from mixed-sex cohorts without sex-stratified summary statistics. These findings highlight the potential role of GM in influencing brain structural integrity. - Source: PubMed
Publication date: 2025/09/04
Zhang LanPang Xiao-WeiZhang Lu-YangZhu Li-FangLi Wan-NingChu Yun-HuiZhou Luo-QiTian Dai-ShiQin ChuanChen Lian