Ask about this productRelated genes to: PROCR antibody
- 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: PROCR antibody
Related articles to: PROCR antibody
- Protein C receptor (PROCR) marks a rare population of mammary epithelial cells with stem-like properties, but their low abundance has hindered characterization of their functional diversity and regulatory programs. Here, we integrate targeted enrichment with single-cell transcriptomic and chromatin accessibility profiling to construct a multimodal atlas of PROCR cells across development. We identify heterogeneous PROCR subpopulations, including a , , population with features consistent with a mammary stem cell (MaSC) state, such as high developmental potency, an EMT-associated program, and an early differentiation position. Integrative analyses reveal dynamic transcriptional regulatory circuits underlying stemness and lineage commitment. Cross-species comparisons uncover analogous PROCR populations in human mammary epithelium, and this stem cell-like signature is enriched in triple-negative and claudin-low tumors. Together, these findings refine the mammary epithelial hierarchy, define regulatory programs underlying stemness and lineage bifurcation, and establish a molecular link between a distinct MaSC state and tumor aggressiveness. - Source: PubMed
Publication date: 2026/09/01
Yan Koon-KiuNekritz ErinXie ZhenJu BenshengDong XinranWerner RachelAlsina-Beauchamp DayaniraRosencrance CelesteMukhopadhyay ParthaPan QingfeiGorbatenko AndrejZhou HongleiYan LeiDing LiangQian ChenxiNatarajan SivaramanChi HongboEaston JohnSilva JoseYu Jiyang - The four-decade evolution of genetically engineered (GE) pigs from the first α-1,3-galactosyltransferase knockout in 2003 to today's 10-gene and 69-edit donors has progressively dismantled the immunologic barriers to xenotransplantation. Hyperacute and acute humoral rejection have been largely overcome through triple knockout of xenoreactive carbohydrate antigens and transgenic expression of human complement regulators. Yet a less appreciated barrier now dominates long-term graft survival: pig-to-human coagulation dysregulation. Molecular incompatibility between porcine endothelial regulators of hemostasis, particularly thrombomodulin, endothelial protein C receptor, and the CD39 axis, and the primate coagulation cascade drives thrombotic microangiopathy and consumptive coagulopathy that erode graft function after immunologic control is achieved. The six reported human cases (Cases 1-6, numbered chronologically) confirm this transition. Notably, the 10-gene configuration now used in most clinical xenotransplants reflects the proprietary design of a single industrial source, not a biologically derived optimum. This review traces the historical development of GE pigs, synthesizes the rationale for integrative endothelial humanization, and argues that scientific progress requires diverse new gene combinations and, ultimately, organ-tailored donor pigs. - Source: PubMed
Publication date: 2026/09/07
Hwang Jeong Ho - Single-cell RNA sequencing (scRNA-seq) profiles cellular heterogeneity but captures only static snapshots, limiting inference of gene expression dynamics. We developed PROFET (particle-based reconstruction of generative force-matched expression trajectories), a framework that reconstructs continuous, nonlinear single-cell trajectories from sparsely sampled scRNA-seq time series. PROFET combines a particle-based gradient-flow algorithm with simulation-free force matching to accurately infer cellular dynamics. Across mouse and human in vitro datasets and an in vivo axolotl regeneration dataset, PROFET achieved 2.6-12.5× lower prediction error than ten state-of-the-art trajectory inference methods. Applying PROFET to newly generated scRNA-seq data from a palbociclib-treated MCF7 cell line and three published breast cancer patient datasets, we reconstructed treatment-response trajectories and identified a resistant cell subpopulation exhibiting large phenotypic shifts and enrichment of the surface markers UNC5B, TLR3, PCDH19, PROCR, SLITRK6, and SEMA6B. PROFET provides a biologically grounded framework for reconstructing cell-state dynamics from static single-cell data across development, regeneration, and therapeutic response. A record of this paper's transparent peer review process is included in the supplemental information. - Source: PubMed
Publication date: 2026/08/28
Cheng Yu-ChenGu HyeminMcDonald Thomas OWu WenboTripathi ShubhamGuarducci CristinaRusso DouglasAbravanel Daniel LBailey MadelineWang YueZhang YunPantazis YannisLevine HerbertJeselsohn RinathKatsoulakis Markos AMichor Franziska - Endothelial cell (EC) dysfunction contributes to venous thrombosis, and disrupting endothelial angiogenic signaling delays venous thrombus resolution. However, the time course of EC appearance during venous thrombus organization and the identity of cells lining the intrathrombotic vessels are largely unknown. - Source: PubMed
Publication date: 2026/07/14
Bochenek Magdalena LNoorali Julie DAderajew AdenMoiko KaterynaZimmer StefanieZifkos KonstantinosWagner MathiasLurz PhilippHobohm LukasSchäfer Katrin - The selection of appropriate in vitro inflammatory models is critical for mechanistic studies of neuroinflammation and the screening of anti-inflammatory therapeutics. Lipopolysaccharide (LPS) combined with interferon-γ (IFN-γ) and LPS combined with adenosine triphosphate (ATP) are widely used to induce microglial inflammation; however, their distinct phenotypic characteristics and optimal applications have not been systematically compared. In this study, we combined transcriptomic profiling with functional assays to compare these two inflammatory paradigms in BV2 microglia. Our results showed that both models activated the chemokine-cytokine inflammatory network and induced the production of inflammatory mediators and chemokines, but exhibited distinct molecular and functional biases. LPS/IFN-γ stimulation preferentially upregulated genes such as Lcn2, Ccl2, Upp1, and Pim2, which are associated with innate immune activation, chemokine-mediated inflammatory responses, and cell survival signaling, and was accompanied by marked increases in NO and TNF-α production. In contrast, the LPS/ATP model preferentially upregulated genes associated with ECM/cell adhesion, inflammatory and cellular homeostatic regulation, oxidative stress, and calcium-dependent secretion, including Thbs1, Thbd, Srxn1, Syt7, and Procr. Functionally, this model exhibited more pronounced IL-1β maturation and release, relatively lower NO production, and greater mitochondrial dysfunction and cell injury. Pharmacological inhibition of NLRP3 with MCC950 significantly attenuated ATP-induced IL-1β maturation, supporting the involvement of the NLRP3 inflammasome in the LPS/ATP model. Overall, the LPS/IFN-γ model is more suitable for investigating the NO/iNOS-TNF-α axis, IFN-γ-mediated synergistic pro-inflammatory responses, and classical pro-inflammatory activation, as well as for screening anti-inflammatory agents. In contrast, the LPS/ATP model is more appropriate for studying IL-1β maturation and release, NLRP3 inflammasome activation, mitochondrial damage, and inflammation-related cell death, as well as for screening inflammasome inhibitors. Our findings provide an empirical framework for rational model selection in microglial inflammation research. - Source: PubMed
Publication date: 2026/08/07
Zhang XinfengLian ZhuoLei SijieYi TanhuiZhao ShuyinLiu MingxiangGui YilingZhu ChengyiXie QianMa Rong