Proteins VSIG2 , Human
- Known as:
- Proteins VSIG2 , Human
- Catalog number:
- C548
- Product Quantity:
- 10μg
- Category:
- -
- Supplier:
- Novoprotein
- Gene target:
- Proteins VSIG2 Human
Related genes to: Proteins VSIG2 , Human
- Gene:
- VSIG2 NIH gene
- Name:
- V-set and immunoglobulin domain containing 2
- Previous symbol:
- -
- Synonyms:
- CTXL, CTH
- Chromosome:
- 11q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-09-02
- Date modifiied:
- 2016-10-05
Related products to: Proteins VSIG2 , Human
Related articles to: Proteins VSIG2 , Human
- As accumulating evidence suggests that PANoptosis plays a significant role in tumour progression, it is essential to elucidate its implications for tumour prognosis and treatment. We aimed to characterize the PANoptotic features of patients with bladder urothelial carcinoma (BLCA) and to develop a novel model to guide clinical diagnosis and treatment, while further investigating the associated molecular mechanisms underlying tumour progression. - Source: PubMed
Publication date: 2026/02/01
Xin ShiyongLi RuixinZhao LeSu JunjieLi GuanyuQin WangZhang ZhengWang ChuZhu YingaoFeng LimingSun XianchaoJin LiangZhai TingshuaiMei WangliGao Zhongwei - Colorectal cancer (CRC) is a global health issue influenced by both genetic and environmental factors. Identifying key genes closely associated with CRC is crucial for understanding its pathological mechanisms and discovering therapeutic targets. This study aimed to integrate multi-omics datasets and Mendelian randomization (MR) approaches to identify CRC-related genes and to clarify their roles in tumor immunity and therapeutic potential. - Source: PubMed
Publication date: 2025/11/26
Zhou ShengyiZhang XinyiWang ShiwenZhou YunfanSun Yizhou - Although B7 family immune checkpoint molecules such as PD-L1/PD-1 have improved the treatment of cancer and autoimmune diseases, more such molecules are still needed to expand therapeutic options. This study focuses on a novel molecule, VSIG2—previous studies suggested that VSIG2 acts as a receptor involved in T cell development, but this study is the first to identify a different mechanism of action, confirming that VSIG2 can function as an immunosuppressive ligand present on the surface of activated antigen-presenting cells. It specifically binds to Nectin-2 and does not interact with well-known immune receptors like PD-1 or CTLA-4; this binding strongly inhibits T cell activation and proliferation. In experiments, the human VSIG2-Ig protein alleviated the symptoms of experimental autoimmune encephalomyelitis, while anti-VSIG2 antibodies inhibited the growth of pancreatic cancer. The interaction between VSIG2 and Nectin-2 can regulate the STAT1/IRF1/GBP2 signaling pathway in T cells, thereby modulating T cell responses, and this axis is expected to serve as a novel therapeutic target for autoimmune diseases and cancer. - Source: PubMed
Publication date: 2025/12/05
Wang XianbinHu RongChen KezhuHe KekeLi YuandiGao JieTian YishenDu GuangshiWang ZuliZhao YouboLai LaijunSu Min - Dysregulation of N6-methyladenosine (m6A) RNA modification plays a critical role in the development and progression of non-small cell lung cancer (NSCLC). To explore the m6A modification landscape in NSCLC, we utilized direct RNA nanopore sequencing (dRNA-seq) to compare m6A patterns between NSCLC and adjacent normal tissues. Our analysis revealed distinct m6A modification differences, with tumor tissues showing reduced m6A density compared to normal tissues. Aberrantly modified genes, such as and , exhibited hypomethylated m6A modifications and were upregulated in NSCLC tissues. We identified 14,419 differentially methylated m6A sites, with 49.5% hypermethylated and 50.5% hypomethylated. Functional enrichment analysis showed that hypermethylated genes were involved in DNA replication and transcription regulation, while hypomethylated genes were linked to cell migration and MAPK signaling. The expression patterns of m6A regulators, including , , , , , and , were consistent across NSCLC subtypes. Furthermore, correlation with clinical data from the TCGA database revealed that m6A-associated DEGs, such as , , , , , , and , were prognostically significant in NSCLC. This study underscores the pivotal role of m6A modifications in NSCLC and highlights the potential of dRNA-seq for identifying RNA epigenetic changes that may serve as novel therapeutic targets. - Source: PubMed
Publication date: 2025/10/24
Li YifeiJiao PengLi DonghangTian YiLi HexinSun GaoyuanWu XiaonanNie XinLi XuXu SiyuanTang XiaokunZhang LiliWan LiZhang LanxinCai JiahuiTang MinLi Lin - As the fifth most common cancer and the third leading cause of cancer death worldwide, gastric cancer (GC) has long been a serious global health challenge. The purpose of this study was to explore the expression of V-set and immunoglobulin domain containing 2 (VSIG2) in GC and to elucidate its role in GC progression and related mechanisms. Western blot analysis, qRT-PCR and immunohistochemical (IHC) staining are used to detect the expression of VSIG2 in GC cells and tissues. Kaplan-Meier survival curve analysis is performed. The effects of VSIG2 on biological effects related to GC progression are detected by CCK-8, EdU, Transwell and wound healing assays and by a nude mouse subcutaneous tumor model and a liver metastasis model. Mechanistically, co-immunoprecipitation, immunofluorescence and ubiquitination experiments are used to explore the regulatory effect of VSIG2 on ANXA2 and the regulatory effect between FBXW10 and ANXA2. VSIG2 is abnormally expressed at low levels in patients with GC and is associated with patient prognosis. Low VSIG2 expression is closely related to tumor size, lymph node metastasis, TNM stage and vascular invasion in GC patients. Functionally, and experiments reveal that VSIG2 could inhibit the growth, proliferation and metastasis of GC. Mechanistically, VSIG2 and ANXA2 interact directly in GCs and co-localize at the cell membrane. Further exploration reveals that highly expressed VSIG2 competes with FBXW10 for binding to ANXA2 and relies on FBXW10-mediated K63 polyubiquitination of ANXA2 to induce membrane localization of ANXA2 and further inactivate NF-κB, thereby suppressing GC progression. In summary, VSIG2 is expressed at abnormally low levels in patients with GC, and its low expression is associated with poor patient prognosis. VSIG2 can inhibit the proliferation and migration of GC via the ANXA2/NF-κB pathway. This study elucidates a new mechanism by which VSIG2 inhibits GC progression, which may provide a new perspective for the diagnosis and treatment of GC patients. - Source: PubMed
Ni QingfengWang YangBian XinyueQu QiuchanShen BoyuanNiu YuanjieYu JiaweiZhu Jianwei