PPARA antibody - middle region (ARP34113_T100)
- Known as:
- PPARA (anti-) - middle region (ARP34113_T100)
- Catalog number:
- arp34113_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- PPARA antibody - middle region (ARP34113_T100)
Related genes to: PPARA antibody - middle region (ARP34113_T100)
- 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 - middle region (ARP34113_T100)
Related articles to: PPARA antibody - middle region (ARP34113_T100)
- The differences in egg production performance among hens are closely linked to the efficiency of follicle selection, which is characterized by granulosa cell differentiation and progesterone production. In this study, by integrating ATAC-seq and mRNA-seq analyses on granulosa cells from pre-hierarchical (Pre-GCs) and hierarchical (Post-GCs) follicles, we set out to identify key regulatory factors involved in chicken follicle selection. - Source: PubMed
Publication date: 2026/04/17
Li DandanQi ChaoSun YiKang LiWei QingqingJiang Yunliang - We previously demonstrated that a clinically relevant dose of pemafibrate (PEM), a selective peroxisome proliferator-activated receptor α (PPARα) modulator (SPPARMα), reduces serum triglyceride (TG) levels in mice via hepatic PPARα activation. However, the specific contribution of hepatocyte PPARα remains unclear. To address this, male -floxed () and hepatocyte-specific -disrupted () mice were fed a diet with or without a clinically relevant dose of PEM (0.00005%) for four weeks. In mice, PEM significantly reduced circulating TG and non-esterified fatty acid levels by enhancing hepatic fatty acid uptake and β-oxidation. In contrast, these effects were absent in mice. Notably, PEM did not activate PPARα in extrahepatic tissues, including white/brown adipose tissue, kidney, and skeletal muscle in either genotype. These findings underscore the essential role of hepatocyte PPARα in mediating the pharmacological effects of PEM at clinically relevant doses. - Source: PubMed
Publication date: 2026/04/06
Zhang ZheZhang XuguangQian ChufangDiao PanNakajima TakeroKimura TakefumiGonzalez Frank JTanaka Naoki - Non-alcoholic fatty liver disease (NAFLD) is characterized by excessive hepatic lipid accumulation and represents a major global health concern. contains numerous phytochemicals associated with diverse biological activities, including hepatoprotective and hypolipidemic effects. This study evaluated the effects of the ethanolic extract of leaves on lipid accumulation in a cellular model of NAFLD, as well as its potential effect on transcriptional factors involved in lipid metabolism. HepG2 cells were exposed to steatogenic conditions and treated with the extract at non-cytotoxic concentrations, quantifying intracellular and extracellular triglycerides and cholesterol levels. Additionally, molecular docking analyses were performed to evaluate the interaction of reported phytochemicals with PPARα and SREBP-1. The results revealed a significant reduction in intracellular lipid content compared to untreated cells, while molecular docking predicted favorable binding interactions between the bioactive compounds in the extract, with higher predicted affinity for PPARα (agonist-like interaction) than for SREBP-1c (antagonist-like interaction). These findings suggest that compounds from leaves reduce lipid accumulation in liver cells and provide preliminary evidence supporting possible interactions with lipid-regulating transcription factors. - Source: PubMed
Publication date: 2026/03/26
Aguillón Osma JohannyLeón Villarreal John SebastiánLoango Chamorro Nelsy - Metabolic dysfunction-associated fatty liver disease (MAFLD) is a growing global health concern linked to gut microbiota dysbiosis. This study aims to evaluate the therapeutic effects of Bacteroidetes on MAFLD, and to explore their mechanisms. - Source: PubMed
Publication date: 2026/04/11
Li XiuxiaZhou GuangpengSun ChangruiShe RuijingFeng WentaoFu XiliangWu ShuangLi DonghuiPan LingaiLiu XingchaoXiong Xuan - Research to date describes the suprachiasmatic nucleus (SCN) of the hypothalamus as the master pacemaker that synchronizes circadian rhythms in peripheral tissues. However, recent high-impact studies demonstrate that non-SCN tissues can also coordinate rhythms in other peripheral tissues. However, the extent to which the cardiac clock regulates peripheral clocks has not yet been tested. Therefore, we investigated the role of the cardiac clock in modulating extra-cardiac circadian function using a model of cardiac-specific deletion of the core clock protein Bmal1 (Bmal1 cKO). Bmal1 cKO mice demonstrated attenuated day-night differences in skeletal muscle core clock gene expression (Bmal1, Clock, Per1) and circadian expressed metabolic genes (Pdk4, Ppara) as well as impaired day-night muscle grip strength. In the kidney, Bmal1 cKO mice had blunted core clock gene and water balance gene expression (Avp) compared to WT mice. Proteomic analysis of serum identified fibulin 5 (Fbln5) as a potential cardiokine mediating peripheral circadian effects, with rhythmic expression of Fbln5 disrupted in the heart and serum of Bmal1 cKO mice compared to WT. Exogenous treatment of synchronized C2C12 myotubes and human renal cells with rFbln5 disrupted rhythmic clock gene expression. In vivo, supplementation of Fbln5 in the drinking water of healthy wildtype C57Bl6 mice also disrupted kidney muscle rhythms. RNA sequencing data suggested that Fbln5 alters circadian output programs via stress-activated mechanotransduction and metabolic remodeling. Importantly, these changes occur without overt SCN dysfunction. Together, we demonstrate a critical role for the heart in regulating peripheral circadian control through the novel circadian cardiokine Fbln5. - Source: PubMed
Bettadapura Sharanya STangeman David CSatyanarayana Sushumna BRuhmann Madison MBonds Willa JEdwards J HarrisonGupta PoojaYusifov AykhanTodd William DBruns Danielle R