ATF5
- Known as:
- ATF5
- Catalog number:
- 002126A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ATF5
Related genes to: ATF5
- Gene:
- ATF5 NIH gene
- Name:
- activating transcription factor 5
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 19q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 2000-03-22
- Date modifiied:
- 2014-11-19
Related products to: ATF5
Related articles to: ATF5
- Biochanin A (BCA) is a natural isoflavone found in chickpeas and soybeans. Although its biological activity is well established, the role of BCA in anti-infective immunity has not yet been fully elucidated. In this study, we demonstrated that BCA exploited the transcription factor ATFS-1 to trigger the mitochondrial unfolded protein response (UPRmt). In Caenorhabditis elegans (C. elegans), BCA increased resistance to Pseudomonas aeruginosa (P. aeruginosa PA14) and other pathogens in a dosage-dependent manner by reducing the intestinal bacterial load rather than directly inhibiting bacterial proliferation. By screening classical signaling pathways, we found that the BCA-mediated protective effect was entirely dependent on the atfs-1 gene, as BCA induced the nuclear translocation of ATFS-1 and upregulated UPRmt and immune effector factors. Notably, this mechanism was evolutionarily conserved. In a mouse model, BCA dose-dependently increased survival rates, reduced bacterial load in the lungs, and upregulated the expression of ATF5 (the mammalian homolog of ATFS-1) and mitochondrial chaperone proteins. This study is the first to reveal a cross-species conserved link between BCA, the mitochondrial stress response, and the host immune system, providing a promising therapeutic target for the management of clinical bacterial infections. - Source: PubMed
Song QiuyuXiao YiXiao XinLiu Fang - Mitochondrial targeting represents a promising antitumor strategy by modulating cell differentiation, metabolic reprogramming, and immune responses. While chlorogenic acid (CGA) has demonstrated the ability to induce tumor cell differentiation and enhance antitumor immunity, the involvement of mitochondrial regulation in these effects remains unclear. This study investigated whether CGA mediates antitumor immune effects through mitochondrial regulation, thereby providing a theoretical framework for natural product-based, mitochondria-targeted therapies. Our findings reveal that CGA inhibits the translocation of mitochondrial transcription factor A (TFAM) into the mitochondria and promotes mtDNA leakage by disrupting the ATF5-mtHSP70 signaling axis. The cytosolic leakage of mtDNA activates the cGAS/STING pathway, triggering the activation of natural killer (NK) cells and cytotoxic T lymphocytes (CTLs), which ultimately facilitates antitumor immunity. In a mouse model, ATF5 knockout enhances cGAS/STING signaling and subsequent immune responses, leading to tumor growth inhibition. These results highlight a novel role of CGA in regulating mitochondrial-associated proteins, positioning it as a potential therapeutic strategy for cancer via the mtDNA-cGAS-STING pathway. - Source: PubMed
Publication date: 2026/08/12
Li RuiZhou PingHu Chu-JuanSi GeRen LingCui Jin-JinHe Ying-YingHan Yan-XingZhang JieLi Wen-BinWang Lu-LuJiang Jian-Dong - Alzheimer's disease (AD) lacks effective therapies, partly due to an incomplete understanding of mitochondrial dysfunction, a key driver of neurodegeneration. Mitochondria activate the unfolded protein response (UPR) to maintain proteostasis, but the roles of matrix- and intermembrane space (IMS)-associated stress responses in AD remain unclear. Here, we used human microglial-like cells expressing mutant amyloid precursor protein together with compartment-targeted mitochondrial proteotoxic stressors to investigate matrix (UPR) and IMS (UPR) stress responses. RNA-seq revealed activation of mitochondrial stress pathways and suppression of synaptic and lipid signaling in AD-like cells. UPR promoted robust immune activation, severe oxidative phosphorylation defects, increased mitochondrial reactive oxygen species, and cell death. In contrast, UPR preferentially induced interferon signaling and suppressed antioxidant pathways. Notably, suppression of ATF5-dependent UPR signaling rescued mitochondrial dysfunction and reduced Aβ release. Together, these findings demonstrate that matrix- and IMS-targeted mitochondrial stress elicit distinct microglial responses and identify mitochondrial proteostasis as a potential therapeutic target in AD. - Source: PubMed
Publication date: 2026/09/02
Shukla ShatakshiKolmetzky DevinGoyani ShanikumarSamantaray KunalSinha AnupriyaKramer Philip ATomar DhanendraJadiya Pooja - Intervertebral disc degeneration (IDD) is associated with the loss of nucleus pulposus derived mesenchymal stem cell (NP-MSC) function, but the contribution of the mitochondrial unfolded protein response (UPRmt) to this process is not well understood. We found that SIRT1 and the UPRmt-related proteins HSP60, ATF5, and CLPP decreased as degeneration progressed in human disc tissues and primary NP-MSCs. In NP-MSCs exposed to tert-butyl hydroperoxide, metformin increased AMPK phosphorylation and SIRT1 expression, enhanced UPRmt signaling, and reduced apoptosis and senescence. Metformin also improved mitochondrial membrane potential and morphology, lowered reactive oxygen species, restored NAD + levels, and favored extracellular matrix synthesis. Blocking SIRT1 with EX527 or SIRT1 siRNA weakened UPRmt activation and largely reversed the mitochondrial, cellular, and matrix effects of metformin. In a rat needle-puncture model, intradiscal metformin preserved disc height and T2 signal, reduced histological degeneration, and increased matrix and UPRmt-related protein expression; these effects were diminished by EX527. Together, these results suggest that reduced AMPK/SIRT1/UPRmt activity contributes to NP-MSC dysfunction during IDD and that metformin may slow disc degeneration by restoring this mitochondrial stress response. - Source: PubMed
Publication date: 2026/09/02
Shao ShanzhongHuang ZhiweiLiu JinrunLi JieWang ZiyuYang RuoyuChang ShengxuanBao GuoqingZhu MingGao SongsenZhang ShengquanZhang SumeiLi XiaochuanTao Hui - Epidermal growth factor receptor pathway substrate 8 (EPS8) is an adaptor protein implicated in tumor progression and therapeutic resistance; however, its role in mitochondrial homeostatic signaling and antioxidant regulation remains unclear. This study examined the effects of EPS8 modulation in lymph node carcinoma of the prostate (LNCaP) and enzalutamide-resistant LNCaP (LNCaP-Enz) cells. - Source: PubMed
Chen Sih-HanWu Chun-HsienHsieh Pei-FangHuang Wen-ChiYang Yu-LinLin Victor CLin Ming-Wei