Ask about this productRelated genes to: PLA1A antibody
- Gene:
- PLA1A NIH gene
- Name:
- phospholipase A1 member A
- Previous symbol:
- -
- Synonyms:
- ps-PLA1
- Chromosome:
- 3q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 2002-11-28
- Date modifiied:
- 2016-10-05
Related products to: PLA1A antibody
Related articles to: PLA1A antibody
- The distinctive flavor and desirable texture of Qiandongnan Xiaoxiang chicken meat make it an ideal model for studying the formation of chicken meat quality traits. This study investigated age-related changes in meat quality, gut microbiota, and the underlying molecular mechanisms in Qiandongnan Xiaoxiang chickens. By integrating multi-omics data, we systematically examined the alterations and interrelationships among serum biochemical indices, gut microbial composition, breast muscle metabolome, and transcriptome in chickens at different ages (60-180 days). The results showed that increasing age significantly affected physiological metabolism, muscle development, and meat quality formation. As age increased, breast muscle pH, shear force, and redness (a*) increased, whereas yellowness (b*) decreased. Serum lipidomic profiling revealed elevated levels of triglycerides, cholesterol, and free fatty acids, accompanied by a reduction in high-density lipoprotein cholesterol. Flavor precursors such as sucrose, arbutin, acylcarnitines, lipid-derived substrates, and bile acid-related metabolites may participate in the maillard reaction, lipid oxidation, or undergo further transformation during processing, thereby promoting aroma formation. With increasing age, lipid metabolism-related signaling pathways, including adipocytokine signaling, fatty acid biosynthesis, fatty acid metabolism, linoleic acid metabolism, glycerophospholipid metabolism, and regulation of lipolysis in adipocytes, were significantly enriched. Transcriptomic analysis identified the key lipid-related gene PLA1A, whose expression pattern was consistent with the observed metabolic changes. Multi-omics analysis identified gut microorganisms (Bifidobacterium, Lachnospiraceae NK4A136 group, and Christensenellaceae R7 group) that were negatively correlated with the PLA1A gene and flavor metabolites such as 4‑aminovaleric acid betaine, danazol, and hetisine. Collectively, these findings elucidate the microbial-metabolic-genetic network underlying meat quality development and provide new insights for optimizing poultry production. - Source: PubMed
Publication date: 2026/04/23
Xie YuxiaoYi LanlanCheng WenjieJia HuijinZhang WanghongSong GuangyaoZhu JunhongZhao Sumei - Tuberculosis (TB) remains a global health threat, and latent TB infection (LTBI) serves as a significant reservoir for new cases. Current diagnostic methods have limitations in accuracy and specificity. This study aimed to identify novel plasma biomarkers for LTBI by integrating metabolomics and transcriptomics. Plasma samples from healthy controls (HC) and LTBI patients were analyzed using liquid chromatography-mass spectrometry (LC-MS)/MS. We identified distinct metabolic signatures characterizing LTBI, and a diagnostic model based on five key metabolites-margaroylglycine, N-palmitoyl tryptophan, oleamide, myristic acid, and pentadecanoic acid-was established, demonstrating discriminatory potential. Multi-omics integration revealed that these metabolites are significantly associated with perturbations in glycerophospholipid and tryptophan metabolism pathways. Validation via qPCR confirmed significant dysregulation of associated genes (, , , , , , and ) in peripheral blood mononuclear cells (PBMCs). External validation in independent cohorts confirmed the consistency of these metabolic alterations. These findings suggest a robust panel of biomarkers for LTBI screening and offer exploratory insights into the metabolic dysregulation underlying latent infection. - Source: PubMed
Publication date: 2026/03/27
Liu DongFeng ZhelongMeng XiangruiLi YanhanZeng YuerongLi YanYan FangWang Yajing - : Metabolic dysfunction-associated steatotic liver disease (MASLD) is a sexually dimorphic condition, with higher prevalence in men than in women. Sex differences in hepatic lipid metabolism and the modulatory role of sex hormones have been described but are still insufficiently understood. The aim of this study was to introduce the variables sex and sex hormones into a human in vitro model of hepatic steatosis. : Primary human hepatocytes (PHHs) were isolated from male and female donors, treated with free fatty acids (FFA) to induce steatosis, and further exposed to physiological concentrations of estrogen, progesterone, or testosterone. Intracellular triacylglyceride (TAG) content, lipid droplet (LD) formation, FFA uptake, and very-low-density lipoprotein (VLDL) excretion were assessed. In parallel, the expression of lipid metabolism-related genes was quantified by qPCR. : FFA treatment induced comparable uptake and intracellular TAG storage in both sexes. However, female PHHs secreted approximately twice as many VLDL particles as male cells. Steatosis significantly increased expression of , , and only in male PHHs. Sex hormones exerted distinct, sex-specific effects: estrogen reduced TAG accumulation in female PHHs; whereas testosterone reduced TAG in male but increased it in female PHHs after prolonged treatment. LD characterization confirmed sex- and hormone-dependent differences in lipid storage patterns. In male PHHs, progesterone promoted lipid storage and increased apoB-100 secretion, accompanied by reduced and expression, and testosterone increased the FFA-mediated even further. : Sex and sex hormones distinctly shape hepatocellular lipid handling under steatotic conditions. While female PHHs demonstrated greater lipid excretion capacity, male PHHs exhibited stronger transcriptional responses. Sex-specific responses to estrogen and testosterone resembled clinical observations on sex hormone effects. These findings highlight the need to account for sex-specific differences in MASLD pathophysiology and therapeutic strategies. - Source: PubMed
Publication date: 2025/11/12
Seidemann LenaRohm Carolin MarieStilkerich AnnaHänsel RenéGötz ChristinaSeehofer DanielDamm Georg - Spleen conventional dendritic cells type 1 (cDC1) take up apoptotic cells (AC) and cross-present associated antigens to CD8 T cells. The receptors promoting AC uptake are incompletely defined. Here, we tested the function of GPR34, a receptor that responds to the phosphatidylserine (PS) catabolite lysoPS. GPR34 deficiency led to reduced AC uptake by cDC1 but not cDC2 or macrophages. Uptake of soluble antigen or heat-killed bacteria was unaffected, whereas uptake of eryptotic RBCs was reduced. Using AC harboring OVA, activation and proliferation of OT-I T cells were compromised in GPR34-deficient mice. Reciprocally, GPR34 overexpression led to enhanced AC uptake and OT-I proliferation. The enzymes PLA1A and ABHD16A have been implicated in generating lysoPS that can act on GPR34. PLA1A but not ABHD16A deficiency was associated with a reduced OT-I response to AC-associated OVA. In conclusion, we identify a receptor requirement for cDC1 efferocytosis and cross-presentation and suggest a model where PLA1A catabolizes PS on AC to generate GPR34 ligands. - Source: PubMed
Publication date: 2025/11/10
Tam HansonShen HaolinXu YingAn JinpingCyster Jason G - Retinal neovascular diseases are leading causes of global blindness. Migrasomes, organelles released during cell migration, play a role in intercellular communication and are present in M2 macrophages, which are critical to the pathology of retinal neovascular diseases. This study investigates the involvement of M2 macrophage-derived migrasomes in ischaemia-induced retinal neovascularization (RNV). Migrasomes are isolated from macrophages and characterized by Western blotting and transmission electron microscopy. Compared with controls, M2 macrophage-derived migrasomes significantly enhance human retinal microvascular endothelial cell (HREC) functions by Cell Counting Kit-8, transwell, and tube formation assays, and markedly contribute to the pathological retinal angiogenesis of oxygen-induced retinopathy (OIR) mice. Triggering receptor expressed on myeloid cells 2 (TREM2) is selected as the potential downstream target of M2 macrophage-derived migrasomes by proteomic analysis. Moreover, the depletion of M2 macrophages in OIR retinas reduces the levels of migrasomes and TREM2. BTC and PLA1A overexpression in HRECs could attenuate decreased HREC functions induced by sh-TREM2 M2 macrophage-derived migrasomes. These findings demonstrate that TREM2-enriched M2 macrophage-derived migrasomes contribute to pathological RNV in vivo and positively regulate HREC functions in vitro through targeting TREM2-BTC/PLA1A, which may serve as biomarkers and therapeutic targets for retinal neovascular diseases. - Source: PubMed
Li BingyanChen JunyuZhu JunyeZhou HaixiangZhang QiuxiangDeng HuiWen HaipengXu FanTang FenYoshida ShigeoZhou Yedi