Recombinant Human CD71 /TFRC Protein
- Known as:
- Recombinant Human CD71 /TFRC Protein
- Catalog number:
- cd-793
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Proxinobio
- Gene target:
- Recombinant Human CD71 /TFRC Protein
Related genes to: Recombinant Human CD71 /TFRC Protein
- Gene:
- TFR2 NIH gene
- Name:
- transferrin receptor 2
- Previous symbol:
- -
- Synonyms:
- HFE3, TFRC2
- Chromosome:
- 7q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-06-03
- Date modifiied:
- 2017-05-05
- 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: Recombinant Human CD71 /TFRC Protein
Related articles to: Recombinant Human CD71 /TFRC Protein
- Poly (ADP-ribose) polymerase inhibitors (PARPi) have reshaped the maintenance treatment of ovarian cancer. However, a significant proportion of patients exhibit primary resistance, highlighting the need for real-world efficacy data and predictive biomarkers, especially in underrepresented populations. - Source: PubMed
Zhang XiuWang ZhibinGu YuhuiFang HuihuiWang YingFang ChaoWu Nayiyuan - Accumulating evidence supports ferroptosis as a key driver for nanomaterial (NM) exposure-induced toxicity. There is considerable interest in the therapeutic potential of ferroptosis inhibition for cells or animals exposed to NMs before clinical applications. This study aimed to synthesize data from published studies for achieving strong evidence about the effects of ferroptosis inhibitors. Fifty-three studies were included after searching PubMed, EMBASE and Cochrane Library databases up to October, 2025. The meta-analysis of in vitro studies (n = 51) showed treatment with ferroptosis inhibitors ferrostatin-1 (Fer-1; standardized mean difference [SMD] = 3.19; 95% confidence interval [CI] = 2.63-3.75) and deferoxamine (DFO; SMD = 3.40; 95% CI = 2.62-4.18) significantly improved the viability of cells exposed to NMs. The pooled results of in vivo studies (n = 8) demonstrated Fer-1 administration suppressed tissue cell death (SMD = -1.38; 95% CI = -2.39 to -0.37) and alleviated damages on the organ function [respiratory frequency (SMD = -1.33; 95% CI = -2.32 to -0.34); enhanced pause (SMD = -1.85; 95% CI = -2.95 to -0.75)] or the body weight (SMD = 1.28; 95% CI = 0.63-1.92) of animals exposed to NMs. The protective mechanisms of Fer-1 or DFO included iron removal (showing reduced iron levels and down-regulated TFRC), anti-oxidation (manifested as inhibited formation of L-ROS, MDA, restoration of GSH, up-regulation of GPX4, down-regulation of ACSL4 and COX2) or anti-inflammation (lowering IL-6, TNF-α and MCP-1). Accordingly, Fer-1 or DFO may be a potentially effective intervention for populations with NM exposure to prevent tissue damages. - Source: PubMed
Liu QiwenLiang YunxiaXie DongliZhao ShuhanLuo Xiaogang - This study investigated the proteomic characteristics and biological functions of hypoxic exosomes derived from hypoxia-preconditioned feline adipose-derived mesenchymal stem cells (ADMSCs), aiming to reveal the remodeling effect of hypoxic preconditioning on the protein composition of exosomes derived from feline ADMSCs and its potential applications. CoCl was used to mimic a hypoxic environment for ADMSCs, and exosomes were isolated by differential ultracentrifugation. The physical properties of the exosomes were characterized by transmission electron microscopy, nanoparticle tracking analysis, and Western blotting. Proteomic analysis revealed that hypoxic preconditioning significantly altered the exosomal proteomic profile, identifying 120 differentially expressed proteins (116 upregulated and 4 downregulated). Bioinformatic analysis indicated significant enrichment of key pathways including the hypoxia-inducible factor-1 (HIF-1) signaling pathway, adenosine monophosphate-activated protein kinase (AMPK) signaling pathway, autophagy, and proteasome function. Gene ontology (GO) functional annotation demonstrated significant enrichment of biological processes such as metabolic processes, cell cycle regulation, and signal transduction in the hypoxia-preconditioned group. Kyoto encyclopedia of genes and genomes (KEGG) analysis further suggested potential biological functions through the regulation of pathways including the cell cycle and renin-angiotensin system. Notably, hypoxia-responsive proteins such as HMOX1 and TFRC were upregulated, while pathways related to the renin-angiotensin system were suppressed. This study systematically elucidates, for the first time, the remodeling effect of hypoxic preconditioning on the proteome of exosomes derived from feline ADMSCs, providing new molecular insights into exosome-mediated intercellular communication. - Source: PubMed
Lou JiaoChen HaiyanFeng EnhuiLi WeinaChen PanlongChen YunlongFan XinyiXu JingmeiFang PingWang YanLu DezhangZhang Shiqiang - Ovarian cancer (OC) is a fatal female malignancy, and Cisplatin resistance severely impacts the clinical management of epithelial ovarian cancer (EOC), the most prevalent histological subtype accounting for over 90% of cases. Exploration of novel effective targets and drugs for treatment of cisplatin-resistant EOC is urgently needed to address the tremendous challenge. In this study, we screened a Traditional Chinese Medicine (TCM) library including 978 monomers and found that Raddeanin A (RA) extracted from Anemone raddeana Regel displayed the powerful cytotoxic effect on cisplatin-resistant EOC cells. Further investigations revealed that RA had potential of inducing ferroptosis via binding to an evolutionarily conserved scaffold protein, VEPH1. Bioinformatics analysis combined with RA-sepharose pull-down assay and immunoprecipitation confirmed that RA interacted with two sites of VEPH1, site 1 (S1) at 212-217 aa and site 2 (S2) at 579-651 aa, and S1 was also involved in VEPH1 binding to and promoting lats1 activation. Moreover, RA bound to and enhanced VEPH1 degradation through the proteasome pathway, and meanwhile inhibited the interaction between VEPH1 and lats1, which in turn suppressed lats1 activation, promoted YAP nuclear translocation to up-regulate the expression of ferroptosis-driven proteins, TFRC and ACSL4, resulting in an imbalance of intracellular iron homeostasis, as well as promotion of lipid peroxidation, and thus inducement of ferroptosis in cisplatin-resistant EOC cells. Importantly, the in vivo results confirmed that RA induced ferroptosis and dramatically suppressed the growth of A2780/DDP transplanted tumours. Taken together, we revealed for the first time that VEPH1 is the direct target for RA, and ferroptosis contributes to RA-triggered anti-tumour effect on cisplatin-resistant EOC, which provides new insights into the therapeutic application of RA against EOC chemoresistance. - Source: PubMed
Publication date: 2026/04/15
Li HuaqiuXing WenxiuDai YuyuanCao ShaoyiYang XinyiZhang YueZeng XiangfengLiu HongjiaoWu Xiaoping - Sensorineural hearing loss (SNHL) induced by noise or aminoglycoside antibiotics is a significant public health concern without any FDA-approved pharmaceutical therapies. Dysregulation of iron homeostasis and its subsequently induced ferroptosis has increasingly been identified as a key mechanism underlying cochlear hair cell (HC) damage. Nevertheless, the therapeutic targets for restoring iron balance for hearing protection remain poorly investigated. In this study, we uncover a previously unrecognized role of the SMO pathway in regulating iron homeostasis. SMO expression was rapidly upregulated and activated in HCs following injury. Both genetic ablation of Smo and pharmacological inhibition of SMO reduced iron accumulation and lipid peroxidation, promoting HC survival and preserving auditory function in mouse models of ototoxic- and noise-induced hearing loss. Mechanistically, SMO inhibition suppressed ATF2 phosphorylation, resulting in downregulation of IRP1, which decreased iron accumulation via downregulation of Tfrc and upregulation of Fpn, ultimately protecting HCs from ferroptosis. Notably, treatment with the SMO inhibitor SANT-1 nearly restored auditory thresholds to baseline levels in mice subjected to ototoxic injury. Our findings identify the SMO-ATF2-IRP1-FPN/TFRC axis as a central regulator of cochlear iron homeostasis and propose SMO inhibition as a promising therapeutic strategy for SNHL through precise modulation of iron metabolism. - Source: PubMed
Publication date: 2026/04/17
Mao HuanyuLi XiangLiao YaqiLiu LimanGao XianLin HailiangNi WenliLi HuaweiChen YanLi Wenyan