Ask about this productRelated genes to: ATG2A antibody
- Gene:
- ATG2A NIH gene
- Name:
- autophagy related 2A
- Previous symbol:
- -
- Synonyms:
- KIAA0404
- Chromosome:
- 11q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2007-07-31
- Date modifiied:
- 2015-09-11
Related products to: ATG2A antibody
Related articles to: ATG2A 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 - Chemotherapy resistance is the main obstacle to breast cancer recurrence, metastasis, and mortality. Drug-tolerant persister (DTP) cells are a novel type of target cell associated with tumor resistance, and autophagy is a key factor in maintaining the survival of tumor DTP cells. However, it is unclear whether the activation of autophagy in breast cancer DTP cells is related to their overexpression of the transcriptional regulatory factor CDCA7. - Source: PubMed
Publication date: 2026/03/11
Wu JinWang ZhaoyuLiu JuanMa QinghuaLi SisiZhou RongMiao JingyaChen QingqiuJiang JunLiu WeiTang Peng - The endoplasmic reticulum (ER) must carefully regulate the levels of nonmembrane lipids such as diacylglycerol (DAG), phosphatidic acid (PA), and triacylglycerol (TAG) to maintain membrane integrity and prevent lipotoxic stress. While ATG2A is well known as a lipid transfer protein essential for autophagosome formation, its role at lipid droplet (LD) contact sites has remained unclear. In our recent work, we show that ATG2A functions beyond its typical role in autophagy as a key regulator of lipid storage, transferring DAG, TAG, and PA from the ER to LDs and recruiting the TAG synthesis enzyme DGAT2 to promote LD expansion. Without ATG2A, lipids accumulate in the ER, leading to smaller, more numerous nucleated LDs rather than proper growth. Notably, ATG2A-mediated DAG transfer recruits DGAT2 to LD surfaces, enabling local TAG synthesis that prevents nonmembrane lipid accumulation in the ER. This cooperative process reveals ATG2A's dual role in both autophagy and lipid storage, highlighting an unexpected link between autophagy machinery and lipid storage. - Source: PubMed
Publication date: 2026/03/18
Elhan HelinKorfhage Justin LMelia Thomas JThiam Abdou Rachid - Chronic and acute pancreatitis (CP and AP, respectively) are debilitating conditions with significant morbidity and mortality, necessitating a comprehensive understanding of their underlying mechanisms. This study provides a high-resolution, multi-omics investigation into the genetic and immune cell underpinnings of pancreatitis, integrating rare familial CP with a large cohort of patients with AP. Utilizing an integrative approach that combined whole-exome sequencing (WES) from two pediatric CP patients and their family members with single-cell RNA sequencing (scRNA-seq) and bulk transcriptomics from a public AP cohort ( = 119), we identified a shared molecular and cellular pathology. WES of the CP family revealed heterozygous mutations in 12 novel genes, including , , and . Functional enrichment analysis highlighted autophagy, cell adhesion, and vesicle-mediated transport as the key biological processes implicated in the pathophysiology of both conditions. Single-cell profiling of peripheral blood mononuclear cells (PBMCs) from the CP family revealed a marked increase in the proportion of naive B cells and an altered activity of CD8 T cells, suggesting a dysregulated B-cell-mediated immune response. This observation was corroborated in the AP cohort, where CIBERSORT analysis revealed a significant increase in both naive B cells and CD8 T cells correlating with the disease severity. Weighted gene co-expression network analysis (WGCNA) on the AP cohort uncovered 14 gene modules associated with disease progression. These modules were significantly enriched for pathways central to the innate immune response, including complement-dependent cytotoxicity and neutrophil degranulation, providing a molecular link to the observed immune cell infiltration. An artificial intelligence (AI)-driven model incorporating 110 CP family-related genes (GTCPFs) demonstrated exceptional predictive capability (average AUC > 0.84) for AP severity, highlighting the translational potential of our findings. The model identified a robust signature of 17 genes, including , , and , which may serve as novel diagnostic and prognostic biomarkers. Our findings provide a unified view of the pathogenesis of pancreatitis, linking novel genetic variants to specific immune cell and transcriptomic signatures. This integrative approach underscores the critical importance of both genetic and immune factors in CP and AP, identifying potential biomarkers and therapeutic targets and paving the way for personalized medicine in the management of these challenging conditions. - Source: PubMed
Publication date: 2026/01/12
Li FuHuang Jin-XinSun Wen-JieZeng Jing-QingGan Ke-XinGong BiaoJi Jian-MeiChen JianDeng Zhao-HuiXu Dong-Liang - - Source: PubMed