Human PROCR / EPCR / CD201 Protein
- Known as:
- Human PROCR / EPCR / CD201 Protein
- Catalog number:
- PRR-H5223
- Product Quantity:
- 1mg
- Category:
- -
- Supplier:
- acrobyosystems
- Gene target:
- Human PROCR / EPCR CD201 Protein
Related genes to: Human PROCR / EPCR / CD201 Protein
- Gene:
- PROCR NIH gene
- Name:
- protein C receptor
- Previous symbol:
- -
- Synonyms:
- EPCR, CCD41, CD201
- Chromosome:
- 20q11.22
- Locus Type:
- gene with protein product
- Date approved:
- 2000-06-26
- Date modifiied:
- 2019-04-23
Related products to: Human PROCR / EPCR / CD201 Protein
Related articles to: Human PROCR / EPCR / CD201 Protein
- Solid‑phase assays for the detection of antiphospholipid antibodies (aPL) are central to the laboratory evaluation of antiphospholipid syndrome (APS). Growing insights into the molecular immunology underlying these assays challenge traditional interpretations. It is now evident that the antigenic drivers are phospholipids (PL)‑binding proteins - primarily β2-glycoprotein I (β2GPI) and prothrombin (PT). β2-glycoprotein I‑dependent aPL represent the dominant subset, recognizing discontinuous conformational epitopes spanning domains I-II (DI-DII). Solid matrices coated with anionic PL or partially oxidized polystyrene amplify DV anchoring through its lysine‑rich cationic loop, thereby increasing local antigen density and molecule orientation, ultimately enhancing functional avidity of intrinsically low‑affinity aPL. These antibodies contribute to reactivity across all three APS laboratory criteria assays: lupus anticoagulant (LA), anticardiolipin, and anti‑β2GPI. Beyond β2GPI, PT‑reactive aPL, detected by phosphatidylserine/prothrombin (aPS/PT) ELISAs, bind epitopes unveiled only when PT engages anionic PL in a Ca²⁺‑dependent conformational transition. Distinct antigenic specificities - type I (open‑conformation fragment‑1 epitope) and type II (C‑terminal Gla domain) - exhibit divergent affinities, matrix‑dependent binding behaviors, and heterogeneous LA activity. Antibodies detected through aPS/PT assays are associated with APS manifestations and often with LA (range 54.8-82.0%). Conversely, a smaller population of 'pure' lipid‑binding aPL, independent of β2GPI or PT, appears to target lysobisphosphatidic acid (LBPA) within the endothelial protein C receptor/LBPA complex, activating pro‑inflammatory/pro‑coagulant pathways. Although these antibodies may contribute to APS pathogenesis in a minority of patients, their detection remains technically challenging and is currently confined to research settings. Understanding the immunological characteristics of aPL subsets is essential for interpreting solid‑phase assays and improving APS management. - Source: PubMed
Publication date: 2026/06/22
Borghi Maria OriettaRaschi ElenaBodio CaterinaDa Via AriannaDevreese Katrien Mj - Endothelial cells expressing the CD157 antigen (CD157 ECs) contribute to vascular regeneration and maintenance in adult tissues, but their molecular identity is not fully defined. Here, we show that CD157-positive ECs in mouse and human tissues share conserved transcriptional profiles enriched for angiogenesis-associated genes. Regulon analysis revealed a gene-regulatory network in which the NFAT pathway contributes to vascular network formation. Integration of mouse and human scRNA-seq datasets revealed human EC clusters with gene expression profiles resembling mouse CD157-positive ECs. The clusters were localized in the large vessel intima and expressed known stem-like EC markers such as BST1 (CD157), PROCR (CD201), and ABCG2. Functionally, human CD157 ECs isolated from muscle exhibited greater proliferative capacity than CD157 ECs. Cell-cell interaction analysis suggested active communication between CD157-positive ECs and surrounding cells, via the CXCL12-CXCR7 axis. Our findings identify a conserved gene signature for CD157 ECs with potential relevance for vascular regeneration. - Source: PubMed
Publication date: 2026/06/04
Iba TomohiroWakabayashi TakuIto RieSugawara AiFujimura SatoshiSawane MikaYoshioka KazuakiMatsui AyaMorishige Jun-IchiNagata NaotoIto YukinobuHorie MasafumiMaeda DaichiTanaka RicaAndo HitoshiTakakura NobuyukiNaito Hisamichi - Malaria and cancer represent intersecting public health challenges in sub-Saharan Africa, where malaria remains endemic and cancer incidence is rapidly increasing. Emerging evidence indicates that chronic or recurrent malaria infection may influence carcinogenesis and tumour aggressiveness through complex biological mechanisms. This narrative review critically synthesizes data from PubMed, Scopus, and Web of Science to elucidate the mechanistic intersections between malaria and cancer risk, progression, and therapeutic response. The review highlights five principal axes linking malaria to oncogenesis: malaria-induced oxidative stress and chronic inflammation driving genomic instability; gut microbiome dysbiosis altering systemic immunity and tumour microenvironment; exploitation of shared molecular targets such as the endothelial protein C receptor (EPCR) and oncofetal chondroitin sulfate by Plasmodium parasites and cancer cells; cooperative interactions between malaria and oncogenic viruses like Epstein-Barr virus in lymphomagenesis; and malaria-associated vitamin D deficiency impairing immune surveillance. Furthermore, pharmacological evidence reveals that several antimalarial agents, including artemisinin derivatives, chloroquine, and quinacrine, possess anticancer properties, while some anticancer drugs exhibit antimalarial activity, underscoring opportunities for dual-action or repurposed therapeutics. The convergence of malaria and cancer biology underscores the urgent need for integrative, multidisciplinary research spanning molecular epidemiology, immunology, and pharmacology. Unveiling these mechanisms may unveil novel biomarkers and therapeutic targets, guiding context-specific interventions to reduce the disproportionate cancer burden in malaria-endemic African populations. - Source: PubMed
Publication date: 2026/04/19
Udobi Magdalene EnoBella-Omunagbe MercyEffiong Paul EtimAfolabi Israel SunmolaChinedu Shalom Nwodo - Hematopoietic stem cells (HSCs) rely on specialized niche cells for maintenance, yet how these regulators functionally integrate to preserve hematopoiesis remains unknown. Here, we identified a subset of Procr+ endothelial cells (ECs) with progenitor-like properties in bone marrow (BM), which is critical for vascular homeostasis and injury regeneration. Endothelial-specific ablation of Procr severely compromises BM vascular integrity and function. Beyond serving as a stem cell marker, Procr serves dual biological functions as a functional signaling receptor in multicellular communication. Mechanistically, Procr binds HSPA8 to promote Foxc2 nuclear translocation, upregulating Dll4 transcription to sustain Dll4/Notch3 activation in mesenchymal stem cells (MSCs), revealing a Procr/HSPA8/Foxc2/Dll4 axis essential for EC and MSC crosstalk. Through the HSPA8/Foxc2/Dll4/Notch3 axis, Procr+ ECs instruct MSCs Notch signaling, coordinating their adipogenic-osteogenic differentiation to maintain HSC self-renewal and myeloid output. Building on this mechanism, we demonstrated conserved functionality of Procr+ EPCs in human BM. Human PROCR+ ECs were found to similarly enhance DLL4/Notch3 signaling in MSCs, consequently preserving HSC function, confirming their therapeutic relevance. Our work highlights Procr⁺ EPCs sustain vascular integrity and govern MSC-dependent HSC maintenance, offering targeted clinical strategies for niche regeneration. - Source: PubMed
Publication date: 2026/05/08
Xu ChangLv XueYang ShangdaLv YanlingZheng YaweiWang Yu-XiangHui YanSun GuohuanZhao XiangnanMa Lan-YueDuan HonglinZhang LinminPu ShuangshuangSun LuLi XialinHe YichengFang WenjiaYang MengSuda ToshioChen QiCheng TaoCheng Hui - Definitive hematopoietic stem cells (HSCs) emerge within intra-aortic hematopoietic cell clusters (IAHCs) located in the dorsal aorta of the aorta-gonad-mesonephros (AGM) region during midgestation in the mouse embryo. Thereafter, HSCs migrate to the fetal liver (FL) and finally settle in the bone marrow (BM). We previously showed that the transcription factor Sox17 is expressed in IAHCs. Overexpression of the Sox17 gene in IAHC cells induces the formation of cell clusters in vitro that resemble IAHCs and retain hematopoietic potential. In addition, a previous report showed that Sox17-transduced hematopoietic stem/progenitor cells (HSPCs) in the BM maintained multipotency. However, whether the ability to form such cell clusters differs among hematopoietic sites has not been fully examined. - Source: PubMed
Publication date: 2026/04/23
Itabashi AyumiYokoi YukiSaito KiyokaTsukahara RyotaMelig GerelAzuma KoyaIizuka NaokiTaga TetsuyaNobuhisa Ikuo