BVES
- Known as:
- BVES
- Catalog number:
- GTX116342
- Product Quantity:
- 0.1 ml
- Category:
- -
- Supplier:
- ACR
- Gene target:
- BVES
Related genes to: BVES
- 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
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- 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 - Although peptide-based delivery strategies show promise for muscle and heart diseases, delivery of biotherapeutics to both skeletal and cardiac muscles remains challenging. Here, we identified a muscle-homing peptide (BV2) against blood vessel epicardial substance (BVES) by phage display. BV2 shows high binding affinity to BVES and is internalized primarily via caveolae-mediated endocytosis. Importantly, BV2 enables efficient delivery of Duchenne Muscular Dystrophy (DMD) phosphorodiamidate morpholino oligomer (PMO), mCherry protein and exosomes to skeletal muscle and heart in vivo. BV2-mCherry protein and BV2-E31R anti-myostatin peptide were effectively delivered to muscle layers when microneedles loaded with these biotherapeutics were implanted on hindlimbs of mice. Muscle mass and myofiber size also significantly increased in muscle atrophy mice grafted with BV2-E31R microneedles. Moreover, significantly enhanced restoration of dystrophin protein was achieved in peripheral and cardiac muscles of dystrophin-deficient mdx and dystrophin/utrophin double-knockout mice when exosomes simultaneously modified with BV2 and PMO. These findings highlight the potency of BV2 in directing targeted delivery of diverse biotherapeutics to muscle and heart, thus providing an effective tool for DMD and other muscular and cardiac disorders. - Source: PubMed
Publication date: 2026/01/04
Wang BiaobiaoCao JiahuiWu JingqiaoZhao YiwenZhang YaoAbendroth FrankLin CaoruiZhong LiYu HuananSeow YiqiOu MeitongVázquez OlallaMei LinYin HaiFangHan Gang