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
- Thyroid hormones are central regulators of metabolic homeostasis and developmental programming. The active hormone triiodothyronine (T3) modulates transcription through nuclear receptors that recruit epigenetic cofactors to remodel chromatin and regulate metabolic gene networks. Although thyroid hormone signaling is known to influence lipid metabolism, whether it coordinates lipid droplet turnover with autophagy-related pathways during early embryonic development remains largely unknown. Here, transcriptomic profiling revealed distinct metabolic signatures between and embryos, with marked differences in fatty acid metabolism. Supplementation with 50 nM T3 enhanced blastocyst formation, particularly when applied from the 4-cell to blastocyst stages, coinciding with elevated thyroid hormone receptor expression. T3 induced robust lipid droplet remodeling, characterized by reduced droplet size, together with increased lipid-mitochondria colocalization and activation of lysosomal and mitochondrial pathways, consistent with enhanced lipid catabolism and organelle coupling. Mechanistically, inhibition of the histone acetyltransferase KAT2B/PCAF abolished T3-mediated developmental gains, reduced H3K9ac and H3K27ac, and resulted in nonselective autophagic stress rather than lipophagy. By contrast, T3 required KAT2B to stimulate cytosolic lipolysis, channel fatty acids into mitochondria, and enhance mitochondrial membrane potential. T3 also upregulated prostaglandin biosynthesis genes and improved outgrowth performance. These findings identify a thyroid hormone-KAT2B epigenetic axis that coordinates lipid droplet remodeling through lipolytic and lipophagic pathways, linking endocrine signaling to organelle crosstalk and mitochondrial activation during early embryogenesis. ART: assisted reproductive technology; ATG5: autophagy related 5; BSA: bovine serum albumin; BSCL2/SEIPIN: BSCL2 lipid droplet biogenesis associated, seipin; CARM1: coactivator associated arginine methyltransferase 1; COCs: cumulus-oocyte complexes; CPT1A: carnitine palmitoyltransferase 1A; CPT2: carnitine palmitoyltransferase 2; CREBBP/CBP: CREB binding protein; DEGs: differentially expressed genes; DGAT1: diacylglycerol O-acyltransferase 1; EP300: E1A binding protein p300; ER: endoplasmic reticulum; H3K9ac: histone H3 acetyl-Lys9; H3K27ac: histone H3 acetyl-Lys27; HCS: high-content screening; HDACs: histone deacetylases; IVC: in vitro culture; IVF: in vitro-fertilized embryos; IVM: in vitro maturation; IVO: in vivo embryos; KAT2A/GCN5: K(lysine) acetyltransferase 2A; KAT2B/PCAF: K(lysine) acetyltransferase 2B; KAT2Bi (Ki): KAT2B inhibition; KD: knockdown; LC3: microtubule associated protein 1 light chain 3; LDs: lipid droplets; LIPE/HSL: lipase E, hormone sensitive type; MGLL: monoglyceride lipase; MMP: mitochondrial membrane potential; mtDNA: mitochondrial DNA; MT-ND1: mitochondrially encoded NADH:ubiquinone oxidoreductase core subunit 1; PA: parthenogenetically activated; PG: prostaglandin; PLA2G4A: phospholipase A2 group IVA; PLIN2: perilipin 2; PLIN3: perilipin 3; PLIN5: perilipin 5; PNPLA2/ATGL: patatin like phospholipase domain containing 2; PPARD/PPARδ: peroxisome proliferator activated receptor delta; PPARs: peroxisome proliferator activated receptors; PRMT1: protein arginine methyltransferase 1; PTGS1: prostaglandin-endoperoxide synthase 1; PTGS2: prostaglandin-endoperoxide synthase 2; PVA: polyvinyl alcohol; RT: room temperature; RT-qPCR: reverse transcription-quantitative polymerase chain reaction; RXR: retinoid X receptor; SIRT1: sirtuin 1; SLC25A20/CACT: solute carrier family 25 member 20; SLC27A4/FATP4: solute carrier family 27 member 4; SUV39H1: SUV39H1 histone lysine methyltransferase; T3: triiodothyronine; T4: thyroxine; TAGs: triacylglycerols; TEM: transmission electron microscopy; THR: thyroid hormone receptor; THRA: thyroid hormone receptor alpha; THRA-i: thyroid hormone receptor antagonist; THRB: thyroid hormone receptor beta; THs: thyroid hormones; ZGA: zygotic genome activation. - Source: PubMed
Publication date: 2026/09/24
Lee Song-HeeZhan Cheng-LinCui Xiang-Shun - Exposure to high and sustained levels of non-esterified fatty acids (NEFA) in the peripartal period is the main cause of fatty liver disease in dairy cows. Rumen-protected choline is often fed as part of the nutritional management of peripartal cows, with in vivo and in vitro data indicating positive effects of this nutrient on alleviating liver lipid accumulation. Although hepatic molecular mechanisms associated with choline supply have been studied using a target gene, protein, or metabolite approach, application of high-throughput technologies could vastly enhance fundamental knowledge on the functional role of choline. The main objective was to challenge isolated hepatocytes with a mixture of NEFA and determine proteome- and metabolome-wide effects in response to choline supply. Three healthy female calves (1 d old, 30-45 kg) were sacrificed to harvest hepatocytes. During a 12 h incubation, isolated hepatocytes were challenged without NEFA (control), 1.2 mM NEFA (c9-18:1, 18:2, 16:0, 18:0, and c9-16:1 at 43.5%, 4.9%, 31.9%, 14.4%, and 5.3% of total NEFA, respectively), or NEFA for 6 h followed by 10 μM choline chloride for another 6 h (NEFA + Chol). iTRAQ labeling-based protein profiling and GC/MS-based metabolomics profiling were used to determine changes in proteins and metabolites. Differentially abundant proteins for each group comparison were determined at a threshold of 1.4-fold change. Differences in metabolite profiles were assessed via pairwise comparisons. A subset of differentially abundant proteins was validated via qRT-PCR and Western blotting. Compared with the control, there were 90 proteins and 22 metabolites in the NEFA group, and 83 proteins and 29 metabolites in the NEFA + Chol. Compared with NEFA, there were 49 proteins and 17 metabolites in the NEFA + Chol group. Greater abundance of hexokinase-1 (HK1), fructose-bisphosphate aldolase (ALDOA), mitochondrial pyruvate carrier 1 (MPC1), and increased concentrations of lactate with high NEFA treatment alone suggested greater glycolytic and TCA cycle activity. Accumulation of triacylglycerol in the NEFA group was associated with lipotoxicity and markers of inflammation, such as greater abundance of prostaglandin reductase 1 (PTGR1), serious cell autophagy processes, such as greater abundance of cell division cycle 42 (CDC42), and NFκB-related proteins. Choline supplementation reduced TAG partly due to greater VLDL secretion driven by greater abundance of diacylglycerol acyltransferase (DGAT1), perilipin 3 (PLIN3), and apolipoprotein C-III (APOC3). In addition, a greater abundance of carnitine O-palmitoyltransferase 1b (CPT1B) with choline suggested enhanced mitochondrial β-oxidation. Activation of the CDC42/JNK pathway and ROS/NFκB axis-related proteins, along with depressed PI3K/AKT/RAC-related proteins, indicated enhanced mitochondrial autophagy in response to NEFA. Overall, data confirmed published effects of choline on TAG accumulation, VLDL secretion, and fatty acid oxidation, while highlighting negative effects of NEFA on the respiratory electron transport chain, autophagy, and inflammatory processes. - Source: PubMed
Publication date: 2026/06/26
Chang YaqiJia BinSi YaranZhang ZexinLiu JiachenGao YueWang JunhaoWang YanhuiLoor Juan JZhang BingbingYang Wei - Recently, immune checkpoint inhibitors (ICIs), especially those that targets PD-1/PD-L1, have significantly altered the treatment approach for NSCLC. Nevertheless, many patients experience different levels of resistance after receiving treatment with ICIs, which restrict their broader use in clinical practice. Therefore, to enhance the overall efficacy of ICIs, there is an immediate necessity to further explain the processes of immune evasion in NSCLC, especially the modulatory mechanism of PD-L1. - Source: PubMed
Publication date: 2026/07/23
Zhou HanqiongFan SongqingOuyang MinZheng Hongmei - Huaier, a traditional Chinese medicinal mushroom, has been shown to have anti-tumor properties in our previous studies. However, its role and underlying mechanisms in regulating doxorubicin (DOX) sensitivity in triple-negative breast cancer (TNBC) remain unclear. - Source: PubMed
Publication date: 2026/07/09
Ma TingtingNiu TongLi YamingYang Qifeng - Reducing reliance on supplemental fish oil is central to sustainable aquaculture, but the molecular consequences of replacing it with vegetable oils remain poorly characterized in the juvenile Chinese soft-shelled turtle (). We evaluated whether full substitution of the supplemental dietary fish oil (FO) with linseed oil (LO) or soybean oil (SO) compromises hepatic lipid metabolism in . Three isonitrogenous and isolipidic diets, sharing identical fish meal and other ingredient bases and differing only in the supplemental lipid (4% FO, LO or SO), were fed to triplicate groups of juvenile turtles (initial body weight 55.0 ± 0.05 g) for 8 weeks. Growth performance, survival, feed conversion ratio, and serum biochemistry were unaffected. However, both vegetable oil diets altered tissue fatty acid composition, raising n-6 PUFA and lowering n-3 LC-PUFA and the n-3/n-6 ratio in liver and muscle (muscle EPA and DHA each decreased by approximately 40%); the SO group additionally exhibited elevated hepatic malondialdehyde, whereas hepatic lipid droplet area and lipid content did not differ significantly among groups. Liver transcriptomic profiling identified 262 (LO vs. FO) and 214 (SO vs. FO) differentially expressed genes, converging on lipid storage and bile acid metabolism. RT-qPCR confirmed the up-regulation of , and and the down-regulation of . Over 8 weeks, replacement of supplemental FO maintained growth without overt impairment while altering tissue fatty acid profiles and the hepatic expression of key lipid metabolism genes. - Source: PubMed
Publication date: 2026/07/02
Li RuiGuo YileiZhao EnhaoGe ChutianSun Jie