FTMT_BOVIN FTMT ELISA tesk kit
- Known as:
- FTMT_BOVIN FTMT Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen16797
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- FTMT_BOVIN FTMT ELISA tesk kit
Ask about this productRelated genes to: FTMT_BOVIN FTMT ELISA tesk kit
- Gene:
- FTMT NIH gene
- Name:
- ferritin mitochondrial
- Previous symbol:
- -
- Synonyms:
- MtF
- Chromosome:
- 5q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-06-25
- Date modifiied:
- 2015-09-11
Related products to: FTMT_BOVIN FTMT ELISA tesk kit
Human ELC ELISA KIT 96 TEST
OxiSelect In Vitro ROS/RNS Assay Kit (Green Fluorescence), Trial Size
OxiSelect Methylglyoxal (MG) Competitive ELISA Kit
OxiSelect Methylglyoxal (MG) Competitive ELISA Kit
OxiSelect TBARS Assay Kit (MDA Quantitation), Trial Size
OxiSelect Total Antioxidant Capacity (TAC) Assay Kit, Trial Size
OxiSelectâ„¢ In Vitro ROS RNS Assay Kit (Green Fluorescence), Trial Size(1-3)-beta-D-glucan Sandwich ELISA, Double Antibody(1-Kit )11,12-EET DHET Immunoassay Kit(1-Kit )11,12-EET_DHET Immunoassay Kit(1-Kit) 11,12-DHET Immunoassay Kit(1-Kit) 14,15-DHET Human Urine ELISA Kit(1-Kit) 14,15-DHET Hypertension ELISA Kit(1-Kit) 14,15-DHET sEH activity ELISA Kit(1-Kit) 14,15-EET DHET Hypertension ELISA Kit Related articles to: FTMT_BOVIN FTMT ELISA tesk kit
- Cervical cancer continues to pose a considerable challenge to global health, necessitating innovative approaches for improved diagnostics and personalized treatment strategies. Prior investigations have suggested that plasma proteins may play a role in the pathogenesis of cervical cancer; however, these studies do not confirm a causal relationship. To address this gap, conducted a large-scale Mendelian randomization (MR) study of the plasma proteome. - Source: PubMed
Publication date: 2026/07/01
Zhao Yan-HongRuan Qing-FenNing Jing-HuaZhang XinQu RunZou JingLiang YiZhang Cheng-GuiZhang Yu-Zhe - Mitochondrial iron handling and immune surveillance are intertwined in tumor biology. Mitochondrial ferritin (FTMT) buffers redox-active iron in mitochondria, while MICB is an NKG2D ligand that can promote anti-tumor cytotoxicity when expressed on tumor cells. However, whether FTMT has a causal relationship with non-small cell lung cancer (NSCLC) risk-and how this might connect to MICB biology-remains uncertain. - Source: PubMed
Publication date: 2026/06/16
Xiao ShouyongWu SiyunShao XianfengChao MingHuang QuiboKe ChenChen JiapingLi GuangjianYe Lianhua - Cerebral ischemia-reperfusion injury (CIRI) remains a major cause of neurological disability and lacks effective neuroprotective interventions. Soy isoflavones (SI), phytoestrogens with antioxidant and anti-inflammatory properties, have shown neuroprotective potential. Given that ferroptosis contributes to CIRI pathogenesis and AMP-activated protein kinase (AMPK) regulates redox homeostasis, iron metabolism, and lipid peroxidation, we investigated whether SI protect against CIRI by activating AMPK and inhibiting ferroptosis. - Source: PubMed
Publication date: 2026/04/02
Wu CailianLuo TiantianHuang JinfengMo Ruikang - Primary osteoporosis is a major age-related disease with a significant global health burden. While iron accumulation is a known risk factor, the mechanisms linking it to bone loss remain unclear. Here, we report that impaired mitophagy in bone marrow mesenchymal stem cells (BMSCs) is a hallmark of osteoporosis and is critically exacerbated by iron accumulation. We found that iron accumulation in BMSCs inhibits mitophagy, leading to mitochondrial dysfunction, increased oxidative stress, and cellular senescence, ultimately impairing osteogenic differentiation. Importantly, targeted activation of mitophagy, either pharmacologically or genetically, restored mitochondrial health, reduced senescence, and rescued bone formation. Conversely, Pink1 deficiency in BMSCs was sufficient to induce osteoporosis. Mechanistically, we identified that the mitochondrial ferritin FTMT is upregulated under iron-loading conditions and binds to PINK1, suppressing its phosphorylation and thereby preventing mitophagy initiation. This pathway is clinically relevant, as BMSCs from osteoporotic patients with high ferritin levels showed elevated FTMT and reduced PINK1 phosphorylation. Therefore, we identify a novel pathway in which FTMT-mediated disruption of mitophagy drives iron-induced osteoporosis. Our findings highlight mitophagy activation as a therapeutic strategy to prevent and treat bone loss under iron accumulation. - Source: PubMed
Publication date: 2026/04/06
Zhang RuizhiWang YikeLi LeiLi JunjieFeng GuangchenHu YutongLiu GongwenWang XiongyiZhang JiajunWei PengLai HoufuZhu KeyuWang XiaoGao XueqinWei WenFang YixuanWang JianrongYuan NaXu Youjia - According to existing research findings, dihydroartemisinin effectively regulates bone metabolism balance, while ferroptosis is closely related to the occurrence of steroid-induced osteonecrosis of the femoral head. As the exact biological mechanism among the three is still unclear, Mendelian randomization, computer-aided drug design, and transcriptomics sequencing were used to explore the specific mechanism of action. - Source: PubMed
Publication date: 2026/03/23
Li YanxinWang YanFeng XiaotianZhang LuluWang QiyuLiu XuezhiMa TianchengZhang PengyuanDu YanQin MengranMa Jianxiong