Platelet ADP receptor, P2Y12 H1_H2
- Known as:
- Platelet ADP receptor, P2Y12 H1_H2
- Catalog number:
- 0702
- Product Quantity:
- 1 kit
- Category:
- -
- Supplier:
- Sacace
- Gene target:
- Platelet ADP receptor P2Y12 H1_H2
Ask about this productRelated genes to: Platelet ADP receptor, P2Y12 H1_H2
- Gene:
- P2RY12 NIH gene
- Name:
- purinergic receptor P2Y12
- Previous symbol:
- -
- Synonyms:
- P2Y12, SP1999, HORK3
- Chromosome:
- 3q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 2002-12-10
- Date modifiied:
- 2019-04-23
Related products to: Platelet ADP receptor, P2Y12 H1_H2
"Recombinant Human Interleukin-18 receptor accessory protein_IL18RAP ""Recombinant Human Interleukin-18 receptor accessory protein_IL18RAP ""Recombinant Human Interleukin-18 receptor accessory protein_IL18RAP ""Recombinant Human Interleukin-18 receptor accessory protein_IL18RAP ""Recombinant Human Interleukin-18 receptor accessory protein_IL18RAP""Recombinant Human Interleukin-18 receptor accessory protein_IL18RAP""Recombinant Human Interleukin-18 receptor accessory protein_IL18RAP""Recombinant Human Interleukin-18 receptor accessory protein_IL18RAP"(Ala1)-PAR-4 (1-6) (mouse)
(Ala1)-Thrombin Receptor-Like 3 (1-6) (mouse), (Ala1)-Proteinase Activated Receptor 4 (1-6) (mouse), (Ala1)-Coagulation Factor II Receptor-Like 3 (1-6) (mouse), AYPGKF 98%(Ala1)-PAR-4 (1-6) amide (mouse)
AYPGKFamide, (Ala1)-Thrombin Receptor-Like 3 (1-6) amide (mouse), (Ala1)-Coagulation Factor II Receptor-Like 3 (1-6) amide (mouse), (Ala1)-Proteinase Activated Recepto(Ala1)_PAR_4 (1_6) (mouse) Salt Trifluoroacetate Binding _ Synonym (Ala1)_Thrombin Receptor_Like 3 (1_6) (mouse), (Ala1)_Proteinase Activated Receptor 4 (1_6) (mouse), (Ala1)_Coagulation Factor II(Ala1)_PAR_4 (1_6) (mouse) Salt Trifluoroacetate Binding _ Synonym (Ala1)_Thrombin Receptor_Like 3 (1_6) (mouse), (Ala1)_Proteinase Activated Receptor 4 (1_6) (mouse), (Ala1)_Coagulation Factor II(Ala1)_PAR_4 (1_6) (mouse) Salt Trifluoroacetate Binding _ Synonym (Ala1)_Thrombin Receptor_Like 3 (1_6) (mouse), (Ala1)_Proteinase Activated Receptor 4 (1_6) (mouse), (Ala1)_Coagulation Factor II(Ala1)_PAR_4 (1_6) (mouse) Salt Trifluoroacetate Binding _ Synonym (Ala1)_Thrombin Receptor_Like 3 (1_6) (mouse), (Ala1)_Proteinase Activated Receptor 4 (1_6) (mouse), (Ala1)_Coagulation Factor II(Ala1)_PAR_4 (1_6) (mouse) Salt Trifluoroacetate Binding _ Synonym (Ala1)_Thrombin Receptor_Like 3 (1_6) (mouse), (Ala1)_Proteinase Activated Receptor 4 (1_6) (mouse), (Ala1)_Coagulation Factor II Related articles to: Platelet ADP receptor, P2Y12 H1_H2
- Neurovascular uncoupling is a critical yet underrecognized pathological mechanism that exacerbates neurological injury after cerebral ischemic stroke. An-Gong-Niu-Huang-Wan (AGNHW), a well-established traditional Chinese formula, has been clinically utilized for stroke management for over two centuries owing to its multi-target neuroprotective properties. However, its potential to ameliorate impaired neurovascular coupling following ischemic insult remains largely unexplored. - Source: PubMed
Publication date: 2026/05/22
Zhang XiaoZhou HongzePei JiaminXu RenhaoXue LupingZhang YuxuanQi PeiyunZhang XiangjianFu LijieZhang CongCui Lili - We evaluated sustained effects of transient H₂O₂ exposure on the oxidative stress index (OSI) and polarization signatures in BV2 microglia, and compared modulation of mitochondrial dynamics by Mdivi‑1 (a putative DRP1‑linked modulator) with antioxidant buffering by N‑acetylcysteine (NAC), carefully under defined conditions. BV2 cells were exposed to H₂O₂ (50 µM, 2 h). Selected arms received 1 h pretreatment with Mdivi‑1 (25 µM) or NAC (5 mM). Doses reflected literature demonstrating robust redox modulation. Dose selection prioritized efficacy with maintained viability. OSI (TOS/TAC) was assessed at 2, 24, and 72 h. Readouts included transcriptional markers (RT‑qPCR), cytokines (ELISA), and viability (WST‑1). Seventy‑two hours was the primary endpoint to test persistence beyond the acute window; 2 h and 24 h were descriptive. Analysis focused on durability at 72 h. Groups contained n = 6 biological replicates. Transient H₂O₂ increased OSI and induced a proinflammatory profile persisting through 24-72 h, with decreased P2ry12 and elevated Nos2/Arg1 ratio and Il1b. Mdivi‑1 improved the phenotype without fully normalizing OSI; it increased P2ry12, lowered the Nos2/Arg1 ratio and Il1b, and improved IL‑6/TNF‑α and viability versus elevated‑OSI. NAC reduced oxidative load but conferred less phenotypic recovery than Mdivi‑1. Viability remained > 80%, consistent with a sublethal stress model. Taken together, these findings indicate that a brief oxidative challenge is associated with a persistent redox-inflammatory bias in BV2 microglia that remains detectable beyond the acute exposure window. Within this experimental setting, Mdivi-1 was associated with broader phenotypic recovery than NAC, while mechanistic conclusions regarding mitochondrial dynamics remain interpretive. - Source: PubMed
Publication date: 2026/05/27
Yıldırım Mehmet EmreAyhan Berkay - Phagocytic and immune-like cells have been observed in the satellite envelope of neuronal somata in peripheral sensory ganglia of many species for several decades. These cells likely play an important role in normal function of sensory neurons and they may also play an important role in neuronal dysfunction and neurodegeneration seen with neuropathy. Recent findings have described a satellite macrophage population transcriptomically similar to microglia in peripheral ganglia of some mammalian species. The function of these cells, and the mechanisms by which they may influence neurons in neuropathy are unclear. We sought to understand the phenotype and localization of these cells in the human dorsal root ganglion (hDRG) using large-scale single nucleus and spatial transcriptomic datasets from individuals with and without a history of peripheral diabetic neuropathy. We observed a large population of macrophages that express classical microglia makers such as and in the hDRG, as previously described. Our findings confirm that these microglia-like cells (MLCs) localize to the satellite envelope around neuronal somata, yet are transcriptomically distinct from all glial cell types characterized in the hDRG. These MLCs exhibit changes in abundance and localization with diabetic painful neuropathy (DPN) in both the hDRG and sural nerves suggesting that they are not exclusively localized to the DRG. We conclude that microglia-like cells are likely the resident tissue macrophage (RTM) of the hDRG, and perhaps the peripheral nervous system (PNS) given their localization to the sural nerve and other ganglia, where they are predicted to regulate homeostatic neuronal functions and response to injury. - Source: PubMed
Publication date: 2026/05/14
Mazhar KhadijahO'Brien Jayden AWilde Michael ASrikanth HarikrushnaaWangzhou AndiPastor VictoriaMaina Charlynn WArefin Nora SMancilla Moreno MarisolSankanarayanan IshwaryaTavares-Ferreira DianaPrice Theodore J - The human dorsal root ganglia (DRG) are increasingly recognized as immunologically active sites within the peripheral nervous system. While single-cell transcriptomics has recently identified myeloid populations with microglia-like profiles in DRG across species, an in-depth, spatially resolved protein-level characterization in human tissue is lacking. Here, we used highly multiplexed Imaging Mass Cytometry (IMC) to map and phenotype myeloid cells in human DRG at subcellular resolution. A 41-marker panel enabled in-depth profiling of immune and neural cell types in situ. We identified a subset of Iba1 myeloid cells co-expressing canonical microglial markers such as P2RY12, TMEM119, and SLC2A5, located in close spatial proximity to neuronal somata. Unsupervised clustering (FlowSOM) of >6000 Iba1 cells identified eight distinct clusters. Among them, distinct myeloid cell subsets exhibited a clear microglial-like signature and were localized near neurofilament neurons. In contrast, Iba1 clusters expressing CD68, HLA-DR, and other activation markers were spatially segregated. These findings provide a spatially resolved, protein‑level atlas of Iba1 myeloid subsets in human DRG and offer a resource for dissecting neuroimmune niches relevant to chronic pain and peripheral neuropathies. - Source: PubMed
Schwabenland MariusOeztuerk BusranurBlank ThomasBeck JuergenBengsch BertramPrinz Marco - Megakaryopoiesis is an elaborate biological process that primarily occurs in the bone marrow. To gain deeper insights into molecular mechanisms driving normal megakaryopoiesis, we utilized an in vitro human megakaryocytic culture system based on mobilized peripheral blood-derived CD34 cells. Following fluorescence-activated cell sorting (FACS) isolation of CD41 and CD41 megakaryocyte (MK) subsets, mature MKs were confirmed through characterization of MK-specific surface markers, ploidy analysis, Giemsa staining, and immunofluorescence. Subsequent bulk RNA sequencing of these distinct populations enabled the identification of differentially expressed genes (DEGs) and enriched pathways. Based on our CD34-derived MK differentiation model, the expression of CD41 was found robustly induced by day 4 and further elevated by day 10. The CD41 population exhibited marked co-expression of CD42b and CD61, a significantly higher proportion of polyploid cells (≥16 N), along with characteristic morphological features of mature MKs, including proplatelet formation, cytoplasmic maturation, and cell size enlargement compared to the CD41 subset. Transcriptomic profiling of these two populations identified 1877 up-regulated and 1817 down-regulated DEGs in CD41 MKs. Protein-protein interaction (PPI) network analysis of the key DEGs revealed hub genes including VWF, PF4V1, SELP, PF4, GP1BA, CD40LG, PPBP, CLEC1B, P2RY12, and THBS1. Functional enrichment underscored the acquisition of migratory, adhesive, and secretory capacities, marked by significant upregulation of platelet activation and wound healing signatures. Pathway analysis further indicated coordinated activation of focal adhesion, cytoskeletal reorganization, glycerolipid metabolism, and neuroactive ligand-receptor interaction during maturation. This study provides an integrative transcriptomic blueprint of human MK maturation and highlights the novel candidate targets for thrombopoiesis. - Source: PubMed
Publication date: 2026/05/15
Zhang ZiyanWang YueLiu Peng