Human VSIG4 Protein
- Known as:
- Human VSIG4 Protein
- Catalog number:
- VS4-H5226
- Product Quantity:
- 1mg
- Category:
- -
- Supplier:
- acrobyosystems
- Gene target:
- Human VSIG4 Protein
Related genes to: Human VSIG4 Protein
- Gene:
- VSIG4 NIH gene
- Name:
- V-set and immunoglobulin domain containing 4
- Previous symbol:
- -
- Synonyms:
- Z39IG, CRIg
- Chromosome:
- Xq12
- Locus Type:
- gene with protein product
- Date approved:
- 2004-09-10
- Date modifiied:
- 2018-07-13
Related products to: Human VSIG4 Protein
Related articles to: Human VSIG4 Protein
- Focused ultrasound (FUS) and microbubbles can transiently increase blood brain barrier (BBB) permeability, yet BBB opening (BBBO) verification relies mainly on contrast-enhanced MRI, offering limited insight into the molecular consequences of barrier modulation. Sonobiopsy, which uses FUS induced BBBO to release brain derived molecules into the bloodstream, provides a molecular readout from blood samples. Nanobubbles (NBs) are smaller agents that circulate more effectively in the brain microvasculature and have shown enhanced BBBO in capillaries. Here, we establish NB-based sonobiopsy as a platform for enhanced biomarker efflux and molecular sensitivity, and apply it to define the proteomic signature of BBBO in healthy and glioblastoma (GBM) models. Plasma collected before and after NB-mediated FUS underwent data-independent acquisition-based mass spectrometry, revealing post-BBBO changes in healthy and tumor bearing mice. In healthy cohorts, 77 proteins were reproducibly altered after BBBO. Six proteins (Dpysl3, Myl1, Mybpc1, Vsig4, Krt33a, Krtap6-5) were detectable only after BBBO in healthy mice. In 005 glioma bearing mice, the BBBO signature identified in healthy animals was preserved with clear pre- vs post-BBBO separation. Candidate BBBO-associated proteins identified in the NB cohort were subsequently evaluated in an MB cohort, where the pre-to-post BBBO changes observed with NBs were not reproduced. These findings establish NB-mediated proteomic sonobiopsy as a promising method for BBBO verification across healthy and disease-relevant conditions and support the development of scalable molecular readouts for BBBO confirmation. This platform may also complement disease-focused sonobiopsy approaches, including protein-based biomarker studies in neuro-oncology. - Source: PubMed
Publication date: 2026/05/02
Gattegno RoniSher DivshaBismuth MikeZohar OrMoskov KerenKabaha SinaFriedmann-Morvinski DinorahIlovitsh Tali - Bacterial extracellular vesicles (bEVs) are increasingly recognized as critical mediators of gut-host interactions; however, their specific role in the aging process remains obscured by fragmented data and disease-specific silos. Current understanding lacks a cohesive mechanism that explains how age-related physiological changes transform bEVs from commensal signals into systemic drivers of pathology. This review synthesizes disparate findings to elucidate a synergistic mechanism: aging compromises intestinal barrier integrity, facilitating bEV translocation, while simultaneously impairing immune clearance capabilities (e.g. loss of Vsig4+ Kupffer cells), leading to their toxic accumulation. We resolve conflicting reports on bEV functionality-such as the paradoxical pro-calcific effects of GG-derived vesicles in chronic kidney disease-by contextualizing them within the host's aging microenvironment. Beyond mapping these interactions across the gut-brain, metabolic, cardiovascular, and bone axes, we identify specific cargo molecules, such as lipopolysaccharide (LPS), curli, and bacterial DNA, that fuel inflammaging. However, translating these insights into therapeutic applications faces significant challenges, including methodological heterogeneity in isolation protocols and unresolved immunogenicity risks. By outlining a strategic roadmap for standardization and rigorous clinical validation, this study redefines bEVs not merely as biomarkers but as actionable targets for delaying aging and mitigating age-related diseases. - Source: PubMed
Publication date: 2026/04/28
Tan JunfeiZubair MuhammadZhang LinLiu LikangLi KangrongWang YihuaYan YongminXu Wenyan - Alcohol-associated liver disease (ALD) has limited therapeutic options due to its complex pathogenesis. This study demonstrates the ALD-protective effects of extracellular nanoparticles derived from Bifidobacterium bifidum (BNPs), focusing on the concept of gut microbiota-derived nanoparticles (GNPs) in disease pathogenesis. When isolated BNPs were administered in an ALD mouse model, they upregulated Vsig4 receptor expression in liver macrophages, improving phagocytic clearance of harmful GNPs that contained bacterial DNA. GNPs activated liver inflammation via the cGAS-STING pathway, exacerbating ALD and liver fibrosis in Vsig4-deficient mice. BNP treatment suppressed the inflammatory cascade, modulated macrophage polarization, and reduced hepatic steatosis and liver injury, while also restoring the balance of the gut microbiota and enhancing intestinal barrier function. These findings reveal the role of GNPs in ALD pathogenesis and present targeted microbial nanoparticle postbiotics as potential therapeutics for treatment of alcohol-associated and other liver diseases. - Source: PubMed
Publication date: 2026/04/30
Gu ZelinMeng ShuhanYao BoqingGao BoyaChen SiyeRen FazhengLi PinglanShao TuoShang Nan - Liver metastases can resist T cell immunotherapies, indicating an adaptation of metastatic tumors toward reduced immunogenicity in the liver. Here we show that VSIG4, an immune checkpoint molecule predominantly expressed by Kupffer cells, has an opposing function in determining the growth of liver metastases with distinct antigenicity by modulating cognate T cell antigen receptor signaling through an interaction with CD5. VSIG4-CD5 engagement impedes activation of low-affinity CD8 T cells while enhancing responses of high-affinity CD8 T cells by rescuing them from activation-induced cell death. This bidirectional regulation favors the outgrowth of poorly immunogenic metastatic tumor clones and fosters an immune landscape that is unfavorable to T cells as metastatic liver cancer progresses. We also show that blockade of VSIG4-CD5 interaction using a nanoantibody to VSIG4 sensitizes liver metastases to anti-PD-L1 therapy, achieving synergistic efficacy in mice. These findings provide mechanistic insights into cancer immunoediting during liver metastasis and a possible approach for treating immunologically cold tumors. - Source: PubMed
Publication date: 2026/04/29
Zhou XiaLiu WeiHu JingYao QiZhang FutingWu QiLi LiyaLi JiajiaZhu LixiaChen ChenZhang QingZhang RenjieLiu JinlingShi ChaoweiZhou HongGuo AoWang JianWang JizhouHu QingsongLi LuJin TengchuanZeng Zhutian - The complement receptor immunoglobulin (CRIg), a key microbial pathogen phagocytosis-promoting receptor, responsible for intravascular clearance of bacteria, is purported to be expressed selectively on tissue-fixed macrophages such as Kupffer cells. However, recently it has been reported that neutrophils can also express functional CRIg following activation by inflammatory mediators. Monocytes have been reported not to express CRIg under non-activated conditions. Thus, investigations were undertaken to examine whether blood monocytes express CRIg under cell activation conditions and its role in anti-microbial immunity. - Source: PubMed
Publication date: 2026/03/13
Perveen KhalidaYang GailinSkurray Cameron DNgo AndyBlack NikkiPutty TrishniPatel AsmitabahenSmall Annabelle GGulam Muhammad YWechalekar Mihir DSadlon TimothyBarry Simon CQuach AlexHii Charles SFerrante Antonio