PPARA antibody - N-terminal region (ARP33066_P050)
- Known as:
- PPARA (anti-) - N-terminal region (ARP33066_P050)
- Catalog number:
- arp33066_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- PPARA antibody - N-terminal region (ARP33066_P050)
Related genes to: PPARA antibody - N-terminal region (ARP33066_P050)
- Gene:
- PPARA NIH gene
- Name:
- peroxisome proliferator activated receptor alpha
- Previous symbol:
- PPAR
- Synonyms:
- hPPAR, NR1C1
- Chromosome:
- 22q13.31
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-01
- Date modifiied:
- 2016-10-05
Related products to: PPARA antibody - N-terminal region (ARP33066_P050)
Related articles to: PPARA antibody - N-terminal region (ARP33066_P050)
- The rising burden of antimicrobial resistance (AMR) necessitates new bioactive molecules that are both sustainable and therapeutically relevant. Endophytic actinomycetes, particularly , represent a valuable but underexplored source of secondary metabolites with pharmaceutical potential. - Source: PubMed
Publication date: 2026/05/14
Pattapulavar VeilumuthuSubburaj SaranyadeviRamanujam SathiyabamaShil RiyankaVelmurugan PriyankaGhatak TapasMuthusamy SanjivkumarSamrot Antony VChristopher John Godwin - Improving feed efficiency in dairy cattle requires a better understanding of tissue-specific mechanisms that support energy and nutrient utilization. Skeletal muscle represents a major proportion of body mass in dairy cows and plays a major role in post-absorptive metabolism. Our previous liver proteomics study highlighted that high-efficiency (HE) cows exhibit enhanced hepatic fatty acid oxidation, supporting lower feed intake without compromising productivity. This study aimed to identify muscle-based metabolic adaptations associated with feed efficiency. Skeletal muscle samples from 8 HE (low residual feed intake, RFI) and 8 low-efficiency (LE; high-RFI) mid-lactation (119 ± 33 DIM) Holstein cows, ranked at the top and bottom 10% of RFI, were analyzed using tandem mass tag proteomics and RT-qPCR to identify differences in skeletal muscle related to feed efficiency. HE cows had significantly greater muscle glycogen content and exhibited a coordinated metabolic shift favoring lipid utilization. RT-qPCR showed increased expression of β-oxidation (PPARA, ACADS, ACADVL, ACOX1) and triglyceride mobilization (ATGL) in HE cows. In contrast, proteomics revealed lower abundance of glycolytic and glycogenolytic enzymes (e.g., ALDOA, PFKM, PGAM2, PYGM, AGL) in HE muscle, indicating reduced glucose and glycogen catabolism. Proteins involved in the SLC2A4 (GLUT4) translocation pathway (ACTG1, YWHAH, YWHAZ) were more abundant in HE cows, suggesting an increased capacity for insulin-stimulated GLUT4 translocation, which may contribute to greater glycogen storage. Proteomics also showed enhanced redox regulation in HE cows, with greater abundance of GSR, CAT, GPX1, and PRDX2, and lower abundance of mitochondrial complexes I (NDUFB8) and III (UQCRC2), major sites of reactive oxygen species formation. These results indicate that skeletal muscle in HE cows adopts a metabolic phenotype characterized by increased reliance on lipid-derived fuels, glucose sparing, and improved oxidative homeostasis. Together with previously reported hepatic adaptations, these muscle-specific responses likely contribute to whole-animal feed efficiency in lactating dairy cows. - Source: PubMed
Publication date: 2026/05/30
Daddam Jayasimha RSura MounicaSarmikasoglou EfstathiosAhmad GhayyoorNaughton SarahMills MorganWhite Heather MVandeHaar MichaelZhou Zheng - Patients with liver cancer frequently exhibit abnormal liver function and disorders in lipid metabolism. This study investigates the effects of Oleanolic acid (OA) on hepatocellular carcinoma (HCC) through the regulation of lipid metabolism. Computational simulations identified six core targets of OA, including PPARα, HMGCR, and ESR1, with stable binding confirmed through molecular docking and dynamics analyses. The experiments demonstrated that OA reduced intracellular lipid accumulation, suppressed cell migration ( < 0.05), and promoted apoptosis. The levels of lipid droplets and triglycerides (TG) were significantly decreased ( < 0.05). The expression levels of lipid metabolism-related genes, including , , , and , were assessed using qRT-PCR ( < 0.05). Additionally, protein expression levels were analyzed through Western blotting ( < 0.05). Furthermore, the combination of OA with the antagonist GW6471 enhanced tumor suppression, while the combination with the agonist Pemafibrate reversed the effects of OA. Compared to OA alone, the antagonist combination significantly reduced PPARα and CPT1A protein expression ( < 0.05), whereas Pemafibrate upregulated these proteins ( < 0.05). In conclusion, OA exerts its anti-lipid metabolism effects in HCC by modulating the PPARα-CPT1A axis, indicating its potential therapeutic value in liver cancer treatment. - Source: PubMed
Publication date: 2026/05/20
Liu YuxinZhang DeruLiu DanWang MengkeLyu HanningSun Yang - Understanding how metabolism governs human hematopoietic stem cells (HSCs) function is essential for advancing regenerative therapies, yet direct metabolic profiling of human HSCs has been limited by their extreme scarcity and the technical limitations of conventional methods. Here, we apply a low-input mass spectrometry-based metabolomics platform, optimized for rare cell populations, to generate metabolic profiles of 13 immunophenotypically defined hematopoietic cell types from adult human bone marrow. Using as few as ~10,000 cells per sample, we detect over 80 metabolites and uncover both conserved metabolic programs in primitive hematopoietic stem and progenitor cells (HSPCs) and lineage-specific metabolic specializations. Notably, we identify L-carnitine-driven fatty acid oxidation (FAO) as a key metabolic feature supporting HSPC function. Mechanistically, L-carnitine activates the PPARA-TFEB signalling axis, promoting mitochondrial metabolism and autophagy to preserve regenerative capacity. Functional assays in primary CD34+ HSPCs derived from healthy donors or patients with aplastic anemia confirm that L-carnitine supplementation improves stem cell function ex vivo and in vivo. Together, this work provides a foundation for human hematopoietic metabolism and reveals a targetable metabolic circuit governing HSPC regenerative fitness with therapeutic potential for improving stem cell-based interventions. - Source: PubMed
Publication date: 2026/05/26
Duan HonglinWang BohongZheng YaweiLv YanlingLu TingLi HaoyuanLi PujiaoLi RuonanXie XiaoweiYang ZiningSun GuohuanZhao XiangnanYang MengHe YichengXu ChangPu ShuangshuangZhang LinminShi JunJiang ErLieCheng TaoHu ZepingCheng Hui - Hepatocellular carcinoma (HCC) exhibits pronounced cellular heterogeneity and dynamic state transitions during tumour progression, yet the emergence of tumour cell states along fate trajectories and their transcriptional regulation remain unclear. Here, we established an integrated framework linking cell fate dynamics with transcriptional regulatory networks using publicly available single-cell RNA sequencing data. Malignant cells were identified by inferred copy number variation, followed by CellRank-based fate inference and SCENIC-based regulatory network reconstruction. We identified three terminal HCC cell states-immune-activated, metabolic, and proliferative hepatocytes-forming a differentiation continuum from stem-like to more mature phenotypes. Each state was governed by a distinct regulatory network with specific core regulators, including IRF3, PPARA, and JUN. Integration with TCGA-LIHC bulk transcriptomic and clinical data revealed that a proliferative state-derived transcriptional signature was associated with poorer overall survival. Together, our study provides a mechanistic framework linking tumour cell fate trajectories, regulatory heterogeneity and clinical outcomes in HCC. - Source: PubMed
Deng BiaolongXu KeZhu YunLin WenhaoLu LangYang TaoZhou XiaoyanChen Yuanyuan