FTH1
- Known as:
- FTH1
- Catalog number:
- Y214092
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- FTH1
Related genes to: FTH1
- Gene:
- FTH1 NIH gene
- Name:
- ferritin heavy chain 1
- Previous symbol:
- FTHL6
- Synonyms:
- FTH, PLIF, PIG15, FHC
- Chromosome:
- 11q12.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-10-05
Related products to: FTH1
anti-FTH1 (C-Terminus)Anti-FTH1, Goat Polyclonal to FTH1, Isotype , Host GoatAntibodies: FTH1 HOST: Goat Clonality: pAbAntigens FTH1, 1-183aa, Human, Recombinant, E.coliBovine Ferritin heavy chain (FTH1) ELISA KitBovine Ferritin heavy chain (FTH1) ELISA KitBovine Ferritin heavy chain (FTH1) ELISA KitBovine Ferritin heavy chain(FTH1) ELISA kitBovine Ferritin heavy chain(FTH1) ELISA kit SpeciesBovineBovine ferritin, heavy polypeptide 1 (FTH1) ELISA kit, Species Bovine, Sample Type serum, plasmaCat Ferritin heavy chain (FTH1) ELISA KitCat Ferritin heavy chain (FTH1) ELISA KitCat Ferritin heavy chain (FTH1) ELISA KitCat Ferritin heavy chain(FTH1) ELISA kitCat Ferritin heavy chain(FTH1) ELISA kit SpeciesCat Related articles to: FTH1
- Hexavalent Chromium [Cr(VI)], a Group 1 carcinogen designated by the International Agency for Research on Cancer (IARC), is a pervasive environmental pollutant. The kidneys are particularly vulnerable to Cr(VI)-induced damage, and emerging evidence suggests that ferroptosis plays a pivotal role in Cr(VI) toxicity. - Source: PubMed
Publication date: 2026/04/14
Qi ChangxiLi MuziYu YueLi JiayiXia YiboLi LinjueCheng GuodongZheng PimiaoLiu YongxiaZhang PuLiu JianzhuZhao Xiaona - Intensive farming and global warming exacerbate the impact of heat stress on the broiler industry, often causing significant heart damage to poultry and thus reducing production performance. Naringenin has garnered significant attention due to its potent antioxidant properties and cardioprotective characteristics. This article aims to explore the role of ferroptosis and ferritinophagy in heat stress-induced heart injury and evaluate the preventive effect of naringenin. The chickens were randomly allocated to four groups for the experiment. The experimental results indicate that heat stress can disrupt the homeostasis of heart antioxidant function and lead to the accumulation of free radicals in chickens. The accumulated reactive oxygen species result in heart damage. Moreover, heat stress upregulates the gene transcription and protein expression levels of ferroptosis-related indicators (GPX4, NRF2, ACSL4, TFR1) and ferritinophagy-related indicators (NCOA4, FTH1, P62, LC3B, BECN1). Meanwhile, naringenin intervention can effectively enhance heart antioxidant function and inhibit ferroptosis and ferritinophagy. It significantly reduces heat stress levels and alleviates heat-stress-induced damage to chicken hearts. Thus, it offers a new way to explore the prevention of heat stress in chickens. - Source: PubMed
Publication date: 2026/04/13
Fang JiahaoJiang ZhenpengLuo JingyanWang ShuliGuo XiaoquanLiu PingZheng ZhanhongCai GaofengGao Xiaona - Ischemic stroke (IS), accounting for about 71% of stroke cases, is the most common form of this significant global cause of disability and mortality. Shunaoxin dropping pills (SNX), a traditional Chinese medicine, have demonstrated notable therapeutic benefits for IS patients. However, preclinical studies investigating its mechanisms remain scarce. This study examined the role of SNX in mitigating cerebral I/R injury by inhibiting ferroptosis, with an emphasis on the AKT/Nrf2/HO-1 signaling pathway mechanisms. LC-MS/MS was used to analyze the chemical composition of SNX. Rats were administered SNX (45 or 90 mg/kg/d) for three consecutive days prior to MCAO model surgery. Neurological impairment in rats was evaluated and histopathological damage was assessed. The levels of Fe, MDA, and GSH in brain tissue were measured using commercial assay kits. The expression of GPX4, SLC7A11, ACSL4 were evaluated via western blot. The expression of FTH1 and FPN1 were detected by immunofluorescence. Network pharmacology identified potential SNX targets linked to ferroptosis and ischemic stroke. The study then investigated the activation of the AKT/Nrf2/HO-1 signaling pathway by SNX. Following SNX treatment, MCAO rats exhibited notable enhancements in neurobehavioral scores, decreased infarct volume, and diminished pathological damage. SNX exerted neuroprotective effects by attenuating lipid peroxidation and inhibiting ferroptosis. Network pharmacological analysis initially suggested, and subsequent experiments indicated, that the inhibition of ferroptosis by SNX has a strong correlation with the activation of the AKT/Nrf2/HO-1 signaling pathway. In conclusion, SNX ameliorates cerebral I/R injury through reducing ferroptosis, likely via AKT/Nrf2/HO-1 pathway activation. - Source: PubMed
Publication date: 2026/04/12
Guo YuyingCheng XueqiSong YanhongLi DongnaDeng HaoQin XiaoliHao HongyingHan YuweiXu WenzheZhao LinnaXu Shixin - Intra-abdominal infection is a major driver of sepsis with limited therapeutic options. Although innate immune memory (trained immunity) has been studied in monocytes and macrophages, its role in neutrophils is unclear. Here, using mouse and zebrafish models of bacterial peritonitis, we show that a low-dose bacterial exposure induces an interferon regulatory factor 5 (Irf5) neutrophil state; upon lethal re-challenge, these cells differentiate into Cd274⁺ checkpoint-enriched and Fth1⁺ ROS-adaptive subsets. Functionally, primed-then-challenged mice exhibit amplified early cytokine responses, increased reactive oxygen species and neutrophil extracellular trap formation, and reduced bacterial burden with improved survival compared with lethal controls. Consistent with a cross-species program, Irf5 overexpression in zebrafish similarly enhances resistance to patient-derived pathogens. Mechanistically, Irf5-MyD88 signaling links priming to neutrophil fate diversification and heightened antibacterial function. These findings suggest Irf5-based modulation may inform future strategies to strengthen innate immunity and improve host resistance in infectious disease settings. - Source: PubMed
Publication date: 2026/04/05
Li LiyuanLiu ChiboZhang MingmingGou YaweiZhang XinfangQi YanLiu LinglingWang RenhaoJiang JiashanWang RuonanWang ShengnanShan WenboZhao XiLi HaokunWang ZhenboLi JingSun Wei - Notably, certain ginsenoside components exhibit distinct bidirectional and context-dependent regulatory effects on ferroptosis depending on the disease setting. In aberrantly proliferating or activated cells, ginsenosides function as ferroptosis inducers, whereas in damaged quiescent cells of normal tissues, they act as ferroptosis inhibitors. The pro-ferroptotic effect is predominantly observed in cells characterized by abnormal proliferation or activation, such as cancer cells and activated hepatic stellate cells in liver fibrosis. In this context, ginsenosides modulate key iron metabolism proteins and suppress antioxidant defense systems (e.g., GPX4, SLC7A11), thereby triggering intracellular iron overload and explosive lipid peroxidation, ultimately culminating in ferroptosis. Conversely, the anti-ferroptotic effect primarily targets damaged non-proliferative cells in normal tissues subjected to pathological insults (e.g., ischemia-reperfusion, inflammation). In this setting, the regulatory focus of ginsenosides shifts toward maintaining iron homeostasis through mechanisms including upregulation of iron storage proteins (e.g., FTH1), downregulation of iron uptake proteins (e.g., TFRC), and inhibition of labile Fe accumulation, thereby blocking ferroptosis initiation. This review systematically elucidates the pharmacological effects and underlying mechanisms by which different ginsenoside components regulate ferroptosis across various disease contexts and cell types, with particular emphasis on their disease- and cell type-dependent bidirectional regulatory characteristics. By highlighting these context-specific effects, we aim to provide novel potential therapeutic targets and mechanistic insights for the precision treatment of diverse pathological conditions, including malignant proliferative disorders, non-malignant aberrantly activated/proliferative diseases such as liver fibrosis, and cell injury/degenerative diseases. - Source: PubMed
Publication date: 2026/03/31
Wang YuanyuanSong MengxueLi ShuaiRen HuizhenLiu ShuangZhang Hui