Rabbit Anti-Human CD234, C-terminus
- Known as:
- Rabbit Antibody toHuman CD234, C-terminus
- Catalog number:
- 129-10121
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Rabbit Anti-Human CD234 C-terminus
Related genes to: Rabbit Anti-Human CD234, C-terminus
- Gene:
- ACKR1 NIH gene
- Name:
- atypical chemokine receptor 1 (Duffy blood group)
- Previous symbol:
- FY, DARC
- Synonyms:
- CCBP1, GPD, Dfy, CD234
- Chromosome:
- 1q23.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2019-04-23
Related products to: Rabbit Anti-Human CD234, C-terminus
Related articles to: Rabbit Anti-Human CD234, C-terminus
- A high rate of metastasis remains a challenge for the treatment of adenoid cystic carcinoma (ACC), yet the underlying mechanism of lung metastasis remains elusive. By integrating single-cell RNA sequencing and bulk transcriptomics with multiplex immunohistochemistry, we identified a metastatic niche consisting of IL1B tumor-associated macrophages (TAMs), CD24 luminal-like tumor cells, ACKR1 endothelial cells (ECs) and HSPA1ACD8 T cells. Importantly, we revealed that IL1B TAMs play diverse roles in the processes of tumor cell intravasation and colonization, two fundamental steps supporting metastatic outgrowth. In primary lesions, IL1B TAMs release elevated levels of VEGFA and MMPs, thereby coupling sprouting angiogenesis with extracellular matrix remodeling to facilitate cancer cell intravasation. In metastatic lesions, IL1B TAMs bind to IL-1R1 on ACKR1 ECs to upregulate the expression of the adhesion molecule SELP, which can attract CD24 luminal-like tumor cells for lung colonization. IL1B TAMs also increase the stress response state of HSPA1ACD8 T-cell recruitment and induce T-cell exhaustion, thereby facilitating the survival of disseminated tumor cells. Mechanistically, MIF derived from CD24 tumor cells increases the transcription of IL1B in TAMs. We also reported that the infiltration of IL1B TAMs increased steadily with increasing lung metastatic progression in mice bearing metastatic ACC cells. Elevated plasma IL-1β and VEGFA levels are associated with increased metastatic burden and poor overall survival in patients with ACC. Our findings reveal the critical role of IL1B TAMs in reshaping the metastatic tumor immune microenvironment and reveal a potential therapeutic vulnerability for metastatic ACC. - Source: PubMed
Publication date: 2026/05/16
Wang YuZheng JianweiZhang KungeMo WeipengYang XiaotianCui PengyuLiu ChaoZheng LeiXia ShunjinSun MengyuWang BoMei MeiZhou XuanRen Yu - Clozapine is licenced for treatment-resistant schizophrenia and psychosis in Parkinson's disease. In the United Kingdom, there is a mandatory requirement for absolute neutrophil count (ANC) and white blood cell count (WBC) monitoring to safeguard against agranulocytosis. Some people have naturally low ANCs without increased infection risk, caused by a homozygous T > C variant in ACKR1, commonly called the Duffy-null genotype. This condition is known as ADAN (ACKR1/DARC-associated neutropenia) and synonyms include DANC (Duffy-null associated neutrophil count) and BEN (benign ethnic neutropenia). It is usual UK practice to lower WBC/ANC thresholds for people confirmed to have ADAN. However, ADAN often remains undetected, resulting in unnecessary discontinuation and exclusion from clozapine. This CERSI-PGx guideline provides a framework to offer ACKR1 genotype testing within the existing clinical pathway. We recommend three eligibility criteria, including pre-emptive testing for all people starting clozapine, testing for people registered in the Central Non-Rechallenge Database and reactive testing following a below-threshold blood result (defined as 'amber' or 'red'). We recommend that people with the Duffy-null genotype should be monitored using revised WBC/ANC thresholds for ADAN. Regardless of ACKR1 genotype, haematology input is required for people returning a WBC < 2.0 × 10/L and/or ANC < 1.0 × 10/L who present with a key clinical feature, such as sustained temperature ≥38°C. Finally, we summarize health economic evidence, estimating in the first year of testing, 129 people with the Duffy-null genotype could be identified, resulting in savings ranging from £42 732 to £727 990. We propose ACKR1 testing as a cost-effective approach for facilitating access to clozapine, the optimal therapy for treatment-resistant schizophrenia. - Source: PubMed
Publication date: 2026/05/13
Murtough StephenStellakis OriellaMills DaisyBjourson BlancaChaplin VickyChauhan DharmishaChipp BevCotic Mariusde Villiers JanaDzahini OlubankéElmslie FrancesEvans KatieGandhi ShreyansHughes Dyfrig AJin HuajiePanconesi DanieleSkowronska AnnaSisodiya Sanjay MSilva EdStinton VickyStuart-Smith SaraTarrant SarahTaylor DavidVarney LaurenWalters James T RWood MichelleWoodley JessicaDello Russo CinziaPirmohamed MunirBramon Elvira - Breast cancer (BC) heterogeneity necessitates prognostic and therapeutic biomarkers. PANoptosis remains incompletely understood with regard to its role in BC immunomodulation and clinical outcomes. Here, we integrated transcriptomic data from 7067 patients with BC across multiple cohorts. Patients were stratified via non-negative matrix factorization based on PANoptosis-related gene expression, revealing three distinct clusters. Cluster C3 exhibited the poorest overall survival, characterized by upregulated lipid metabolism and suppressed immunity. A prognostic signature was constructed using a random survival forest model and served as an independent prognostic factor. Single-cell RNA sequencing of 31 tumors identified IL-33-expressing endothelial subclusters (ACKR1 and FBLN5) as key regulators of the tumor immune microenvironment. Reduced IL-33 expression correlated with increased M2 macrophages and CD4 T cell depletion, while sex-specific analysis revealed IL-33 as a predictor of immunotherapy response. Our findings underscore the role of PANoptosis and IL-33 endothelial cells in shaping BC immunity and prognosis. - Source: PubMed
Publication date: 2026/04/15
Qi YuanLi ZehaoJia LanningYang ShuxianLi ZhigaoLi YingpuZhang Sifan - To investigate the role of the CXCL signaling pathway in angiogenesis of endometrial cancer and evaluate its potential as a therapeutic target. - Source: PubMed
Publication date: 2026/05/01
Zhao KeyuanJiang Yanjiao - Diabetic wounds, particularly diabetic foot ulcers, represent a significant clinical challenge owing to impaired vascularization, persistent inflammation, and dysfunctional extracellular matrix remodeling. Although adipose-derived stem cells offer therapeutic potential, their heterogeneity and functional impairment within the diabetic microenvironment limit their efficacy. Using single-cell RNA sequencing of human adipose and diabetic wound tissues, we identified a distinct CCL2-expressing ADSC subpopulation that is enriched in obese individuals and exhibits elevated stemness, unique metabolic profiles, and enrichment in pathways related to ECM organization and tissue development. This subpopulation functions as a key communication node, engaging with fibroblasts, macrophages, and endothelial cells through ligand-receptor interactions such as CCL2-ACKR1, TGFB1-TGFBR1, and IL34-CSF1R. Exosomes secreted by these CCL2-positive ADSCs were found to be enriched in CCL2, TGFB1, and IL34. In a diabetic mouse wound model, CCL2-ADSC-derived exosomes significantly accelerated wound closure compared with conventional exosomes, promoting angiogenesis, collagen deposition, and M2-macrophage polarization while reducing pro-inflammatory cytokines. In vitro, these exosomes reversed high-glucose-induced suppression of endothelial cell proliferation, migration, and tube formation. Mechanistically, CCL2 carried by the exosomes activates the PI3K/AKT/mTOR/HIF-1α signaling axis in endothelial cells via ACKR1, an effect abolished by CCL2 neutralization or ACKR1 knockdown. Together, these results demonstrate that the CCL2-positive ADSC subpopulation exerts multi-cellular and multi-target therapeutic actions, and that exosomes derived from this subpopulation offer a potent cell-free strategy to enhance diabetic wound healing by improving vascularization, modulating immune responses, and supporting ECM remodeling. - Source: PubMed
Zhao SongyunChen WanyingLiu KaiboXie JiahengChen YanmingDai HaoLu ZhongqiuChen LongwangHe YucangYu HuaLi Liqun