Ask about this productRelated genes to: M6PRBP1 antibody
- Gene:
- PLIN3 NIH gene
- Name:
- perilipin 3
- Previous symbol:
- M6PRBP1
- Synonyms:
- TIP47, PP17
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-16
- Date modifiied:
- 2014-11-19
Related products to: M6PRBP1 antibody
Related articles to: M6PRBP1 antibody
- We and others have shown that elevated human Group IIA secreted phospholipase A (hGIIA) has both catalysis-dependent and -independent functions that are associated with both acute and chronic inflammatory disorders including cancer. Our novel inhibitors that selectively block hGIIA's catalysis-independent function slow tumor growth in animal models via interaction with vimentin. The mechanism of this interaction and its consequences for cancer aggressiveness remains unexplored. - Source: PubMed
Publication date: 2026/05/18
Andarva MonavvarElias Maria GeorgeSajinovic MilaMann Timothy JZhou Jasmine MMellick Albert SRoberts Tara Laurinede Souza PaulScott Kieran F - Lipid metabolic reprogramming is increasingly recognized as a critical feature of prostate cancer progression, but the lipid metabolism-related genes that remain continuously dysregulated from normal tissue to primary tumor and metastatic disease have not been systematically characterized, and their biological and prognostic relevance remains incompletely understood. - Source: PubMed
Publication date: 2026/05/25
Li RongnaHe HongyingSun HuiLong YiliHuang NanZhu YingbingChen HongtaoJiang GuanminChen Xiaohui - BACKGROUND: Macrophage–myofibroblast transition (MMT) promotes tumor progression. Studies have primarily emphasized macrophage-intrinsic regulation; however, whether lung adenocarcinoma (LUAD) cells actively drive MMT in tumor-associated macrophages (TAMs) remains unclear. METHODS: We integrated LUAD single-cell RNA sequencing (scRNA-seq) and bulk transcriptomic datasets, applying MMT-infiltration-stratified differential analysis to identify tumor cell-derived upstream regulators of MMT. Multiple machine learning algorithms were used to construct an MMT-related risk score. SHAP analysis prioritized key genes, and NicheNet inferred tumor–macrophage ligand–receptor–target axes. Tumor cell–conditioned medium (CM)–driven MMT induction in M2 macrophages was examined by dual immunofluorescence and in vitro experiments. RESULTS: Single-cell analysis showed that M2 macrophages in LUAD exhibit variable activation of an MMT-related transcriptional program. Tumor-level differential analysis across MMT infiltration strata identified tumor cell-derived candidate regulators of MMT. A 9-gene MMT prognostic risk model was established using univariate Cox regression and machine learning analyses. This model achieved a higher C-index than previously reported models, and high-risk tumors displayed an immunosuppressive infiltration pattern. SHAP analysis identified PLIN3 as a key driver. NicheNet analysis suggested that PLIN3-high tumor cells may induce MMT through TGF-β1-related signaling. Immunohistochemistry demonstrated PLIN3 upregulation in LUAD tissues, while immunofluorescence further revealed enrichment of CD68⁺α-SMA⁺ macrophages around tumor cells in PLIN3-high samples. LUAD cell-derived CM induced MMT in M2 macrophages. PLIN3 knockdown in LUAD cells attenuated CM-induced MMT, whereas PLIN3 overexpression enhanced it. PLIN3 knockdown also suppressed LUAD cell migration, invasion, and colony formation. CONCLUSION: High PLIN3 expression in LUAD promotes MMT through tumor–macrophage crosstalk in the tumor microenvironment. - Source: PubMed
Publication date: 2026/04/07
Tian KangMa GuoyuanGuo DeyuJiang HuiZhao XinjieWang GuanghuiDu JiajunPang Zhaofei - Viruses hijack host metabolic resources for replication. Previous studies have shown that classical swine fever virus (CSFV) infection induces host lipid metabolic reprogramming.However, research into the exact regulatory mechanisms between CSFV and lipid metabolism remains limited. Lipophagy refers to the degradation of lipid droplet contents to release free fatty acids(FFAs), CSFV induces autophagy to promote its replication, the regulatory mechanism between CSFV and lipophagy is unclear. In this study, we found that lipid droplets(LDs) initially accumulate and then decrease following CSFV infection. Autophagy activity was negatively correlated with lipid drople levels. Subsequent experiments revealed that CSFV induces lipophagy in Hepatic stellate cells(HSCs)and upregulates perilipin3(PLIN3) expression, a LD-associated protein that facilitates viral replication. Further studies demonstrated that PLIN3 activates the AMPK signaling pathway to promote lipophagy-mediated FFAs release. This FFA increase could be blocked by autophagy inhibitors. Notably, exogenous FFA addition reversed the shPLIN3-induced impairment of CSFV replication. Overall, this finding provides new insights into the mechanisms of virus-host lipid metabolism interactions. - Source: PubMed
Publication date: 2026/02/25
Li BingkeZou LinkeSun ChenchenJiang JiananLi ShurouWang JiaxinHe YintaoQin YuweiZeng SenSong YiwanZeng WeijunYi LinFan ShuangqiChen JindingWu Keke - To investigate the fillet quality traits (texture, flavor, nutritional value) formation and the mechanism of muscular lipid deposition in triploid rainbow trout, low (20%) and high (30%) lipid diets were manufactured and fed market-size triploid rainbow trout (∼3.2 kg) for 77 days. Results showed that the width of the myosepta (MS) was significantly increased, and nonanal, (E, Z)-2,6-nonadienal, octanal, 1-octen-3-ol, and hexanal emerged as the top five contributors to the overall odor profile of the fish fillets, following exposure to the high-lipid (HL) diet. Lipidomic profiling demonstrated that triglycerides (TG) were the predominated lipid class in both muscle fibers (MF) and MS fractions. The HL diet differentially modulated lipid composition: it upregulated TG content in MF, while reducing TG content and promoting the accumulation of phosphatidylcholine (PC) in MS. Gene expression analysis showed tissue-specific regulation of lipid metabolism. In MF, the upregulation of fatty acid binding protein 1 () and perilipin-3 (), and the downregulation of , peroxisome proliferator activated receptor α (), , acyl-CoA oxidase (), and carnitine palmitoyltransferase 1 (), were induced by the HL diet, which collectively promoted TG synthesis and storage, which may be one of the underlying mechanisms contributing to the formation of a more intense odor profile in MF. In MS, HL diet exposure induced the upregulation of , , , , and , and the downregulation of and , thereby promoting TG mobilization and catabolism, and stimulating PC accumulation, and represent a potential mechanism contributing to the increased width of MS. The findings of this study will lay a theoretical foundation for elucidating the quality formation and the heterogeneity of muscular lipid deposition in rainbow trout. - Source: PubMed
Publication date: 2026/01/11
Shen FenghuangHuang DongSun GuoliangWu ZezhongMa RuiMeng Yuqiong