PNPLA2 _ Desnutrin
- Known as:
- PNPLA2 _ Desnutrin
- Catalog number:
- Y213921
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- PNPLA2 _ Desnutrin
Related genes to: PNPLA2 _ Desnutrin
- Gene:
- PNPLA2 NIH gene
- Name:
- patatin like phospholipase domain containing 2
- Previous symbol:
- -
- Synonyms:
- desnutrin, TTS-2.2, ATGL, FP17548, iPLA2zeta
- Chromosome:
- 11p15.5
- Locus Type:
- gene with protein product
- Date approved:
- 2004-09-06
- Date modifiied:
- 2015-11-23
Related products to: PNPLA2 _ Desnutrin
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- Pigment epithelium-derived factor (PEDF) promotes photoreceptor survival through its receptor PEDF-R, a phospholipase involved in retinal lipid metabolism. To define the in vivo function of the PEDF/PEDF-R axis, we generated mice lacking (PEDF) and (PEDF-R). Combined loss of and resulted in severe retinal degeneration characterized by outer nuclear layer (ONL) thinning, outer segment (OS) shortening, reduced rhodopsin and cone opsin expression, increased TUNEL-positive nuclei, and enhanced retinal autofluorescence associated with altered lipid distribution. Lipid-associated markers, including TIP47, PLIN5, and BODIPY, exhibited abnormal distribution patterns in mutant retinas, indicating disrupted lipid storage and trafficking. Loss of PEDF/PEDF-R signaling also impaired photoreceptor-rod bipolar cell connectivity, as demonstrated by reduced PKCα/synaptophysin colocalization, and resulted in diminished electroretinographic responses. Lipid Imaging mass spectrometry revealed decreases in some lipid abundances in photoreceptor outer segment and inner segment/outer nucleus layer, while lipids containing arachidonic acid and docosahexaenoic acid-containing lipids showed increased abundance. Together these findings identify the PEDF/PEDF-R signaling axis as a key regulator of retinal phospholipid homeostasis that couples lipid metabolism to photoreceptor survival and visual function. - Source: PubMed
Publication date: 2026/08/09
Bernardo-Colón AlexandraCrawford Susan EAgbaga Martin PaulWang ZhenSchey KevinBecerra S Patricia - Objective Pediatric obesity is associated with early metabolic complications and increased risk of persistent obesity in adulthood. Beyond fat accumulation, obesity may induce long-lasting molecular alterations in adipose tissue, described as "obesogenic memory." However, whether such intrinsic alterations are already present in pediatric adipose progenitor cells remains poorly understood. This study aimed to develop an in vitro model of adipogenesis using pediatric adipose-derived mesenchymal stem cells (hMSCs) and to investigate whether obesity is associated with intrinsic metabolic reprogramming of adipose progenitors. Methods hMSCs were isolated from periumbilical subcutaneous adipose tissue obtained from pediatric subjects with normal weight (NW), overweight (OW) and obesity (OB). Cells were expanded and induced to undergo adipogenic differentiation for up to 14 days using defined adipogenic media. Differentiation was evaluated through morphological analysis, lipid accumulation (BODIPY staining), gene expression profiling by RT-qPCR, and protein analysis by Western blot. Results Two differentiation protocols efficiently induced adipocyte maturation without cytotoxicity. hMSCs derived from NW and OB subjects showed comparable adipogenic differentiation capacity, with similar lipid droplet accumulation and expression of canonical adipogenic markers including C/EBPα, PPARγ, and FABP4. Despite this comparable differentiation efficiency, OB-derived adipocytes exhibited altered transcriptional regulation of genes involved in lipid metabolism, including pathways associated with lipogenesis, lipolysis, and fatty acid β-oxidation. Protein analyses further revealed dysregulated expression of key metabolic regulators such as SCD1, SREBP1, PNPLA2, and FADS1, suggesting altered lipid metabolic programming. Conclusions Pediatric obesity does not impair adipogenic differentiation but is associated with intrinsic metabolic alterations in adipose progenitor cells. These findings support the presence of an early obesogenic memory in adipose tissue that may contribute to long-term metabolic dysfunction. - Source: PubMed
Publication date: 2026/08/14
Dardi MarkoBerardo ClarissaPelizzo GloriaBonnet MaximeDestro FrancescaCapelo GersonCeresola MicheleLai AlessiaCarelli StephanaZuccotti GianVincenzoCalcaterra Valeria - Perturbation of macropinocytosis triggers methuosis, a non-apoptotic cell death characterized by cytoplasmic vacuolization. However, the regulatory mechanisms of methuosis remain poorly defined. Lipid metabolism dysregulation is implicated in various cell death pathways, while its role in methuosis has remained elusive. Herein, LXX-8250, an isopropanolamine derivative of β-elemene, induced a vacuolization-associated cell death in breast and liver cancer cell lines. This process was accompanied by massive macropinocytosis, thereby confirming the occurrence of methuosis. Mechanistically, hypoxia-inducible lipid droplet-associated protein (HILPDA), a key regulator that promotes intracellular triacylglycerol (TAG) accumulation, was identified as the direct target of LXX-8250. By suppressing HILPDA, LXX-8250 inhibited diacylglycerol O-acyltransferase 1 (DGAT1) and activated adipose triglyceride lipase (ATGL). Consequently, lipid droplets and cellular TAG levels were reduced, while the subsequent increased diacylglycerol (DAG) stimulated macropinosome formation, leading to methuosis in these cells. In this study, we discover a novel methuosis agonist LXX-8250, and elucidate the critical role of HILPDA repression-dysregulated lipid metabolism in methuosis. Our study highlighted the potential of targeting this pathway as a therapeutic strategy to trigger cancer cell death. - Source: PubMed
Wang JieZhai ChuanxinZhang ChengfeiFan AnlianJalal SajidZhang TingXu TingGao ChuanzhouChen XinranTeng HongmingLuo YuanyuanLi CongHuang Lin - By integrating transcriptomics and network pharmacology, we systematically investigated the potential hemostatic mechanism of (BS). - Source: PubMed
Yang TaoXiong YanYang LingWang Xing-GangHuang YongFu Zhi-Li - Vein occlusion (VO), including deep venous thrombosis (DVT) and retinal vein occlusion (RVO), is a common cause of multiple diseases that severely compromise the quality of life of affected individuals. Epidemiological evidence indicates that VO prevalence increases in cold seasons, yet the underlying mechanism remains unknown. Here, we show that cold exposure markedly elevates peripheral platelet counts, thereby aggravating VO in mouse models. Cold-augmented thrombocytopoiesis depends on the activation of adipose thermogenesis and subsequent increase in circulating free fatty acid (FFA) levels. Mechanistically, FFA-β-oxidation promotes acetyl-CoA production, which upregulates and stabilizes C/EBPα by shifting the balance between p300 acetyltransferase and SIRT1 deacetylase. Acetyl-C/EBPα transcriptionally upregulates GATA-1 and NF-E2 for megakaryocyte maturation and platelet production. Depletion of adipose triglyceride lipase PNPLA2, megakaryocyte-specific knockout of key β-oxidation enzyme CPT1α, or pharmacological inhibition of CPT1α and p300 abolishes cold-augmented thrombocytopoiesis and alleviates DVT and RVO in mouse models. In healthy volunteers, tolerable cold exposure activates adipose thermogenesis, increases circulating FFA levels, and increases platelet counts. Moreover, a retrospective cohort study of 425 patients reveals elevated platelet counts and higher DVT incidence during cold seasons. Similarly, increased platelet counts are observed in 448 patients with RVO at the time of diagnosis in cold seasons. Our study provides novel mechanistic insights into the increased VO risk induced by cold exposure and proposes a new therapeutic paradigm for VO by targeting megakaryocyte metabolism. - Source: PubMed
Publication date: 2026/07/30
Xie SisiChen KaihongSun XiaotingYe YingChen RuiboJiang ChenyuChen MingjiaLv XueLi HuilanLiao YingChen WeihuaDeng LinCai LinliLiang YuWei QiaolingZuo JiYu GuohuaYang LiboJi JiansongLin LiTao WeiZhao ChenYang YunlongCao Yihai