CD71
- Known as:
- CD71
- Catalog number:
- 1F-235-T100
- Product Quantity:
- 100 tests
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- CD71
Related genes to: CD71
- Gene:
- TFRC NIH gene
- Name:
- transferrin receptor
- Previous symbol:
- -
- Synonyms:
- CD71, TFR1, p90
- Chromosome:
- 3q29
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2014-11-19
Related products to: CD71
Related articles to: CD71
- Radiation-induced oral mucositis (RIOM) is the most common complication in patients receiving radiotherapy for head and neck, to which ferroptosis is an important contributor. Transferrin receptor (TFRC) -mediated endocytosis is a critical source of iron. Accordingly, we proposed that inhibiting ferroptosis by disrupting TFRC mediated-iron uptake. In this study, we developed endosome-targeting self-assembling nanoparticles (CB NPs) integrated into a detachable microneedle patch (CBT@MNs) for precise and synergistic RIOM therapy. This system integrated the clinically conventional drugs chloroquine and baicalin and loaded into MN patch for mucosal drug delivery. In the tongue mucosa, the MN tips released CB NPs. Upon entering endosomes through the endocytosis pathway, CB NPs disrupted endosomal acidification through the proton sponge effect, which may block TFRC recycling, achieving long-term inhibition of ferroptosis and inflammation efficacy. In rat models of RIOM, CBT@MNs dramatically attenuated mucosal ulceration and accelerated healing via anti-inflammation, angiogenesis, and collagen deposition. Transcriptomic analysis further revealed that CBT@MNs suppressed ferroptosis and inflammatory signaling. This radioprotective strategy for inhibiting ferroptosis and regulating redox homeostasis provided a novel approach for designing tissue engineering materials. - Source: PubMed
Publication date: 2026/09/03
Xiao YanxuanSun PengchengXu WenjieHao XinyanTang TiantianLiu XinyingHuang HaiGong ZhaojianWu Junyong - The discovery of ferroptosis and cuproptosis has significantly expanded the landscape of programmed cell death. Artesunate (ART), a semisynthetic derivative of artemisinin, exhibits pleiotropic pharmacological activities beyond its canonical antimalarial role, including anticancer and neuroprotective effects. However, a comprehensive review systematically integrating ART's roles in modulating both ferroptosis and cuproptosis remains lacking. This review bridges this gap by synthesizing recent advances. The distinct core mechanisms of ferroptosis and cuproptosis are first outlined. Extensive evidence is then summarized regarding ART-induced ferroptosis in cancers, primarily through disrupting iron homeostasis (e.g., stabilizing transferrin receptor (), promoting ferritinophagy) and impairing antioxidant defenses (e.g., suppressing the System Xc/ glutathione peroxidase 4 (GPX4) axis, targeting peroxiredoxins). In contrast, the anti-cuproptotic effect of ART is currently restricted to Parkinson's disease (PD) models, mediated by the upregulation of astrocytic metallothionein 2A (MT2A) to chelate excess copper-the only validated cuproptosis-related mechanism of ART to date. The crosstalk between ferroptosis and cuproptosis at shared metabolic nodes, including glutathione depletion, mitochondrial dysfunction, and reactive oxygen species (ROS) amplification, is further delineated as a hypothesis-generating framework. This interplay suggests a theoretical potential for ART-when combined with functional nano-materials-to synchronously engage both death pathways, though direct experimental validation of such dual-pathway synergy for ART as a single agent remains lacking. Finally, translational prospects of ART in cancer therapy, neurodegenerative diseases, and hepatic fibrosis are discussed, together with current challenges and future directions. ART acts as a context-dependent modulator: pro-ferroptotic activity is evident across multiple disease models, whereas anti-cuproptotic activity is currently limited to PD and requires further validation. Systematic characterization of ART's context-specific effects suggests a preclinical rationale for the future design of ART-based combination strategies targeting metal-dependent cell death, pending further validation. - Source: PubMed
Publication date: 2026/09/02
Feng KaiXia YayiLiu JingshengYang Mingxuan - Tailored flax-reinforced composites (TFRC) are being investigated as a sustainable alternative to conventional glass- and carbon-fiber-reinforced composites, having a lower fiber volume than these and the structure of the laminate with two plies (two identical layers of alkali-treated flax yarns) is unidirectional, weakly twisted, oriented at ±45°, and reinforced by stitching; it is also impregnated with bio-resin and has robust reinforcement through controlled lamination. TFRC has shear-dominated behavior under both tensile and compressive loading, due to the off-axis orientation of the fibers, but the damage evolution differs significantly. Under tensile loading, the material exhibits a lower strength (55.2 MPa), whereas under compression loading, the composite achieves a higher apparent strength (99.1 MPa). The paper provides a comprehensive analysis for structural and mechanical characterization using the following: nondestructive evaluation using ultrasound to detect internal discontinuities and assess homogeneity; optical microscopy to evaluate fiber-matrix integration and porosity reduction; and Dynamic Mechanical Analysis to assess thermomechanical transitions and storage modulus stability. Finite element simulations have been used to determine elastic properties and validate the matrix-dominated shear response. The results confirm that the [±45°] sequences of TFRC optimize mechanical response and interfacial adhesion, promoting TFRC as an ecological solution for structural systems where progressive energy dissipation is preferred. - Source: PubMed
Publication date: 2026/08/26
Bencze AndreiBergant ZoranArnăutu IrinaŠturm RomanChlada MilanSteigmann RozinaStanciu Mariana DomnicaSavin Adriana - Ovarian cancer (OV) is a highly lethal gynecological tumor, often developing platinum chemotherapy resistance and treatment failure. With their diverse and complex structures, natural products offer potential solutions to drug resistance. This study systematically examines chaetocin's effects on cisplatin-resistant OV cells and its underlying molecular mechanisms. We utilized a cell counting Kit-8, transwell assays, flow cytometry, immunohistochemistry, and western blotting to evaluate chaetocin's effects on cisplatin-resistant OV cells. Proteomic analysis and bioinformatics were utilized to identify the molecular targets of chaetocin, which were validated via cell transfection and co-immunoprecipitation. Additionally, a cisplatin-resistant OV xenograft model was developed for in vivo studies. Chaetocin suppressed the malignancy of cisplatin-resistant OV cells in a dose-dependent manner to suppress cell proliferation, impede cell migration and invasion, and induce both cell apoptosis and cell cycle arrest. Furthermore, in vivo studies showed that chaetocin inhibited tumor growth in a cisplatin-resistant OV xenograft model. In terms of mechanism, chaetocin induced ferroptosis in these cells, inhibiting TFRC ubiquitination and upregulating its expression by reducing the levels of cullin1 and its neddylation binding (cullin1-NEDD8). Our study uncovers a previously unrecognized mechanism: Chaetocin induces ferroptosis by inhibiting TFRC neddylation to upregulate its expression in OV. Unlike its known role as an SUV39H1 inhibitor, chaetocin functions through the neddylation-TFRC-ferroptosis axis, a pathway not previously linked to this compound. Moreover, while neddylation has recently been reported to regulate ferroptosis via SLC7A11, our study reveals an entirely distinct mechanism involving TFRC-mediated iron transport. This epigenetic regulation stabilizes TFRC, sensitizing resistant cells to ferroptosis, providing a dual-mechanistic insight not found in existing literature. By linking chaetocin's gene regulation to iron-dependent cell death, we offer new insights and potential therapies for cisplatin-resistant OV. - Source: PubMed
Publication date: 2026/09/14
Xie HanfeiDai WuminSun LuGong WangangZhu TaoZhang Yingli - Esophageal squamous cell carcinoma (ESCC) is a highly aggressive malignancy with a dismal prognosis, mainly due to cisplatin resistance and severe adverse effects of conventional therapies. Wogonin, a natural flavonoid, exhibits anticancer activity in several cancers, but its efficacy and potential molecular mechanisms in ESCC remain unclear. - Source: PubMed
Publication date: 2026/08/29
Wei ChengmingShi MeinaWei LiujiaoWei Caituan