Ask about this productRelated genes to: PPARGC1A antibody
- 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
Related articles to: PPARGC1A antibody
- Adaptive thermogenesis is a fundamental defense against obesity through energy dissipation, yet the molecular mechanisms that couple energy sensing to transcriptional control remain incompletely understood. Here, we identify Feimin as a key activator of adaptive thermogenesis that connects AMP-activated protein kinase (AMPK) signaling to nuclear transcriptional regulation in adipose tissue. Upon cold exposure, AMPK phosphorylates Feimin, promoting translocation of Feimin into the nucleus, where it directly interacts with PGC1α to drive thermogenic gene expression. Conversely, obesity attenuates Feimin phosphorylation and nuclear localization, leading to impaired thermogenic capacity. Adipose-specific knockout abolishes cold-induced thermogenesis and exacerbates diet-induced obesity, phenotypes that cannot be rescued by a nuclear localization-defective Feimin mutant. Together, these findings delineate an AMPK-Feimin-PGC1α signaling axis essential for thermogenic regulation and identify Feimin as a promising therapeutic target for obesity and metabolic disorders. - Source: PubMed
Publication date: 2026/05/01
Peng YingShi XiaoliuWang YazhuoJia LiangjieLi TiantianCai ZixinLi HaoZhang JingjingWang Yiguo - Early brain injury after subarachnoid hemorrhage (SAH) involves oxidative stress and ferroptosis. Sestrin2 (SESN2) regulates redox homeostasis, but its role in SAH-induced ferroptosis remains unclear. - Source: PubMed
Zhang YiWan XichenZhang HongyanChen ZhaoyanXiao ShiningWang WansongWang JunZheng RenliChen XiupingYang Youqing - RATIONALE AND OBJECTIVES: Remarkable intratumor heterogeneity of mitochondrial redox state was found in malignant tumors by optical redox imaging (ORI) of reduced nicotinamide adenine dinucleotide (NADH), oxidized flavoproteins (Fp) containing flavin adenine dinucleotide, and the optical redox ratio (ORR = Fp/(NADH + Fp)), with higher and lower ORR corresponding to more oxidative and more reductive redox status, respectively. Our previous reports suggested that ORR can be a biomarker for cancer aggressiveness or risk of progression. Our goal here is to explore the molecular basis of the ORR's biomarker value for breast cancer by investigating the expression and activity of PGC1α, a master regulator of mitochondrial metabolism and cancer progression. MATERIALS AND METHODS: Intratumor redox subpopulations were isolated from triple-negative breast cancer (TNBC) MDA-MB-231 mouse xenografts and grouped according to high, medium, and low levels of ORI indices (ORR, Fp, or NADH). Gene expression and associated gene networks were obtained by RNA sequencing and bioinformatics analysis, respectively. PGC1α gene expression was validated by RT-PCR. The role of PGC1α in TNBC progression was further investigated by knocking down PGC1α (validated by western blot and RT-qPCR) in MAD-MB-231 cells and measuring the changes in ORI indices and invasiveness in vitro. RESULTS: PGC1α was upregulated in the subpopulation with a high ORR compared to that with a medium ORR. A PGC1α associated gene network with 21 differentially expressed genes (DEGs) was also identified, implicating regulation of redox signaling, metabolism, and cancer progression. Important signaling regulating genes SIRT1 and FOXO1 were upregulated, whose activities influence the NAD/NADH ratio or are influenced by the NAD/NADH ratio. Decreased ORR and invasiveness were observed in vitro in PGC1α knockdown MDA-MB-231 cells, supporting the association of higher PGC1α expression with more oxidative redox status. CONCLUSION: ORI-based redox subpopulations in TNBC tumors exhibited differential expression of PGC1α gene that was associated with a gene network, providing a possible molecular basis underlying the potential value of ORR as a prognostic biomarker. - Source: PubMed
Publication date: 2025/12/18
Lin ZhenwuWen YuXu He NZhang LijunZeng ChenboLin Tony RFloros JoannaMach RobertLi Lin Z - Skeletal muscle is an indispensable tissue and loss of skeletal muscle mass and function can severely impact quality of life. Dexamethasone-treated C2C12 myotubes are an increasingly common model for studying skeletal muscle pathology (such as atrophy). While many features of this model are well-established (reduced myotube size, reduced anabolic signaling, and increased atrophic signaling), the mechanisms by which dexamethasone leads to mitochondrial dysfunction are less explored. This work assessed the effect of dexamethasone-mediated mitochondrial dysfunction on Yin Yang 1 (YY1) expression. YY1 interacts with various signaling pathways, including the mechanistic target of rapamycin (mTOR) and peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (Ppargc1a/PGC-1α), all of which have been shown to be down-regulated following dexamethasone treatment. - Source: PubMed
Publication date: 2026/04/20
Klein Alexa JTravis Kipton BZimmerman John MVaughan Roger A - Postoperative cognitive dysfunction (POCD) in the elderly is a serious clinical concern. Although microglial phagocytosis is known to depend on mitochondrial metabolism, and its dysregulation can lead to abnormal synaptic pruning and neuronal injury, the molecular link between these processes in POCD pathogenesis requires further elucidation. In this study, we established a POCD animal model of aged mice using isoflurane exposure and partial hepatectomy to investigate how anesthesia and surgery impacted synaptic plasticity via microglial phagocytosis. Our findings demonstrated that anesthesia and surgery significantly reduced hippocampal peroxisome proliferators-activated receptor γ coactivator-1α (PGC-1α) expression, leading to impaired mitochondrial energy metabolism, abnormal microglial phagocytosis and excessive synaptic pruning, which was associated with synaptic deficits and cognitive dysfunction. Importantly, the treatment with the PGC-1α activator ZLN005 or AAV-mediated overexpression of PGC-1α not only successfully restored PGC-1α level in the hippocampus of aged mice, but also effectively ameliorated mitochondrial dysfunction, reversed abnormal microglia-mediated synaptic pruning, restored synaptic plasticity, and improved POCD. Our findings identify microglial PGC-1α as a critical mediator in the pathogenesis of POCD, linking mitochondrial energy metabolism with microglia-mediated synaptic pruning, and highlight the potential of microglial PGC-1α as a promising therapeutic target for prevention and treatment of POCD. - Source: PubMed
Publication date: 2026/03/25
Wu XuyangXu MaokaiHuang YongxinChen PinzhongWu LiangChen AndiWei JianjieChen YingjieLin YongbaoLin YingcengLin ZheLin YingXue FushanChen XiaohuiZheng Xiaochun