CXCR4 Antibody
- Known as:
- CXCR4 Antibody
- Catalog number:
- 1009
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- CXCR4 Antibody
Related genes to: CXCR4 Antibody
- Gene:
- CXCR4 NIH gene
- Name:
- C-X-C motif chemokine receptor 4
- Previous symbol:
- -
- Synonyms:
- LESTR, NPY3R, HM89, NPYY3R, D2S201E, fusin, HSY3RR, NPYR, CD184
- Chromosome:
- 2q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-09-17
- Date modifiied:
- 2019-04-23
Related products to: CXCR4 Antibody
Related articles to: CXCR4 Antibody
- Metastatic progression of prostate cancer involves complex remodelling of signalling networks that cannot be fully explained by changes in individual pathway activity. In this study, we performed a systems-level analysis of signalling module interactions using transcriptomic data from primary prostate tumours in the TCGA-PRAD cohort (n = 550) and metastatic tumours from the SU2C cohort (n = 118). The framework integrates thirteen metastasis-associated signalling modules encompassing oncogenic, inflammatory, stress-response, angiogenic and mechanotransduction pathways. Module activity scores were computed for key cancer-related signalling pathways and used to construct module co-occurrence networks. While differences in median pathway activity between cohorts were modest, metastatic tumours exhibited substantial rewiring of pathway coordination. Notably, this rewiring reflects changes in pathway coordination rather than absolute activity levels, supporting a network-centric view of established metastatic disease. Network analysis identified the CXCR4 signalling axis as a central hub showing increased connectivity with inflammatory and growth-factor pathways, including NF-κB, MAPK, and hypoxia modules. Unsupervised clustering of pathway activity profiles revealed two distinct signalling states characterized by differential androgen receptor signalling and activation of metastasis-associated pathways. These signalling states were significantly associated with PTEN and TP53 alterations. A logistic regression classifier based on module activity achieved moderate discrimination between primary and metastatic tumours (AUC = 0.685), indicating that coordinated pathway activity captures biologically relevant features of disease progression. Overall, our findings highlight the importance of network-level approaches for understanding metastatic prostate cancer and identify CXCR4-centred signalling architecture as a key component of metastatic signalling rewiring. - Source: PubMed
Publication date: 2026/09/03
Dzik RadosławChwał JoannaTkacz Ewaryst J - Psoriasis vulgaris (PV) and atopic dermatitis (AD) are chronic inflammatory skin diseases characterized by distinct dominant T cell subsets, yet emerging evidence suggests overlapping immune mechanisms. Whether a shared Treg abnormality underlies both diseases remains unclear. - Source: PubMed
Publication date: 2026/08/20
Lin YitingSu XiaoleiJin MingzhuWang YuqiLi YaoyaoZong BingquanSong HaoranLv YajieLiu ZhenhuaWang GangWu Shengxi - Neutrophils serve host defense through phagocytic activity in acute kidney injury. However, excessive neutrophil activation drives tissue damage during systemic inflammation. NOD-like receptor family pyrin domain-containing 3 (NLRP3) has been reported to regulate neutrophil function in inflammatory conditions, but it remains unclear how NLRP3 modulates neutrophil function in the kidney. We investigated the role of NLRP3 in regulating neutrophil phagocytic activity and infiltration in the kidney. knockout (KO) and KO/lysozyme M-GFP mice were analyzed by time-lapse imaging and intravital imaging under naïve and LPS-treated conditions. KO neutrophils exhibited enhanced motility and phagocytic activity against pHrodo particles. The enhanced phagocytic activity was confirmed at both cellular and tissue levels in deficient kidneys . deficient kidneys showed increased neutrophil infiltration accompanied by upregulation of and and downregulation of and under naïve and LPS-treated conditions. Despite increased infiltration, deficient kidneys under LPS treatment displayed reduced and expression and attenuated tissue damage. Collectively, these findings suggest that NLRP3 suppresses neutrophil effector function at the cellular level. At the tissue level, NLRP3 amplifies inflammatory tissue injury in the kidney. - Source: PubMed
Publication date: 2026/08/06
Yang HaesungPark Koung-MinLim Keum-YoungHyun Young-Min - Sepsis remains a major cause of mortality, largely due to acute lung injury (ALI) driven by excessive neutrophil mediated inflammation. We recently identified a pathogenic subset of DLL4⁺ neutrophils that expands in inflamed lungs and promotes ALI, yet the underlying mechanisms remain unclear. Here, we investigated how DLL4⁺ neutrophils modulate alveolar macrophage (AM) function to exacerbate lung injury. AMs were treated with DLL4⁺ neutrophils or recombinant DLL4 (rmDLL4), and macrophage polarization was assessed by flow cytometry. Conditioned medium was subsequently applied to bone marrow-derived neutrophils (BMDNs) to evaluate neutrophil aging and CD47 expression (don't eat me signal on neutrophils). We showed that DLL4⁺ neutrophils activate the Notch1 signaling pathway in AMs, promoting toward a proinflammatory M1 phenotype. M1 cells markedly upregulate leukotriene B4 (LTB4) production through 5-lipoxygenase activation (5-LOX), inducing the accumulation of aged neutrophils (CXCR4CD62L). These aged neutrophils markedly increase CD47 expression, leading to impaired macrophage mediated phagocytosis and amplified lung inflammation. Importantly, we developed a novel DLL4-Notch1 inhibitory peptide (NDI) that reprograms AMs toward an anti-inflammatory M2 phenotype, reduces LTB4 release and aged neutrophils, lowers CD47 expression in a murine model of sepsis. Together, we identify DLL4⁺ neutrophils as key orchestrators of macrophage dysregulation in sepsis-induced ALI and demonstrate NDI may represent a potential therapeutic candidate in sepsis-induced ALI. - Source: PubMed
Publication date: 2026/09/03
Jin HuiHolland SaoirseJha AlokAziz MonowarWang Ping - Extramedullary hematopoiesis is increasingly recognized as an important mechanism by which peripheral tissues augment immune responses during inflammation and infection. However, the mechanisms governing recruitment, retention, and local differentiation of circulating hematopoietic stem and progenitor cells (HSPCs) within human tissues remain poorly understood due to the lack of physiologically relevant experimental models. Here, we developed a human skin-on-a-chip microphysiological platform to investigate the role of circulating hematopoietic stem and progenitor cells (HSPCs) in cutaneous immune responses and their potential contribution to extramedullary hematopoiesis. The device recapitulates key features of human skin, including a perfusable vascular endothelium, fibroblast-populated dermis, and keratinocyte epidermis. Upon stimulation with pro-inflammatory cytokines or a TLR2 agonist, endothelial activation significantly increased ICAM-1 and VCAM-1 expression and enhanced recruitment of both neutrophils (PMNs) and HSPCs. While PMNs readily underwent transendothelial migration into the dermal compartment, HSPCs remained localized to the vascular niche. Notably, HSPCs adhered robustly and persisted on inflamed endothelium independent of SDF-1/CXCR4 signaling. Under granulopoietic conditions, these retained HSPCs differentiated locally within the vascular compartment into PMN-like cells capable of phagocytosis and exhibiting pathogen-responsive gene expression profiles. These findings provide evidence in a human model that circulating HSPCs can contribute to host defense localized granulopoiesis without tissue infiltration, and suggests that the vascular niche itself may serve as a site of immune cell production during infection. The platform further offers a foundation for developing HSPC-based therapeutic strategies to combat antibiotic-resistant skin infections. - Source: PubMed
Publication date: 2026/09/03
Cirves Evan PWallace Stormy KChiaramonte Bella SJudy MadisonShirure Venktesh SShergill Bhupinder SGeorge Steven C