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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- The present study aimed to investigate lipolytic function in cumulus cells (CCs) from women with polycystic ovary syndrome (PCOS), with a particular emphasis on the role of androgen excess. - Source: PubMed
Publication date: 2026/08/31
Zarezadeh RezaFattahi AmirHamdi KobraNikanfar SabaNouri MohammadDarabi Masoud - To summarize recent advances in adult-onset disorders of muscle lipid metabolism, with particular emphasis on fatty acid β-oxidation disorders (FAODs), multiple acyl-CoA dehydrogenase deficiency (MADD) and MADD-like disorders, and neutral lipid storage disease with myopathy (NLSDM). - Source: PubMed
Publication date: 2026/09/03
Liewluck TeerinLaforêt Pascal - 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