BVES antibody
- Known as:
- BVES (anti-)
- Catalog number:
- orb129542
- Product Quantity:
- 200 ug
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- BVES antibody
Related genes to: BVES antibody
- Gene:
- BVES NIH gene
- Name:
- blood vessel epicardial substance
- Previous symbol:
- -
- Synonyms:
- HBVES, POP1, POPDC1
- Chromosome:
- 6q21
- Locus Type:
- gene with protein product
- Date approved:
- 2000-01-10
- Date modifiied:
- 2015-08-24
Related products to: BVES antibody
Related articles to: BVES antibody
- The Popeye domain-containing protein 1 (Popdc1, also known as Bves) is a transmembrane protein whose dysfunction is closely associated with various diseases. Clinical studies have identified that mutations in the bves gene predispose individuals to limb-girdle muscular dystrophy. However, a marked reduction in Bves protein expression has been observed in patients with heart failure, highlighting a critical unresolved challenge in understanding its role in disease pathogenesis. In this study, we discovered that bves deficiency drives cardiac contractile dysfunction, thereby revealing a novel mechanism underlying heart failure pathogenesis. The study found that bves knockout led to cardiac contractile dysfunction in zebrafish during both embryonic and adult stages, with a significant reduction in ejection fraction. Twelve-month-old bves knockout zebrafish exhibited ventricular dilation, increased cardiomyocyte size but significantly decreased cell numbers, and aggravated fibrosis of atrioventricular valves. Transmission electron microscopy revealed widened Z-lines and shortened I-bands in myocardial fibers of the bves knockout group. Collectively, these findings provide compelling evidence that bves knockout induces heart damage. Transcriptome analysis showed disrupted expression of ATP synthesis-related genes and activation of the mitochondrial autophagy pathway following bves knockout. In bves knockout zebrafish, myocardial mitochondria exhibited abnormal structure and impaired oxidative respiratory function, with upregulated expression levels of a series of protein complexes in the mitochondrial electron transport chain. These studies have for the first time established that myocardial mitochondrial structural/functional damage caused by bves deficiency may be associated with the pathogenesis of heart failure, providing a new perspective for the occurrence and development of heart failure. - Source: PubMed
Publication date: 2026/08/22
Cai WanwanZhou WanbangLei JunrongWu XiushanWang HaochenXu JiaoHuang ChengWu QiongZhou SongSun KangZhang ZhilongZhang JishengOuyang JingyingYuan WuzhouJiang ZhigangWen MingLiu XianchuLi YongqingZheng Lan - Recent studies have shown that UFMylation plays an important role in cancer, but its specific function in gastric cancer (GC) remains to be fully elucidated. This study aimed to develop a prognostic signature based on UFMylation-related genes (URGs) for survival prediction in GC. - Source: PubMed
Publication date: 2026/07/27
Chen GuohaoGao XianDai LingchenDeng ShukangWang HaoyangHuang XinkunFeng Ying - The Popeye domain-containing protein 1 (Popdc1), also known as Bves, plays a crucial role in maintaining skeletal muscle homeostasis, with its variants leading to limb-girdle muscular dystrophy type R25. Skeletal muscles of patients with the homozygous missense variant of Bves exhibit impaired membrane trafficking, while skeletal muscle fibers in homozygous mutant zebrafish are significantly reduced and disorganized. However, the mechanism by which the absence of induces skeletal muscle atrophy remains unclear. In this study, we discovered a novel mechanism whereby deficiency drives skeletal muscle atrophy by disrupting mitochondrial structure and function. Our findings indicate that knockout leads to a significant decrease in zebrafish's ability to swim, atrophy of skeletal muscle tissue, loss of cell membrane localization signals, and abnormalities in mitochondrial structure and function. After an 8-week intervention of regular aerobic exercise, the symptoms of skeletal muscle atrophy in knockout zebrafish were significantly alleviated, and the expression levels of genes and proteins related to mitochondrial were effectively rescued. These findings establish a connection between deficiency-induced disruption of mitochondrial structure and function and the onset and progression of skeletal muscle tissue atrophy symptoms, thereby laying a molecular foundation for exercise rehabilitation strategies in atrophic myopathy. - Source: PubMed
Publication date: 2026/06/20
Cai WanwanZhou WanbangWu XiushanLei JunrongWang HaochenWu QiongZhou SongSun KangLi XiuyanZhang ZhilongZhang JishengOuyang JingyingLi YongqingJiang ZhigangLiu XianchuYuan WuzhouZheng Lan - Mytilus coruscus (M. coruscus) is a high-value marine aquaculture species with significant economic importance. Traditional semi-artificial seed collection methods in coastal waters are insufficient to meet current demands for improved M. coruscus varieties exhibiting desirable traits such as enhanced growth rates and larger body size. Long non-coding RNAs (lncRNAs) are known to regulate critical cellular processes, including proliferation, development, and the cell cycle. To investigate potential regulatory influences on M. coruscus growth, comparative transcriptomic analyses were performed on specimens exhibiting divergent growth phenotypes (fast-growing and slow-growing) reared under identical conditions. Foot tissue samples were aseptically collected from each group for full transcriptome sequencing. Sequencing analysis identified 91 differentially expressed long non-coding RNAs (DE-lncRNAs), comprising 55 upregulated and 36 downregulated transcripts. GO analysis showed that the target or source genes of these differentially expressed RNAs were mainly enriched in the categories of biological processes, cellular components, and molecular functions. KEGG pathway analysis revealed several signaling pathways potentially involved in growth regulation, notably TGF-beta, VEGF, Wnt, and mTOR signaling pathways. Among the identified DE-lncRNAs, MSTRG.10759.1 exhibited the highest expression levels and is predicted to regulate the BVES and RASV genes, as well as the ST13/HIP protein. Interaction network analysis of lncRNA-mRNA pairs highlighted two core target genes, PLOD1 and ANK, suggesting their potential regulatory roles in mussel growth. These findings offer new perspectives on the molecular mechanisms underlying growth in mytilids and provide foundational data for the development of molecular marker-assisted breeding strategies to produce fast-growing mussel strains. - Source: PubMed
Publication date: 2026/05/11
Zhao XinyuDong Xiangli - Aberrant DNA methylation induces abnormal expression of drug-resistance genes, promoting drug resistance. This study identified specific DNA methylation patterns driving LUAD chemoresistance and explored their mechanisms. Blood vessel epicardial substance (BVES) expression and methylation were analyzed by using TCGA and MethylMix. Primers for the BVES CpG island were designed with MethPrimer. Pathways for BVES were analyzed by gene set enrichment analysis. Methylation-specific quantitative PCR detected the levels of BVES methylation. Quantitative reverse transcription polymerase chain reaction evaluated BVES expression, and western blot analyzed the expression of BVES, LC3, and P62. The cell counting kit-8 was used to determine IC50 and cell viability. Cell proliferation assessment was achieved by colony formation assay, and apoptosis was evaluated by flow cytometry. LC3 expression was observed through immunofluorescence. The findings displayed hypermethylation of BVES in LUAD tissues and cells, which was further elevated in the setting of cisplatin (DDP) resistance. The overexpression of BVES in A549/DDP cells substantially repressed their proliferation in response to DDP and markedly amplified the apoptotic effects induced by DDP. In the rescue experiments, autophagy stimulants effectively eliminated the DDP sensitivity enhancement caused by BVES overexpression in A549/DDP cells. In vivo assays confirmed that BVES overexpression suppressed autophagy and augmented the therapeutic impact of DDP. BVES hypermethylation, through the promotion of autophagy, reinforces resistance to DDP in LUAD. This study indicates that repressing BVES methylation and upregulating its expression may be a strategic way to combat cisplatin resistance in LUAD patients. - Source: PubMed
Publication date: 2026/04/15
Tan XiaoliLv XiaodongChen RuruXu YufenChen Wenyu