CD71
- Known as:
- CD71
- Catalog number:
- 11-353-C025
- Product Quantity:
- 0.025 mg
- 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
- This study aims to leverage publicly available databases to systematically investigate the pathogenic mechanisms of osteoarthritis (OA), with particular focus on the role of myeloid cell differentiation (MCD)-related genes. Comprehensive multidimensional analyses were performed to elucidate the potential mechanisms through which these genes contribute to the pathophysiological processes of OA. The findings of this study are expected to provide a theoretical foundation for targeting MCD-related abnormalities in OA. - Source: PubMed
Publication date: 2026/06/17
Liu JiamingZhang XinyuXu HaiFu XueyiSheng DuanyangHuang YingheHuang YuanxinLv XianglongLu Wei - Breast cancer (BRCA) remains a major health burden. Ferritinophagy, a selective form of autophagy regulating iron homeostasis, has been linked to tumor progression. This study aims to explore ferritinophagy-associated biomarkers and develop a prognostic model in BRCA through integrative multi-omics analysis. - Source: PubMed
Publication date: 2026/06/24
Luo WenXu PengWu HaoMa XiaobinKang Huanfeng - Brain microvascular endothelial cells (BMECs) form the blood-brain barrier (BBB), a highly selective interface that restricts paracellular diffusion and regulates the transport of nutrients and drugs into the central nervous system via specialized transporters and receptors. Tight junction-associated protein 1 (Tjap1), also termed protein incorporated later into tight junctions (Pilt), has been localized to tight junctions (TJs) in epithelial cells and to the trans-Golgi network in fibroblasts; however, its expression, subcellular localization, and functional significance in BMECs are still unknown. We characterized Tjap1 subcellular localization in mouse and human BMEC cell lines as well as primary mouse BMECs by immunofluorescence with and without pharmacological Golgi disruption by treatment with Brefeldin A, Golgicide A or Pitstop 2. CRISPR/Cas9-mediated Tjap1 knockout cells were generated and examined with regard to their Golgi morphology using immunostaining. Tjap1 mRNA localization was examined by RNAscope in situ hybridization. Quantitative real-time PCR and Western blot was performed to assess the expression of BBB-associated efflux transporters, solute carrier transporters, and cellular receptors in control and Tjap1 knockout cells. Tjap1 predominantly localized to the cis-Golgi compartment, co-localizing with Gm130 rather than Tgn38, and was absent from TJs in BMECs. Tjap1 knockout induced pronounced Golgi fragmentation BMECs. Importantly, Tjap1 knockout significantly downregulated mRNA-expression of Abcb1a, Abcb1b, Abcc4, Slc2a1, Slc7a1, Slc7a5 and Tfrc, while Abcg2 was upregulated. At the protein level, a decrease in the protein levels of Abcb1, Abcc4, Slc2a1, Slc7a1, and Tfrc was observed in Tjap1 knockout cEND cells. In BMECs, Tjap1 is a cis-Golgi-associated protein required for the structural integrity of the Golgi apparatus. Its deletion is associated with Golgi fragmentation and significant alterations in the mRNA and protein expression of drug transporters and receptors at the BBB. These findings identify Tjap1 as a candidate regulator of both Golgi architecture and the BBB transporter profile in vitro, with potential implications for modulating drug transport across the BBB. - Source: PubMed
Publication date: 2026/05/28
Mi JunqiaoSchoder AnnabelleSun AiliMeybohm PatrickBurek Malgorzata - Intervertebral disc degeneration (IVDD) is a major contributor to chronic low back pain, yet its molecular mechanisms remain incompletely understood. Emerging evidence suggests that ferroptosis, an iron-dependent form of regulated cell death, may play a key role in the degeneration of nucleus pulposus cells (NPCs). However, its involvement in IVDD has not been systematically explored. Resveratrol (Res), a natural polyphenol with antioxidant and cytoprotective effects, shows therapeutic potential, but its regulatory role in ferroptosis during IVDD is unclear. In this study, bulk transcriptome analysis identified 22 ferroptosis-related differentially expressed genes, among which five hub genes (GPX4, FTH1, HMOX1, NCOA4, and TFRC) were strongly linked to ferroptosis and oxidative stress pathways. Single-cell transcriptome data further revealed dynamic expression of these genes in NP cells, showing decreased GPX4 and FTH1 and increased HMOX1, NCOA4, and TFRC along the differentiation trajectory. High-dimensional weighted gene co-expression network analysis (hdWGCNA) confirmed significant associations between ferroptosis-related gene modules and IVDD pathology. Validation using human clinical samples, NP cell models, and animal experiments demonstrated that Res alleviates IVDD by modulating hub gene expression and suppressing NP cell ferroptosis. Overall, this study highlights ferroptosis as a key mechanism driving IVDD and identifies resveratrol as a promising therapeutic candidate targeting NP cell ferroptosis. - Source: PubMed
Publication date: 2026/06/22
Wang XiaoqiangLv JialeZhou DaqianCai WeiyeSong ChaoFu ZhijiangLiu Zongchao - Attention deficit hyperactivity disorder (ADHD) is one of the most prevalent and heritable of neurodevelopmental disorders. To characterize the genetic variants contributing to this heritability, we studied families with members affected by ADHD. Genome-wide array data were obtained on two cohorts: NHGRI Family Cohort (359 nuclear families,1538 individuals) and NCR Family Cohort (25 multigenerational and 132 nuclear families, 631 members). A meta-analysis of family-based association tests (FBAT) of the two cohorts identified three genome-wide significant associations, one upstream from TFRC, and two that were intronic to GSDME and to TRIM31, with the last gene previously implicated in ADHD. Genes associated with ADHD (MAGMA, gene-based association P < 0.05) overlapped with genes implicated in ADHD by prior case/control genome-wide association studies. Meta-analyses of the linkage signals identified one significant linkage region (LOD > 3) on 19p13.2-13.11 that encompassed a genome-wide significant variant in the FBAT of the NHGRI Family Cohort (rs55741253, P = 2.68 × 10). Additionally, two of the five linkage regions that reached a LOD > 2 in our meta-analysis replicated significant linkages from prior studies (prior studies reporting 13 linkages with LOD > 3.0; hypergeometric test of overlapping linkage signals, P < 0.01). Using neuroimaging data from the NCR cohort, we found genes associated with ADHD overlapped with genes associated with the brain's total surface area and a feature of functional connectivity, reflecting the interaction between the brain's default mode and task positive networks. Such work begins to delineate the neural substrates of the discovered genetic associations with familial ADHD. - Source: PubMed
Publication date: 2026/06/22
Justice Cristina MAhn KwangmiJung BenjaminNorman Luke JSudre GustavoSharp WendyBouyssi-Kobar MarineChoudhury SaadiaGligorovic SteviKundzicz PaulAcosta Maria TShaw Philip