Rabbit Anti-Human CD234, N-terminus
- Known as:
- Rabbit Antibody toHuman CD234, N-terminus
- Catalog number:
- 129-10122
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Rabbit Anti-Human CD234 N-terminus
Related genes to: Rabbit Anti-Human CD234, N-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, N-terminus
Related articles to: Rabbit Anti-Human CD234, N-terminus
- 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 - Microvessels within atherosclerotic plaques are crucially involved in disease progression. Here, we generated a transcriptomic atlas of human atherosclerosis at single-cell resolution, encompassing 17,367 vascular endothelial cells (VECs) from five scRNA-seq studies, and verified key morphological characteristics using histology. SULF1 arterial endothelial cells (ArtECs) represented the primary subcluster undergoing endothelial-to-mesenchymal transition (EndMT). Capillary-like endothelial cells (CapECs) were identified as primary mediators of angiogenesis, and a trajectory model illustrated the transition between tip and stalk cells, with subclusters of ArtECs and CapECs predominantly expressing CXCL12, thereby driving the CXCL12/CXCR4 signaling axis. The largest plaque EC cluster, exhibiting the most heterogeneity, was found among post-capillary venule endothelial cells (VenECs), particularly ACKR1NR2F2 VenECs, which displayed distinct inflammatory transcriptional signatures characterized by adhesion molecules and chemokines. Overall, this atlas of atherosclerosis underscores endothelial heterogeneity and identifies SULF1 ArtECs and VenECs as potential therapeutic targets for EndMT and leukocyte recruitment, respectively. - Source: PubMed
Publication date: 2026/04/17
Wu YanzhaoXue ZhiweiSun TaoYu YindaLiang XiangjunXing WenchenMu FeiyuZhang ZhihanLv MeilinLing LuHan MengtaoCheng LianGisterå AntonWang Donghai - Ulcerative colitis (UC) is characterized by chronic colonic mucosal inflammation, with its pathogenesis involving multidimensional interactions and limitations in clinical treatment. Dietary restriction (DR) is a commonly used approach for UC patients to alleviate symptoms, and exploring the role of DR-related genes in UC could provide new directions for the development of precision therapies. - Source: PubMed
Publication date: 2026/03/25
Li YingyingXu MinLi WenZhang HaoHe QijinZhang Shuyi - Tertiary lymphoid structures (TLSs) are critical components of the tumor microenvironment in HCC. However, the role of TLS-related molecules in predicting HCC outcomes and guiding immunotherapy remains unexplored. This study aimed to develop TLS-related gene signature (TLSRS) to predict prognosis and immunotherapy response in patients with HCC. - Source: PubMed
Publication date: 2026/03/26
Li Jian-RongPan Li-XinSu Jia-YongTian WeiLin Lei-PoHuang Zhi-HaoLuo Cheng-PiaoLi Zhen-ZhenMa LiangGuo Ping-PingMa Yi-LiZhong Jian-Hong - The formation of the premetastatic niche prepares distant tissues for tumor cell engraftment. Endothelial cells are critical mediators of premetastatic niche formation, orchestrating extravasation of circulating tumor cells and critical pro-tumor immune cells, such as neutrophils. In mouse models of breast cancer, we show that primary tumors upregulate the non-signaling chemokine receptor ACKR1 in the endothelium of the lung premetastatic niche. ACKR1-expressing venules were found to be preferential sites of neutrophil and tumor cell localization within lung tissue. A newly generated conditional ACKR1 allele was used to show that endothelial-specific removal of ACKR1 expression significantly reduces metastatic engraftment in the lung. When ACKR1 is activated by tumor-secreted factors, endothelial ACKR1 functions to promote neutrophil recruitment within the lung parenchyma. We conclude that ACKR1 is a critical component of the endothelial response to tumors at the metastatic site of the lung, leading to neutrophil recruitment and promotion of tumor cell metastasis. - Source: PubMed
Publication date: 2026/03/18
Roach S TannerWang QianxunPatel RishiThomas SerenaAguilar BraulioEwenighi ChinweRaasch LaurenMuller William ANaiche L AKitajewski Jan