Ask about this productRelated genes to: VEZT antibody
- Gene:
- VEZT NIH gene
- Name:
- vezatin, adherens junctions transmembrane protein
- Previous symbol:
- -
- Synonyms:
- DKFZP761C241
- Chromosome:
- 12q22
- Locus Type:
- gene with protein product
- Date approved:
- 2006-01-27
- Date modifiied:
- 2014-11-19
Related products to: VEZT antibody
Related articles to: VEZT antibody
- Gastric cancer is a leading cause of cancer-related death, particularly in East Asia, yet its genetic basis remains incompletely understood. Using genome-wide association study data from BioBank Japan, we show that gastric cancer shares significant genetic associations with 25 other phenotypes, most notably cardiovascular conditions such as angina pectoris and myocardial infarction. Mendelian randomization supports a causal role of these traits in gastric cancer risk. Multitrait analysis of GWAS reveals a novel pleiotropic locus at 12q22 (rs12814712) that is shared between gastric cancer and cardiovascular traits. Functional experiments demonstrate that the risk allele at this locus reduces transcriptional activity and downregulates the expression of nearby genes, particularly VEZT. In gastric cancer cells, overexpression of VEZT and NR2C1 suppress proliferation and migration, whereas their knockdown promotes malignancy. Our analysis identifies rs12814712 as a novel susceptibility locus for gastric cancer and underscores its regulatory role in disease-related gene networks. - Source: PubMed
Publication date: 2026/03/15
Ding HuanxinLiu ChuxuanSun QingJiang YueXu QianZhu ZhenguoJin XinHuang QiboLi YueSong YingchaoLiu ZenglinYu TianmingShi BowenTan DelinLi LinzehaoMentch FrankGlessner JosephChang XiaoHakonarson HakonZhang Guangyong - Endometriosis is a heterogeneous gynecological disease manifesting in three distinct phenotypes: superficial peritoneal endometriosis (SUP), ovarian endometrioma (OMA), and deep infiltrating endometriosis (DIE). While Genome-Wide Association Studies (GWAS) have identified numerous susceptibility loci-such as , , and -the functional translation of these genetic risks into phenotype-specific pathophysiology remains unclear. - Source: PubMed
Publication date: 2026/02/10
Situmorang HerbertPramayadi Cepi TeguhKurniawan Riyan HariPriangga Muhammad DwiMirza Muhammad SyauqiGunardi Eka RusdiantoSurya Ilham Utama - Adenomyosis and endometriosis are complex, estrogen-dependent gynecological conditions increasingly diagnosed in adolescents. While traditionally considered diseases of reproductive-age women, emerging evidence suggests a possible developmental origin in some cases, with genetic and epigenetic susceptibility playing a central role. Understanding the contribution of hereditary and molecular factors in adolescent-onset forms may offer insights into early pathogenesis, personalized risk stratification and tailored prevention strategies. The objectives of this study were to explore the current evidence supporting a genetic contribution to the development of adenomyosis and endometriosis in adolescents and to identify specific genetic variants, molecular pathways and epigenetic mechanisms potentially involved in early-onset disease. A narrative literature review was conducted using PubMed and Scopus databases up to September 2025. Studies investigating the genetic basis of adenomyosis and endometriosis in adolescents, including familial aggregation, twin studies, GWAS and candidate gene analyses, were included. Evidence from familial clustering and twin studies suggests a significant heritable component in both conditions. Genome-wide association studies have identified susceptibility loci, particularly involving , and , that may be relevant to adolescent-onset disease. Candidate gene studies further highlight the roles of estrogen signalling, inflammatory pathways, extracellular matrix remodelling and emerging epigenetic alterations, including aberrant DNA methylation and chromatin remodelling, which may influence early lesion development. However, most data are derived from adult cohorts, with limited adolescent-specific analyses. Genetic and epigenetic predispositions appear to contribute significantly to the pathogenesis of endometriosis and possibly adenomyosis in adolescents. Further studies targeting early-onset disease are needed to unravel developmental mechanisms and gene-environment interactions unique to this population. - Source: PubMed
Publication date: 2025/12/05
Palumbo MarioDella Corte LuigiAscione MarioD'Angelo GiuseppeColacurci DarioBaldini Giorgio MariaPellicano MassimilianoGiampaolino PierluigiBifulco Giuseppe - Growth traits are crucial for poultry breeding and production. Marker-assisted selection (MAS) and genomic selection (GS) of growth traits require a substantial number of accurate genetic markers. A genome-wide association study (GWAS) for body size traits was performed on 248 Luning chickens to identify significant single-nucleotide polymorphisms (SNPs) and insertions and deletions (INDELs) related to the growth and development of chickens. A total of 30 significant SNPs and 13 INDELs were obtained for body size traits. Two notable regions, spanning from 43.072 to 43.219 Mb on chromosome 1 and from 4.751 to 4.800 Mb on chromosome 11, were found to be significantly associated with growth traits in the GWAS of both SNPs and INDELs. Some genes, including , , , , , , , , , and , were identified as important candidate genes for the growth of chickens. The results provide valuable information for understanding the genetic basis of growth traits which is beneficial for the subsequent selective breeding in Luning chickens. - Source: PubMed
Publication date: 2025/03/27
Li ZhiyiNong YiLiu YuanWang ZiWang JiayanLi Zhixiong - Endometriosis (EM) is a common multifactorial gynaecological disorder. Although Genome-Wide Association Studies have largely been employed, the current knowledge of the genetic mechanisms underlying EM is far from complete, and other approaches are needed. To this purpose, whole-exome sequencing (WES) was performed on a deeply characterised cohort of 80 EM patients aimed at the identification of rare and damaging variants within 46 EM-associated genes and novel candidates. WES analysis detected 63 rare, predicted, and damaging heterozygous variants within 24 genes in 63% of the EM patients. In particular, (1) a total of 43% of patients carried variants within 13 recurrent genes (, , , , , , , , , , , , ); (2) a total of 8.8% carried private variants within eight genes (, , , , , , , ); (3) a total of 24% carried variants within three novel candidates (, , ). Finally, to deepen the polygenic architecture of EM, a comprehensive evaluation of the analysed genes was performed, revealing a higher burden ( < 0.05) of genes harbouring rare and damaging variants in the EM patients than in the controls. These results highlight new insights into EM genetics, allowing for the definition of novel genotype-phenotype correlations, thereby contributing, in a long-term perspective, to the development of personalised care for EM patients. - Source: PubMed
Publication date: 2023/07/27
Santin AuroraSpedicati BeatriceMorgan AnnaLenarduzzi StefaniaTesolin PaolaNardone Giuseppe GiovanniMazzà DanielaDi Lorenzo GiovanniRomano FedericoBuonomo FrancescaMangogna AlessandroConcas Maria PinaZito GabriellaRicci GiuseppeGirotto Giorgia