Ask about this productRelated genes to: VSIG1 antibody
- Gene:
- VSIG1 NIH gene
- Name:
- V-set and immunoglobulin domain containing 1
- Previous symbol:
- -
- Synonyms:
- MGC44287, GPA34
- Chromosome:
- Xq22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-09-02
- Date modifiied:
- 2019-03-21
Related products to: VSIG1 antibody
Related articles to: VSIG1 antibody
- V-set and immunoglobulin domain-containing 1 (VSIG1) is a member of the immunoglobulin superfamily that has attracted increasing attention as a differentiation-associated protein in gastrointestinal neoplasia. Although initially described as a gastric-specific marker, accumulating evidence indicates that VSIG1 more accurately reflects gastric-enriched epithelial differentiation rather than strict anatomical origin. This conceptual shift has implications for phenotype-oriented tumor classification and diagnostic interpretation in the context of lineage plasticity. A structured and transparently reported literature search was conducted in PubMed/MEDLINE, Web of Science, and Scopus, covering studies published between 2000 and 2024. Eligible studies included original research and relevant reviews evaluating VSIG1 expression in normal tissues and digestive tract tumors, with emphasis on immunohistochemical patterns and clinicopathological correlations. In gastric cancer, VSIG1 expression consistently correlates with preserved glandular architecture and epithelial differentiation, whereas reduced or absent expression accompanies dedifferentiation and architectural disorganization. Outside the stomach, VSIG1 positivity is uncommon but reproducible in tumors exhibiting gastric-type or mixed differentiation, including settings of hepato-gastric phenotypic overlap. These patterns support interpretation of VSIG1 as a context-dependent indicator of lineage engagement and differentiation state rather than tumor origin or aggressiveness. Current data on independent prognostic value are limited and partially conflicting, and predictive roles remain unsupported, while functional data remain limited. - Source: PubMed
Publication date: 2026/03/08
Satala Catalin-BogdanPatrichi GabrielaGurau Alina-MihaelaOnofrei Popa AndreeaMihalache Daniela - Tetraodontiformes species exhibit several evolutionary innovations, notably the convergent evolution of two traits in some clades: defensive body inflation and the loss of acid-peptic digestion. It has been widely believed that the evolution of body inflation drove the loss of gastric digestion, as ingesting seawater during inflation would hinder acidification and ultimately lead to the loss of gastric digestion. Leveraging accumulating genome resources, we investigated the presence, synteny, gene expression, and rapid evolution of nine genes associated with acid-peptic digestion across seven species from four Tetraodontiformes families, representing two branches that underwent convergent evolution. In the first evolutionary branch, all agastric species-including the species lacking inflation capability (Mola mola)-exhibit loss or pseudogenization of eight gastric-function-related genes. Among these, only pga1 is retained, though it lacks digestive functionality. In another branch, the greenfin horse-faced filefish (Thamnaconus septentrionalis), which possesses a functional stomach, maintains solely pga2 as its single pepsinogen gene, with pga1 and pgc having been lost, while slc26a9 and vsig1 show evidence of rapid evolution. These findings suggest that the convergent loss of gastric digestion likely occurred before the evolution of body inflation in both branches, supporting an "unfunctional-stomach-first" evolutionary scenario. - Source: PubMed
Publication date: 2025/07/01
Liu ChangLin LeiDu ShengLiu KaiqiangJi HonglongWang QianHe YangbinShao Changwei - The stomach has been a highly conserved organ throughout vertebrate evolution; however, there are now over 20 lineages composed of monotremes, lungfish and teleost fish displaying a secondary loss of stomach function and morphology. This "agastric phenotype" has evolved convergently and is typified by a loss of gastric glands and gastric acid secretion and a near-to-complete loss of storage capacity of the stomach. All agastric species have lost the genes for gastric enzymes ( and ) and proton pump subunits ( and ), and gastrin () has been lost in monotremes. As a key gastric hormone, the conservation of gastrin has not yet been investigated in the lungfish or agastric teleosts, and it is unclear how the loss of gastrin affects the evolution and selection of the native receptor (), gastrin-releasing peptide () and gastrin-releasing peptide receptor () in vertebrates. Furthermore, there are still many genes implicated in gastric development and function which have yet to be associated with the agastric phenotype. We analysed the evolution, selection and conservation of the gastrin pathway and a novel gastric gene repertoire (, , , , and ) to determine the correlation with the agastric phenotype. We found that the loss of gastrin or its associated genes does not correlate with the agastric phenotype, and their conservation is due to multiple pleiotropic roles throughout vertebrate evolution. We found a loss of the gastric gene repertoire in the agastric phenotype, except in the echidna, which retained several genes (, and ). Our findings suggest that the gastrin physiological pathway evolved differently in pleiotropic roles throughout vertebrate evolution and support the convergent evolution of the agastric phenotype through shared independent gene-loss events. - Source: PubMed
Publication date: 2025/08/05
Dann JacksonGrützner Frank - Porcine deltacoronavirus (PDCoV) is an enteropathogenic coronavirus that causes acute diarrhea, vomiting, dehydration, and even death in piglets, resulting in serious economic losses to the pork industry worldwide. PDCoV has received much attention owing to its broad host range, including humans, posing a potential threat to public health. However, the prevalence, characteristics, and host cellular gene expression of PDCoV remain poorly understood. - Source: PubMed
Publication date: 2025/03/26
Yang XiaozhuYin HanweiLiu MengyuanWang XuemeiSong TaoSong AiaiXi YiboZhang TingSun ZilongLi WeiNiu ShengZainab FarwaWang ChenyangZhang DingWang HaidongYang Bo - Cell surface proteins, targeted by approximately 70 % of current pharmaceuticals, offer promising prospects for therapeutic and biotechnological advancements. The recent identification of cell surface proteins, differentially expressed by rabbit spermatozoa, could support technologies to enable sperm sex selection. However, a more detailed knowledge of the rabbit sperm plasma membrane proteome is crucial to such developments. Hence, the primary objective of this study was to conduct a shotgun proteomic (LC-MS/MS) analysis of New Zealand White rabbit spermatozoa protein lysates enriched in cell surface proteins isolated through biotinylation. This approach was designed to provide an overall characterization of this proteome and so determine an expanded list of protein candidates with potential for rabbit sperm sexing. The most promising targets were identified through functional annotation (UniProt and eggNOG-mapper v.2.1.9) and topology prediction (DeepTMHMM v.1.0.13). Additionally, a statistical overrepresentation test (PANTHER 18.0) and analysis of protein-protein interactions (STRING v.12.0) were conducted. Among the 859 detected proteins, 803 had Gene Ontology information, with 574 predicted as globular proteins, 152 as transmembrane proteins, and 133 possessing only a signal peptide. The combined data identified 107 proteins as potential cell surface targets, including three transmembrane proteins encoded by the X chromosome (ADGRG2, ATP6AP2, and VSIG1). Furthermore, two proteins (BCAP31 and PGRMC1), previously identified as putative rabbit X-targets, were recognized. This study enhances our comprehension of rabbit spermatozoa proteomics. Further validation of the utility of these five proteins to differentiate between X- and Y-sperm will determine their suitability for integration into sperm sexing technologies. - Source: PubMed
Publication date: 2025/04/02
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