Ask about this productRelated genes to: TFAM antibody
- Gene:
- TFAM NIH gene
- Name:
- transcription factor A, mitochondrial
- Previous symbol:
- TCF6, TCF6L2
- Synonyms:
- -
- Chromosome:
- 10q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1991-09-13
- Date modifiied:
- 2016-10-05
Related products to: TFAM antibody
Related articles to: TFAM antibody
- This study explores the protective role of melatonin against Bisphenol A (BPA)-induced oxidative stress in the testes of adult mice. - Source: PubMed
Publication date: 2026/06/15
Liu JingjingZhang WanshengQi QiLi ShuangWang XuenanPan Xiaoyan - FAPS-C1, the novel pectic polysaccharide with excellent hypouricemic activity, was screened during a 28-day fermentation of Astragalus membranaceus for in vitro uric acid-lowering activity in HK-2 cells. The structure analysis results indicated that the major monosaccharide composition of FAPS-C1 consisted of arabinose (Ara), galacturonic acid (GalA), galactose (Gal), mannose (Man), glucose (Glc), and rhamnose (Rha) in a molar percentage of 26.582: 27.585: 12.789: 12.679: 7.345: 2.603. The molecular weight of FAPS-C1 was 5462 Da. FAPS-C1 was identified as homogalacturonan (HG) containing short rhamnogalacturonan-I (RG-I) regions. The main chain of FAPS-C1 was composed of →4)-α-GalpA-(1→ repeating units, interspersed with→2)-α-Rhap-(1→ residues. In vitro experiments demonstrated that FAPS-C1 (5 μM) significantly (p < 0.05) decreased uric acid levels in XOD-induced HK-2 cells. Mechanistic investigations indicated that FAPS-C1 may activate the PGC-1α/DRP1/NRF1/TFAM/Cyt.C signaling pathways, thereby modulating the mitochondrial dynamics network and significantly reducing uric acid levels. Furthermore, in vivo pharmacokinetic analysis revealed that fluorescein isothiocyanate-labeled FAPS-C1 reached a relatively late peak time. Biodistribution studies suggested that FAPS-C1 predominantly accumulated in the colon, small intestine, and kidneys, supporting the notion that this macromolecular compound was poorly absorbed and that the kidney was an important target organ for FAPS-C1. In conclusion, FAPS-C1, a novel pectin-like polysaccharide from fermented Astragalus membranaceus, holds potential as a therapeutic agent for hyperuricemia. - Source: PubMed
Publication date: 2026/06/15
Yin ZhichengLi JieBi SixueZhang MeijuanSun MengWang ZijianWang XiaojieSun ShengqianZhang Jiayu - Mitochondrial biogenesis is essential for maintaining energy homeostasis and chondrocyte function in articular cartilage, and its impairment contributes to cartilage degeneration and osteoarthritis pathogenesis. PACAP (pituitary adenylate cyclase-activating polypeptide) has recently emerged as a regulator of cellular metabolism, but its role in chondrocyte mitochondrial biology remains unclear. In this study, we investigated whether PACAP38 promotes mitochondrial biogenesis in rat primary chondrocytes. Cells were treated with PACAP38 (50 or 100 nM) for 48 h. PACAP38 enhanced mitochondrial function in a dose-dependent manner, as evidenced by increased complex I activity, maximal oxygen consumption rate (OCR), and ATP production. PACAP38 also increased the mtDNA/nDNA ratio and the protein expression of mitochondrial complex subunits NDUFB8 and MTCO2, indicating enhanced mitochondrial biogenesis. MitoTracker red staining further revealed that PACAP38 significantly increased mitochondrial mass. Mechanistically, PACAP38 upregulated the expression of Nrf1 and TFAM, two key transcription factors for mitochondrial biogenesis, at both mRNA and protein levels. Moreover, PACAP38 increased SIRT1 expression and decreased acetylated PGC-1α levels. Notably, shRNA-mediated silencing of either SIRT1 or its downstream target PGC-1α abolished the upregulation of Nrf1 and TFAM, the increase in mitochondrial mass, and the enhancement of ATP production. Collectively, these findings demonstrate that PACAP38 promotes mitochondrial biogenesis in rat primary chondrocytes through the SIRT1/PGC-1α signaling pathway, suggesting a potential therapeutic target for cartilage degenerative diseases. - Source: PubMed
Publication date: 2026/06/10
Xiong Liwei - Icariin (ICA), a major flavonoid isolated from the traditional oriental herbal medicine Epimedium, exhibits various pharmacological activities, including anti-inflammatory and antioxidant properties. It has been demonstrated in previous studies that the NLRP3 inflammasome contributes to the progression of diabetic cardiomyopathy (DCM), and that ICA exerts a protective effect in DCM. However, the mechanism by which ICA may attenuate DCM by inhibiting the NLRP3 inflammasome still needs to be elucidated. - Source: PubMed
Publication date: 2026/05/29
Sun MinHuang HuiWei ChaoXing YuanWu Bing - Mitochondrial transplantation is an emerging therapeutic strategy for various diseases associated with mitochondria dysfunction; however, conventional isolation methods require fresh tissue due to the fragility of isolated mitochondria, limiting clinical application. We previously developed a novel isolation method to recover high-quality mitochondria (Mitochondria oRganelle Complex; MRC-Q) from cryopreserved cell stocks. In this study, we characterized the biological profiles of MRC-Q and investigated its intracellular behavior and metabolic impact on recipient cells. MRC-Q maintained exceptionally high structural integrity of both outer and inner membranes, respiratory capacity, and high catalase activity even after cryopreservation and thawing. When delivered to human fibroblasts and vascular endothelial cells, RFP-labeled MRC-Q was rapidly internalized as independent puncta without fusing with the endogenous mitochondrial network. MRC-Q treatment significantly enhanced cellular respiration and ATP levels, and upregulated the expression of electron transport chain components and mitochondrial transcription factor A (TFAM). Furthermore, MRC-Q conferred dose-dependent resistance to HO-induced oxidative stress. These results suggest that MRC-Q acts not only as a transient energy source but also as a biological catalyst that triggers endogenous mitochondrial biogenesis. Our findings demonstrated that MRC-Q is a scalable and potent candidate for next-generation mitochondrial replacement therapy. - Source: PubMed
Publication date: 2026/06/07
Shibata TakahiroEl-Darawish YosifSakakibara KeiichiTakeda MasaeHayashi JunkoNitta YoshiharuOhta YoshihiroYamada YumaTsai RickOta HisashiSuganuma Masashi