Ask about this productRelated genes to: CD182 antibody
- Gene:
- CXCR2 NIH gene
- Name:
- C-X-C motif chemokine receptor 2
- Previous symbol:
- IL8RB
- Synonyms:
- CMKAR2, CD182
- Chromosome:
- 2q35
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-19
- Date modifiied:
- 2016-03-14
Related products to: CD182 antibody
Related articles to: CD182 antibody
- Brain abundant membrane attached signal protein 1 (Basp1), a member of the neuronal growth-associated protein family, was originally identified for its high expression in the central nervous system. Recent evidence suggests its involvement in peripheral diseases through modulation of myeloid cell function; however, the molecular mechanisms remain poorly defined. In this study, by re-analyzing single-cell RNA sequencing data from peripheral blood of TBI patients and validating results in a mouse TBI model via flow cytometry, we demonstrated that Basp1 was specifically upregulated in neutrophils after injury. Using tamoxifen-induced lineage tracing (Basp1⁺-TdTomato⁺), we further confirmed that Basp1-expressing neutrophils represented the majority of infiltrated neutrophils in the brain during acute TBI. Bulk RNA-seq comparing Basp1⁺ and Basp1 neutrophils revealed Basp1's central role in regulating neutrophil migration and neutrophil extracellular traps (NETs) formation. Silencing Basp1 impaired both processes in vitro, and real-time PCR analysis indicated correlated downregulation of key chemotaxis-related (Itgb2, Cybb, Mmp9, Actn1, Cxcr2, Pik3cb) and NETs-related genes (Fcgr1, H3c1, Tlr2). Protein docking and co-immunoprecipitation assays demonstrated a direct interaction between Basp1 and Vimentin in neutrophils, suggesting a mechanism by which Basp1 promotes cytoskeletal rearrangement essential for migration and NETs formation. Notably, conditional KO Basp1 in myeloid cells significantly reduced neutrophil infiltration and NETs formation after TBI. Our work identifies Basp1 as a critical molecular mediator of neutrophil-driven inflammation in TBI, providing a potential therapeutic target not only for TBI but also for other neuroinflammatory conditions. - Source: PubMed
Publication date: 2026/05/18
Sun JianbinLi TaoZhang TongYang TengMa PengjiaoZhou RuitianTan MenglanHuang YvshaHe WenhuiDai Shuang-ShuangLiu Yang-Wuyue - The extensive application of bisphenol A (BPA), an endocrine-disrupting substance in polymer-based products and consumer commodities, has sparked concerns over its carcinogenic potential. However, the molecular mechanisms underlying BPA-induced gastric carcinogenesis remain poorly understood. We used network toxicology and molecular docking analysis to uncover the pivotal targets and mechanisms underlying BPA-associated gastric carcinogenesis. Potential BPA-related targets and differentially expressed genes in gastric cancer (GC) were collected from publicly available databases to identify hub genes. A prognostic risk assessment model utilizing hub genes, with molecular docking simulations, was performed to confirm the binding interactions between BPA and target proteins. A total of 27 potential targets associated with both BPA exposure and GC were identified. The protein-protein interaction network analysis revealed 19 hub genes, with core targets including MMP9, ADRB2, PTGS1, SLC6A4, ERBB2, MAPT, AR, SLC6A3, CNR1, PDE5A, DRD2, KCNH2, MC4R, CALCR, CHRM1, ADRB3, CXCR2, MMP1, and SHBG. Enrichment analysis demonstrated these hub genes were significantly involved in neuroactive ligand-receptor interaction, calcium signaling pathway, cGMP-PKG signaling pathway, and chemical carcinogenesis-receptor activation pathways. Prognostic analysis identified six hub genes (CALCR, ADRB3, CNR1, HRH2, KCNH2, and AR) significantly associated with patient survival. Molecular docking simulations demonstrated robust interaction affinities of BPA with the identified core target proteins. This study reveals that BPA may influence GC development and progression through multiple targets and signaling pathways, particularly involving G protein-coupled receptor signaling, hormone regulation, and neurological pathways. - Source: PubMed
Publication date: 2026/05/14
Yu Wen-YanZhang Yue - Macrophage migration inhibitory factor (MIF) is a pleiotropic inflammatory cytokine and atypical chemokine that regulates both innate and adaptive immunity. Its broad expression and stress-induced release make MIF a key determinant of inflammation, cardiovascular diseases, and cancer. MIF acts as an upstream regulator within a complex ligand-receptor network comprising the more recently discovered MIF paralog, D-dopachrome tautomerase (D-DT, MIF-2), its cognate receptor CD74, and the chemokine receptors CXCR2, CXCR4, and ACKR3/CXCR7. MIF-driven effects, including leukocyte recruitment, cell migration, and inflammatory signaling, largely depend on the specific MIF receptor repertoire of the involved cell types, which can dynamically change in inflammatory settings. Here, we describe an optimized protocol for the ibidi 3D µ-Slide chemotaxis assay to study MIF-mediated pro-migratory effects on human neutrophils, a prototype of innate immune cells, and CD4 T cells, a cornerstone of adaptive immunity. Additionally, we discuss the application of current inhibitor strategies to selectively target and identify the receptor pathways involved. - Source: PubMed
Zhang ZhishenKapurniotu AphroditeBernhagen JürgenHoffmann Adrian - Colorectal cancer (CRC) remains a major global health burden and a leading cause of cancer-related morbidity and mortality. Current blood-based biomarkers lack sufficient sensitivity and specificity, particularly for early detection. In this context, circulating immune-cell transcriptomic profiling has emerged as a promising minimally invasive approach. This systematic review was conducted following a PROSPERO-registered protocol (CRD42024604757) and PRISMA 2020 guidelines to evaluate the diagnostic and prognostic potential of circulating monocyte-related transcriptomic profiles in CRC. Of 295 records identified, six studies met the inclusion criteria. The available evidence consistently supports the diagnostic value of circulating transcriptomic profiles in distinguishing patients with CRC from healthy individuals and in reflecting tumour-associated immune alterations. Monocyte-related signatures, including CXCR2 monocytes, were associated with disease stage and metastatic features. Epitranscriptomic modifications, such as m6A and m5C, further reinforced their diagnostic relevance, with some studies reporting higher diagnostic accuracy than classical biomarkers. In contrast, evidence for prognostic value remains limited, heterogeneous, and often indirect, largely due to small sample sizes, methodological variability, and reliance on public datasets. Overall, circulating immune-cell transcriptomic profiles are promising non-invasive biomarkers for CRC detection and characterization, although their prognostic utility remains unclear. Methodological heterogeneity limits clinical applicability, highlighting the need for standardized, CRC-specific studies with cell-type-resolved approaches. - Source: PubMed
Publication date: 2026/05/06
Podadera-Herreros AliciaPilo JesúsRego-Calvo AlejandroOrtega-Castan MaríaMuriel-López CarolinaHinojosa-Nogueira DanielMoreno-Indias IsabelAmaya-Campos María Del MarAlcaide-García JuliaBoughanem HatimGarcía Flores Libia AlejandraMacías-González Manuel - Cardiovascular disease (CVD) remains the leading cause of mortality among various diseases in China, with both the incidence and mortality rates associated with CVD continuing to rise. Obesity, as a key risk factor for CVD, exacerbates the disease burden. Concurrently, the rates of overweight and obese individuals among Chinese college students have been increasing annually. Maximal fat oxidation (FATmax)-intensity training, which precisely identifies the optimal exercise intensity for fat oxidation, can effectively improve cardiorespiratory function, regulate metabolic levels, and reduce the risk of chronic diseases. Thus, this study aimed to investigate the effects of FATmax-intensity exercise on cardiovascular disease risk factors in obese college students and to explore the associated underlying mechanisms. - Source: PubMed
Publication date: 2026/04/17
Yang JinZhu HaimeiSun FeiyiPei Zuowei