CD71 (human) _ Clone SOM4D10
- Known as:
- CD71 (H. sapiens) _ Clone SOM4D10
- Catalog number:
- T-1372.0200
- Product Quantity:
- 200ìg
- Category:
- -
- Supplier:
- New Immunology
- Gene target:
- CD71 (human) _ Clone SOM4D10
Related genes to: CD71 (human) _ Clone SOM4D10
- 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 (human) _ Clone SOM4D10
Related articles to: CD71 (human) _ Clone SOM4D10
- Plasmacytoid dendritic cells (pDCs) are specialized antiviral sentinels defined by rapid type I interferon (IFN‑I) production, yet their proteomic organization and metabolic requirements remain incompletely understood. We established the steady‑state proteome of murine splenic pDCs directly ex vivo using deep, absolute quantitative mass spectrometry and compared it with conventional dendritic cell subsets and human pDCs. pDCs exhibited a highly conserved proteomic architecture across species, with selective divergence in central carbon metabolism, amino‑acid utilization, and nutrient transporter expression. Notably, pDCs expressed exceptionally high levels of the transferrin receptor (TFRC) in both mice and humans and displayed robust transferrin‑mediated iron uptake relative to other splenic immune populations. Despite this, pDCs did not demonstrate increased total cellular iron or enhanced ferritin‑based storage. Instead, proteome‑wide iron mapping revealed preferential allocation of iron to functional iron-sulfur and heme‑containing proteins, particularly within mitochondrial pathways. Detection of the iron exporter ferroportin indicated coordinated iron import and efflux, establishing sustained iron flux rather than net accumulation. Functional assays showed that iron availability does not constrain TLR9‑induced IFN‑I or TNF production. Together, these data define a conserved iron‑handling program in pDCs characterized by high TFRC expression, balanced iron flux, and targeted redistribution into essential protein systems. - Source: PubMed
Corkish CarrieO'Shaughnessy SimonLin ClaireWugk SophiaKenny SarahSinclair LindaCloonan SuzanneFinlay David - The prognosis of cervical cancer (CESC) is closely associated with the differentiation of myeloid cells within the tumor microenvironment (TME), including myeloid-derived suppressor cells (MDSCs) and tumor-associated macrophages (TAMs). These myeloid cells modulate CESC progression and treatment response by regulating immunosuppressive and activating pathways. The current study aimed to identify prognostic gene signatures and elucidate the biological pathways involved in myeloid cell differentiation (MCD) in CESC. - Source: PubMed
Publication date: 2026/05/27
Wen XiaominZheng WenlanZhai TingtingWang QiLiang YongZhang Xin - Recent research indicates that ferroptosis plays a role in Ischemic Stroke (IS). This study aims to investigate the causal connections and underlying mechanisms involving Ferroptosis-related genes, Gut Microbiota (GM), and IS using the Mendelian Randomization (MR) approach. - Source: PubMed
Publication date: 2026/06/12
Rong ChunshuWei ZhenWang XueXie DongeWang XuZhao Dexi - Atrial fibrillation (AF) is a common cardiac arrhythmia often accompanied by structural remodeling of the atria, particularly fibrosis, and disruption of normal mitochondrial function. N(1)-methyladenosine (m1A), a methylation of RNA, is gaining attention for its role in diverse biological processes. This study aimed to explore the role of the m1A methyltransferase tRNA methyltransferase 10C (TRMT10C) in AF pathogenesis. In the study, TRMT10C and m1A methylation levels were upregulated in AF rats, accompanied by excessive mitochondrial fission and myocardial fibrosis. Knockdown of TRMT10C inhibited the expression levels of mitochondrial fission-related proteins Drp1 and Fis1, reduced collagen deposition (collagen I, Postn, collagen III, and fibronectin), and AF progression. In vitro results showed that TRMT10C knockdown inhibited TGF-β1-induced cardiac fibroblasts proliferation and migration, whereas overexpression of transferrin receptor (TFRC) reversed this effect. Mechanistically, TRMT10C enhanced the stability of TFRC mRNA by promoting m1A methylation, driving mitochondrial fission and fibrosis. Collectively, our findings elucidate a novel TRMT10C-TFRC mA axis driving pathological mitochondrial dynamics and fibrosis in AF, offering new insight into cell-signaling pathways underlying atrial disease and potential therapeutic targets. - Source: PubMed
Publication date: 2026/06/10
Li NijinaZhang Hao - Physiological bilirubin exerts protective effects against ischemic stroke, but its role in post-stroke white matter injury (WMI) remains unclear. Here, through integrated epidemiological, genetic, and mechanistic studies, we demonstrate that mild elevation of serum bilirubin mitigates ischemic WMI by modulating B cell immunometabolism. Prospective cohort and Mendelian randomization analyses revealed an inverse association between bilirubin levels and WMI severity. In experimental models, bilirubin suppressed B cell activation and neuroinflammation by targeting transferrin receptor (TFRC), thereby reducing iron overload, restoring glucose metabolism, and improving mitochondrial homeostasis. Single-cell profiling further linked bilirubin-mediated B cell modulation to attenuated microglial activation via Fcγ receptor signaling. The existence of a bilirubin-B cell immunometabolism axis bridges preclinical findings with clinical relevance. Our findings establish bilirubin as a key immunometabolic checkpoint in B cells and propose TFRC blocking as a therapeutic strategy for ischemic WMI. - Source: PubMed
Publication date: 2026/06/09
Chen LianPang Xiao-WeiMei Zhi-ChengZhang LanChu Yun-HuiTian Meng-LuZhu Li-FangZhou Luo-QiYang ShengDong Ming-HaoShang KeXiao JunGong Jian-KeWang WeiTian Dai-ShiQin Chuan