ATF5 antibody - N-terminal region (P100653_P050)
- Known as:
- ATF5 (anti-) - N-terminal region (P100653_P050)
- Catalog number:
- p100653_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- ATF5 antibody - N-terminal region (P100653_P050)
Related genes to: ATF5 antibody - N-terminal region (P100653_P050)
- 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 antibody - N-terminal region (P100653_P050)
Related articles to: ATF5 antibody - N-terminal region (P100653_P050)
- Traumatic brain injury (TBI) induces secondary neuronal damage, in which mitochondrial dysfunction plays a central role. Mitochondrial heat shock protein 70 (mtHsp70) is a key mitochondrial chaperone involved in protein folding and proteostasis, yet its role in TBI pathology remains unclear. In the present study, we investigated the neuroprotective function of mtHsp70 and its underlying mechanisms using a controlled cortical impact (CCI) mouse model. We found that CCI selectively reduced mtHsp70 levels within mitochondria, accompanied by its cytoplasmic accumulation, while total cellular mtHsp70 expression remained unchanged. Stereotactic AAV-mediated overexpression of mtHsp70 in the cortex significantly reduced neuronal apoptosis, improved motor and cognitive behavioral outcomes, and increased neuronal survival following CCI. In vitro, mtHsp70 overexpression in HT22 cells attenuated H₂O₂-induced neuronal injury, improved mitochondrial respiration (OCR), and reduced mitochondrial protein aggregation. Mechanistically, mtHsp70 overexpression increased the expression of mitochondrial unfolded protein response (UPRmt)-related proteins, including HSP60 and Lonp1, and restored mitochondrial membrane potential. Importantly, ATF5 knockdown attenuated mtHsp70-induced upregulation of UPRmt-associated proteins and diminished mitochondrial respiratory improvement, suggesting that mtHsp70-mediated protection is dependent on ATF5-associated UPRmt signaling. Together, these findings indicate that mitochondrial mtHsp70 deficiency contributes to neuronal injury after CCI, whereas restoration of mtHsp70 improves mitochondrial proteostasis and neuronal survival. Targeting the mtHsp70-UPRmt pathway may represent a potential therapeutic strategy for TBI. - Source: PubMed
Publication date: 2026/04/16
Zhang YuanqingJin YiHan RunzeShen YuchengWang ZongqiSun XiaoouLiu Jiangang - Protein arginine methyltransferase 5 (PRMT5) is overexpressed in B-cell lymphomas, including diffuse large B-cell lymphoma (DLBCL) and mantle cell lymphoma (MCL). While PRMT5 is known to regulate multiple oncogenic pathways, including PI3K-AKT signaling, its role in lipid metabolism and ferroptosis, a regulated, iron-dependent cell death driven by lipid peroxidation, remains poorly understood. Here, we identify a novel role for PRMT5 in suppressing ferroptosis in DLBCL and MCL cells through upregulation of SLC7A11, which imports cystine for glutathione (GSH) biosynthesis. This effect is mediated by the AKT-MYC-ATF5 signaling axis. ATF5, a MYC-regulated transcription factor overexpressed in these lymphomas, induces SLC7A11 expression. In addition, ATF5 promotes the expression of ATF4, another key regulator of the ferroptotic response, which forms heterodimers with ATF5 to further reinforce this regulatory network. PRMT5 inhibition sensitizes lymphoma cells to ferroptosis inducers such as dimethyl fumarate (DMF), an electrophile that irreversibly depletes GSH via succination. Notably, combined treatment with the PRMT5 inhibitor GSK3326595 and DMF synergistically enhances anti-tumor activity in a patient-derived xenograft (PDX) model. These findings reveal a previously unrecognized PRMT5-ATF5-SLC7A11 axis that drives ferroptosis resistance in B-cell lymphomas and provide a strong rationale for targeting PRMT5 to potentiate ferroptosis-based therapies in relapsed or refractory disease. - Source: PubMed
Publication date: 2026/04/17
Liu YunxiaChen RuoyuGao XiaoyueZhu FenNi QinyuBates Paul DWu SunnyZai ZhuoyanObernberger Victoria AWeerawardhene KavinuTourdot Taylor KPetta SophieConyers Madison JCapitini Christian MRui Lixin - Intervertebral disc degeneration (IVDD) is a major contributor to low back pain (LBP) and one of the foremost causes of disability worldwide. Oxidative stress-induced senescence of nucleus pulposus progenitor cells (NPPC) and mitochondrial dysfunction are key drivers of IVDD. The mitochondrial unfolded protein response (UPR), orchestrated by the Silent Information Regulator 1 (SIRT1)-Activating Transcription Factor 5 (ATF5) axis, plays a pivotal role in maintaining mitochondrial proteostasis. However, its involvement in IVDD remains insufficiently characterized. Luteolin (Lut), a naturally occurring flavonoid with well-documented antioxidant and anti-senescence properties, has emerged as a promising disease-modifying candidate. - Source: PubMed
Publication date: 2026/04/16
Wu HuofengZai ShuangjiaYou XuanLiu ChenLi ZhaoyuLi ZhengguangMei YuhuiHua BenkuiTao YupingWu YimingZhang Liang - Acute kidney injury (AKI), whether induced by nephrotoxins like glycerol or by gamma radiation, is characterized by severe oxidative stress and subsequent mitochondrial dysfunction. We investigated the protective mechanism of sodium propionate (SP) against AKI in a rat model. Six experimental groups were established: (I) control rats were given saline; (II) rats were administered SP (37.5 mg/kg, p.o.) for two weeks; (III) rats were given an intramuscular injection of glycerol 10 mL/kg body weight; (IV) rats were given glycerol followed by SP treatment for two weeks; (V) rats were exposed to fractionated gamma-radiation (8 Gy; delivered as 2 Gy x 4 times); and (VI) γ-irradiated rats were treated with SP for two weeks. In comparison to AKI rats, SP treatment significantly preserved renal function, reduced serum urea and creatinine, and improved histopathological features. Biochemically, SP reduced lipid peroxidation and protein oxidation (malondialdehyde MDA, protein carbonyl PC, and lipofuscin) while restoring antioxidant defenses as reduced glutathione (GSH) and methionine sulfoxide reductase A (MSRA). SP restored mitophagy flux by increasing microtubule-associated protein light chain 3 (LC3II/LC3I) ratio and PTEN-induced putative kinase 1 (PINK-1) levels, promoting p62 clearance, and downregulating the mitochondrial stress marker, activating transcription factor 5 (ATF5), relative to the untreated AKI groups. These findings demonstrate that SP confers protection against AKI by attenuating oxidative stress and re-establishing mitochondrial quality control through re-establishment of autophagic flux. Hence, SP represents a promising candidate for therapeutic intervention in nephrotoxin- and γ-radiation-induced renal injury. - Source: PubMed
Publication date: 2026/04/12
Habieb Mahmoud EAli Maha MAbd-ElRaouf AmiraAbdou Fatma Y - In skeletal muscle, the mitochondrial network is highly regulated by quality control (MQC) processes including the Integrated Stress Response (ISR) and the mitochondrial Unfolded Protein Response (UPR), controlled in part by the transcription factor, Activating Transcription Factor 5 (ATF5). With age, mitochondrial health and function become altered in muscle, but the role of ATF5 in regulating these processes has not yet been evaluated. This study therefore aimed to evaluate the role of ATF5 in mediating mitochondrial quality control and function during aging. To investigate this, we utilized young (4-6 months) and middle-aged (14-16 months; denoted as aged) ATF5 whole-body KO and WT male mice. The normal age-related decline in muscle mass was prevented in the absence of ATF5. This was accompanied by an attenuated rise in important protein degradation regulators, indicating that ATF5 regulates muscle protein turnover with age. Aged ATF5 KO muscle exhibited greater muscle fatiguability than WT counterparts, accompanied by accelerated mitochondrial ROS production. The expression of the co-regulatory ISR/UPR transcription factors, CHOP and ATF4, was attenuated in response to acute contractile activity in the absence of ATF5. The lack of ATF5 led to a reduction in the levels of LonP and was accompanied by an increase in mitochondrial:nuclear derived protein imbalance. Collectively, these results suggest that ATF5 functions to maintain mitochondrial quality control and muscle endurance at the expense of muscle mass, and its absence attenuates the normal compensatory stress response to contractile activity with age. - Source: PubMed
Publication date: 2026/03/27
Sanfrancesco Victoria CHood David A