VAT1

Last update 08 May 2025

Basic Info

Synonyms

FLJ20230, Synaptic vesicle membrane protein VAT-1 homolog, VAT1

+ [2]

Introduction

Possesses ATPase activity (By similarity). Plays a part in calcium-regulated keratinocyte activation in epidermal repair mechanisms. Has no effect on cell proliferation. Negatively regulates mitochondrial fusion in cooperation with mitofusin proteins (MFN1-2).

100 Clinical Results associated with VAT1

100 Translational Medicine associated with VAT1

0 Patents (Medical) associated with VAT1

Literatures (Medical) associated with VAT1

01 Feb 2025·International Immunopharmacology

Identification and validation VAT1 in gastric cancer through bioinformatics and experimental analysis

Article

Author: Du, Yan ; Mao, Pengxue ; Qiu, Zhisheng ; Hu, Yongli ; Da, Mingxu

This study investigated the expression pattern of Vesicular Amine Transporter 1 (VAT1) in gastric cancer (GC) and its impact on prognosis, alongside evaluating its potential as a biomarker for immunotherapy and chemotherapy. Analysis of transcriptomic data, supported by experimental validation, revealed that VAT1 is highly expressed in GC and is associated with poor prognosis. Kaplan-Meier and ROC analyses demonstrated VAT1's potential in GC diagnosis, while multivariate analysis confirmed its role as an independent risk factor. Gene set enrichment analysis indicated that VAT1 plays a role in regulating the MAPK signaling pathway and epithelial-mesenchymal transition (EMT) in GC. Immune infiltration analysis showed a positive correlation between VAT1 and immune cells, particularly macrophages, and a negative correlation with chemotherapy sensitivity. In vitro and in vivo experiments further confirmed VAT1's critical role in promoting GC cell proliferation and inhibiting apoptosis. Overall, VAT1 holds significant value not only in GC diagnosis and prognosis but also as a potential target for immunotherapy and overcoming drug resistance.

01 Feb 2025·Heliyon

A VAT1-related gene signature predicts radioresistance in gliomas

Article

Author: Shan, Xia ; Qiu, Xiaoguang ; Yang, Pei ; Wang, Kuanyu ; Huang, Ruoyu ; Sun, Zhiyan

BackgroundRadiotherapy is a vital postoperative adjuvant treatment for gliomas. However, radioresistance seriously affect the treatment efficacy. Excavating the feature of radioresisrtance in gliomas comprehensively are necessary.MethodsIn the training set, 191 patients from the Chinese Glioma Genome Atlas (CGGA) were included, of which all patients had received postoperative radiotherapy. The epidemiological data and RNA sequencing data of 430 patients with whole grade glioma were obtained from the Cancer Genome Atlas (TCGA), which was used for validation.ResultsBased on the Lasso regression analysis, five-gene signature was established which was associated with VAT1-related radioresistance in gliomas. High-risk patients showed higher proportion of elders, high-grade glioma, oligodendroglial histology and IDH wild type. The risk score was identified as an independent prognostic factor in the CGGA dataset, and the high-risk score impaired the overall survival time. The biological processes of positively expressed genes of risk score were functionally involved in inflammatory and immune response. And the activation of signaling pathways in high-risk score group also showed close correlation with tumor occurrence, progression and immune microenvironment. What's more, the immune cell infiltration analysis showed that high-risk score indicated decreased CD8⁺ T cell and the upregulation of the immune checkpoints, which probably promoted the immunosuppressive microenvironment.ConclusionThe five-gene signature can predict the survival of patients with glioma received postoperative radiotherapy efficiently. The immunosuppressive microenvironment, as a feature of glioma, potentially devote to the radioresistance.

01 Jan 2025·Cardiovascular Therapeutics

Exploring Potential Drug Targets in Multiple Cardiovascular Diseases: A Study Based on Proteome‐Wide Mendelian Randomization and Colocalization Analysis

Article

Author: Dong, Xueyan ; Chen, Chen ; Fan, Maoxia ; Huang, Libin ; Gao, Wulin ; Li, Na

Background: Cardiovascular diseases (CVDs) encompass a group of diseases that affect the heart and/or blood vessels, making them the leading cause of global mortality. In our study, we performed proteome‐wide Mendelian randomization (MR) and colocalization analyses to identify novel therapeutic protein targets for CVDs and evaluate the potential drug‐related protein side effects.Methods: We conducted a comprehensive proteome‐wide MR study to assess the causal relationship between plasma proteins and the risk of CVDs. Summary‐level data for 4907 circulating protein levels were extracted from a large‐scale protein quantitative trait loci (pQTL) study involving 35,559 individuals. Additionally, genome‐wide association study (GWAS) data for CVDs were extracted from the UK Biobank and the Finnish database. Colocalization analysis was utilized to identify causal variants shared between plasma proteins and CVDs. Finally, we conducted a comprehensive phenome‐wide association study (PheWAS) using the R10 version of the Finnish database. This study was aimed at examining the potential drug‐related protein side effects in the treatment of CVDs. A total of 2408 phenotypes were included in the analysis, categorized into 44 groups.Results: The research findings indicate the following associations: (1) In coronary artery disease (CAD), the plasma proteins A4GNT, COL6A3, KLC1, CALB2, KPNA2, MSMP, and ADH1B showed a positive causal relationship (p‐fdr < 0.05). LAYN and GCKR exhibited a negative causal relationship (p‐fdr < 0.05). (2) In chronic heart failure (CHF), PLG demonstrated a positive causal relationship (p‐fdr < 0.05), while AZGP1 displayed a negative causal relationship (p‐fdr < 0.05). (3) In ischemic stroke (IS), ALDH2 exhibited a positive causal relationship (p‐fdr < 0.05), while PELO showed a negative causal relationship (p‐fdr < 0.05). (4) In Type 2 diabetes (T2DM), the plasma proteins MCL1, SVEP1, PIP4K2A, RFK, HEXIM2, ALDH2, RAB1A, APOE, ANGPTL4, JAG1, FGFR1, and MLN demonstrated a positive causal relationship (p‐fdr < 0.05). PTPN9, SNUPN, VAT1, COMT, CCL27, BMP7, and MSMP displayed a negative causal relationship (p‐fdr < 0.05). Colocalization analysis conclusively identified that AZGP1, ALDH2, APOE, JAG1, MCL1, PTPN9, PIP4K2A, SNUPN, and RAB1A share a single causal variant with CVDs (PPH3 + PPH4 > 0.8). Further phenotype‐wide association studies have shown some potential side effects of these nine targets (p‐fdr < 0.05).Conclusions: This study identifies plasma proteins with significant causal associations with CVDs, providing a more comprehensive understanding of potential therapeutic targets. These findings contribute to our knowledge of the underlying mechanisms and offer insights into potential avenues for treatment.

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VAT1

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