Ask about this productRelated genes to: VAPA antibody
- Gene:
- VAPA NIH gene
- Name:
- VAMP associated protein A
- Previous symbol:
- -
- Synonyms:
- hVAP-33, VAP-A
- Chromosome:
- 18p11.22
- Locus Type:
- gene with protein product
- Date approved:
- 1999-03-19
- Date modifiied:
- 2016-10-05
Related products to: VAPA antibody
Related articles to: VAPA antibody
- Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy with a poor prognosis, in which the role of lipophagy, a selective autophagic process degrading lipid droplets (LDs), remains poorly characterized. This study investigated lipophagy and its key regulator, , in PDAC progression. Through immunofluorescence analysis of patient samples, transgenic mouse tissues, and cell lines, we find that lipophagy is elevated in PDAC and correlates with poor prognosis. Single-cell transcriptomic analysis identified as a critical lipophagy regulator and an independent clinicopathological indicator. Functional assays, including orthotopic and subcutaneous xenografts, demonstrated that promotes tumor growth. Mechanistically, OSBPL10 functionally cooperates with VAPA/VAPB to facilitate rapid lysosomal repair via ATG2A, thereby promoting lipophagy and lipid mobilization. Inhibition of lysosomal function abrogated the pro-lipophagic and pro-tumorigenic effects of OSBPL10. Collectively, our findings demonstrate that upregulated drives PDAC progression by enhancing lipophagy through ATG2A-mediated rapid lysosomal repair, highlighting OSBPL10 as a potential therapeutic target in PDAC. - Source: PubMed
Publication date: 2026/03/25
Duan ZonghaoMa XueshiyuYu FengZhang JunfengHua RongLiu WeiLiu DejunYang JianyuFu XueliangYang MinweiYao HongfeiJiang ShuhengHu LipengMutailifu MusitabaYang XiaomeiSun YongweiYao LinliHuo Yanmiao - The glycolipid transfer protein (GLTP) has been proposed to function as a sensor and regulator of glycosphingolipid homeostasis in the cell, as levels of GLTP directly influence the quantities of many glycosphingolipids. Furthermore, through its interaction with the endoplasmic reticulum membrane protein vesicle-associated membrane protein-associated protein A (VAPA), GLTP may also be involved in regulating intracellular vesicular transport. Here we show that GLTP knockout (GLTP KO) leads to the sequestration of coat protein complex II coat proteins Sec23 A and Sec31 A at the ER exit sites. The intracellular localization of the small GTPase Sar1A is altered in GLTP KO cells and in cells expressing a GLTP mutant incapable of VAPA binding, indicating a correlation between the inhibition of the GLTP/VAPA interaction and the altered localization of Sar1A. We also observed alterations in the intracellular localization of the Sar1A-activating GEF Sec12 in GLTP KO cells, implying a Sec12-activating role of the GLTP/VAPA interaction. Knockout of GLTP does not alter the amounts of other lipid transfer proteins or glucosylceramide synthase, indicating that a decrease in the levels of these proteins is not responsible for the decreased glycosphingolipid levels associated with GLTP KO. We propose a role for GLTP in modulating the coat protein complex II vesicle trafficking pathway, thereby indirectly regulating the cellular glycosphingolipid homeostasis by controlling the vesicular ceramide transport from the endoplasmic reticulum to the Golgi. Moreover, the discovery that GLTP localizes to the nucleus at the onset of the DNA-replicating S-phase of the cell cycle introduces an entirely new and unexpected dimension to GLTP's in vivo function. - Source: PubMed
Publication date: 2026/03/17
Nurmi HenrikEnglund LindaHenriksson AlinaLönnfors MaxMattjus Peter - Growth of filamentous fungi is highly polarized requiring the coordinated apical delivery of cell wall components and plasma membrane (PM) material, primarily lipids and proteins, to hyphal tips via conventional vesicular secretion. Fungal growth also requires the tight coordination of exocytosis (secretion) with endocytosis and recycling of proteins and lipids, which occurs in a defined region behind the growing tip known as the endocytic collar. Here, we genetically characterized proteins tentatively implicated in the formation of endoplasmic reticulum-plasma membrane (ER-PM) contact sites, including Scs2/VAP, tricalbins and Ist2 homologues, in . We showed that among these proteins, only the single Scs2/VapA homologue is essential for normal fungal growth, and this requirement is due to the critical role of VapA in maintaining the polarized localization of apical cargoes, such as the lipid flippases DnfA and DnfB or the SNARE protein SynA. In mutants, these cargoes lose their polarized localization, a phenotype that correlates with the mislocalization of the AP-2 cargo adaptor complex, which is essential for the endocytosis and recycling of apical membrane components. Further analysis provides evidence linking the defect in apical cargo endocytosis observed in mutants to altered membrane lipid partitioning, suggesting that VapA contributes to lipid domain organization critical for cargo recycling. Strikingly, deletion of VapA does not impair the localization or endocytosis of non-polarized (subapical) plasma membrane transporters, indicating that the trafficking and biogenesis of polarized (apical) versus non-polarized (subapical) cargoes are differentially dependent on membrane lipid composition and domain-specific organization. - Source: PubMed
Publication date: 2026/02/04
Georgiou XeniaPoliti SofiaAmillis SotirisDiallinas George - Colorectal cancer (CRC) is a leading cause of cancer-related deaths, with the tumor microenvironment (TME) influencing disease progression and therapeutic response. Tumor endothelial cells are crucial in CRC initiation, progression, and metastasis, yet their specific mechanisms are not fully understood. - Source: PubMed
Publication date: 2026/02/16
Zhou WentingWang RuiLiu XueniYang ZhengfengYuan YixinPeng XiaoPeng Zhihai - Understanding the genetic foundations of dementia is critical to unraveling its complex molecular basis. Given that a clinical diagnosis of Alzheimer's disease (AD) dementia often results from interplay between multiple underlying neuropathologic co-morbidities, previous genome-wide association studies (GWAS) of clinically diagnosed AD are restricted in their ability to translate genetic associations to potential targeted therapeutics. The current study seeks to address these limitations by presenting the largest GWAS to date (n=12,509) of neuropathologic hallmarks of AD and AD related dementias (ADRDs). We further performed a candidate-variant analysis using loci previously identified in GWAS of clinically diagnosed AD dementia and Parkinson's disease (PD). Finally, we conducted heritability and genetic correlation analyses using linkage disequilibrium (LD) score regression. We found broad genome-wide significant associations with across AD and ADRDs but not cerebrovascular disease and vascular brain injury. We further identified 12 significant loci across 10 neuropathologic phenotypes, including 5 loci previously implicated in GWAS of clinical AD and ADRDs (variants on and ) and 7 novel genome-wide associations (variants on and ). Our analysis of AD and PD clinical candidate variants demonstrated several that were associated with AD neuropathologic change and Lewy body disease, as well as substantial overlap with neuropathologic lesions other than the primary neuropathologic hallmarks of these diseases. Heritability analyses demonstrated heritability that was high for amyloid plaques (78%) relative to prior clinical AD heritability analyses, intermediate for TDP-43 inclusions (41%), and low for remaining AD and ADRD pathologic features. This study underscores the importance of investigating the underlying neuropathologic hallmarks of AD and ADRDs as a step toward refining the translation of genetic associations to biomarker interpretation and development of targeted therapeutics. - Source: PubMed
Publication date: 2026/01/23
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