PPARGC1A antibody - N-terminal region (ARP31507_P050)
- Known as:
- PPARGC1A (anti-) - N-terminal region (ARP31507_P050)
- Catalog number:
- arp31507_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- PPARGC1A antibody - N-terminal region (ARP31507_P050)
Related genes to: PPARGC1A antibody - N-terminal region (ARP31507_P050)
- Gene:
- PPARGC1A NIH gene
- Name:
- PPARG coactivator 1 alpha
- Previous symbol:
- PPARGC1
- Synonyms:
- PGC1, PGC1A, PGC-1alpha
- Chromosome:
- 4p15.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-08-02
- Date modifiied:
- 2016-10-05
Related products to: PPARGC1A antibody - N-terminal region (ARP31507_P050)
Related articles to: PPARGC1A antibody - N-terminal region (ARP31507_P050)
- Mitophagy plays a critical role in the pathology of Parkinson's disease (PD) via mitochondrial quality control, making it a promising therapeutic target. However, the precise mechanistic role of mitophagy in PD pathogenesis and progression remains unclear. - Source: PubMed
Publication date: 2026/04/17
Li XuesongZhang YujiaYang QianwenGong JunweiZhang NingningHuang YifanChen TaoZhou DiZou ZhaoGuo Zongduo - Porcine in vitro embryo production often relies on serum-supplemented media, yet fetal bovine serum (FBS) is chemically undefined and introduces batch-to-batch variability. Here, we tested whether the relatively defined N2B27 formulation improves porcine parthenogenetic embryo development compared with FBS-containing culture media and whether any developmental effects are associated with coordinated changes in oxidative stress, mitochondrial status, and apoptosis. After parthenogenetic activation, embryos were cultured in PZM-3 to the morula stage (96 h) and then transferred to PZM-3 (PZM), PZM-3 supplemented with 10% (v/v) FBS (PZM + FBS), or N2B27 for an additional 72 h. At 168 h, we assessed intracellular ROS and mitochondrial superoxide, ΔΨm and biogenesis-related indices, and apoptosis. N2B27 significantly increased blastocyst formation and hatching rates compared with both PZM conditions. In parallel, N2B27-derived blastocysts exhibited markedly lower intracellular ROS (-66.0% vs PZM; -45.9% vs PZM + FBS) and mitochondrial superoxide, higher ΔΨm, and increased expression of PPARGC1A, POLG, and TFAM. Although the number of TUNEL-positive nuclei did not differ among groups, total cell numbers increased and the apoptotic index decreased (-70.5% vs PZM; -53.5% vs PZM + FBS). These findings support N2B27 as a defined alternative to FBS-supplemented culture for mechanistic and applied embryo production, in association with reduced oxidative stress, improved mitochondrial status/biogenesis-related signatures, and attenuated apoptosis. - Source: PubMed
Publication date: 2026/04/06
Kim Dong-WookHeo JuyoungHam JaehyungHaomiao ZhengJawad AliJin HuijinSeo JaehyeokLee SeokyungOh AramLee Chang-KyuHyun Sang-Hwan - Neonatal mice achieve scar-free healing after spinal cord injury (SCI) by restoring microglial homeostasis, unlike adults, where persistent microglial dyshomeostasis drives scar expansion through mechanisms that remain elusive. Using RNA sequencing, we identified protein arginine methyltransferase 6 (PRMT6) as a key regulator of this disparity, upregulated in activated microglia at adult SCI lesions but maintained at low levels in neonatal microglia after injury. In adult mice, Prmt6 deficiency restored microglial homeostasis, evidenced by increased P2Y12/TMEM119 and reduced CD68, while reducing scar formation and enhancing axonal regrowth and motor recovery. Microglia-specific Prmt6 knockdown or PRMT6 inhibitor administration recapitulated these effects. Mechanistically, PRMT6 deposits H3R2me2a at the Ppargc1a promoter to repress peroxisome proliferator-activated receptor-γ coactivator-1α（PGC-1α）, thereby inhibiting fatty acid oxidation (FAO) and disrupting microglial homeostasis. Loss of Prmt6 alleviates this epigenetic repression, restoring FAO and microglial homeostasis. These findings establish PRMT6 as a novel epigenetic regulator linking microglial dyshomeostasis and metabolic dysfunction to maladaptive scar formation in adult SCI, highlighting PRMT6 inhibition as a promising therapeutic strategy to reprogram microglial metabolism and promote neural repair. - Source: PubMed
Publication date: 2026/04/17
Peng WeilinWu ZhengqiangXiong YuGao ZhongyaLiu YishanWang ZiyiWang HaibinHan ChaofengChu WenxiangLu Xuhua - Glucagon activates amino acid catabolism and gluconeogenesis in adults. Elevated glucagon concentrations in the fetus occur in pregnancy complications such as fetal growth restriction and hypoxia, yet the impact of chronic fetal hyperglucagonemia is unknown. Using chronically catheterized pregnant sheep, glucose tracers, and liver tissue biopsies, we investigated the effects of nine days of glucagon infusion at 5 or 50 ng·kg-1·min-1 in late-gestation fetal sheep that increased plasma glucagon concentrations by 800%. Glucagon-infused fetuses were euglycemic and exhibited lower plasma and hepatic amino acid concentrations. They also had increased hepatic mRNA expression of amino acid catabolism genes, including ARG2, GLS2, BCAT1, BCAT2, GLUL, HAL, UROC1, and PPARGC1A. Metabolite profiling in liver tissue revealed enrichment of pathways associated with amino acid degradation, elevated tri- and diphosphate nucleotides, and changes in fatty acid metabolites, supporting enhanced hepatic energy metabolism from amino acid oxidation. Hepatic glycogen content was reduced in glucagon-infused fetuses and the gluconeogenic genes PCK1 and G6PC1 were increased, though fetal glucose production was not detected. These findings demonstrate that in the fetal liver, chronic hyperglucagonemia activates amino acid catabolic pathways, indicating a physiological role for glucagon in regulating fetal amino acid homeostasis. These findings have implications for understanding fetal hepatic adaptations during chronic fetal hyperglucagonemia that can occur in the setting of fetal growth restriction or hypoxia. - Source: PubMed
Publication date: 2026/04/15
Tanner Amelia RCilvik Sarah NNguyen Marjorie ABrown Laura DAnthony Russell VWright Clyde JWesolowski Stephanie RRozance Paul J - Hybridization effectively enhances breeding efficiency and significantly boosts sheep productivity. However, the epigenetic mechanisms underlying the superior production performance of crossbreds remain largely elusive. In this study, Hu sheep were crossbred with Suffolk rams used as the paternal line. We integrated RNA-seq, ATAC-seq, and CUT&Tag (H3K4me3, H3K4me1, H3K27ac, and H3K27me3) techniques to characterize epigenetic regulatory differences in the longissimus dorsi muscle between Hu sheep (HU) and crossbred progeny (SH). Phenotypic and transcriptomic analyses revealed that SH crossbred sheep exhibited superior growth performance ( < 0.05), and the upregulated genes in the Apelin signaling pathway were significantly correlated with eye muscle area ( < 0.05). Utilizing a Hidden Markov Model, we annotated 15 distinct chromatin states in both HU and SH sheep, systematically characterizing the dynamic epigenomic landscapes across the two breeds. In contrast to SH sheep, the genome of HU sheep exhibited enrichment of repressive chromatin modifications typified by H3K27me3. Strong active enhancers (EnhA) were significantly enriched within upregulated genes in SH. A total of 1862 SH-specific and 691 HU-specific EnhA elements were characterized in this study. Motif analysis revealed that SH-specific EnhA were enriched for myogenic MEF2 family motifs ( < 0.05), which promote muscle and vascular development. By integrating multi-omics data, we constructed a putative regulatory network potentially modulated by SH-specific enhancers, identifying , , and as the core hub genes. Collectively, this study provides a robust data resource, identifying candidate genes and regulatory elements associated with crossbreeding-related muscle phenotypes. - Source: PubMed
Publication date: 2026/04/04
Cheng JiangboXu DanTian HuibinZhang XiaoxueZhao LimingZhang RunanWang JianlinXiao JinyuLi FadiWang WeiminZhang Deyin