Ask about this productRelated 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
- Abdominal aortic aneurysm (AAA) is a chronic degenerative disease characterized by localized aortic dilation and persistent inflammation. While neutrophil extracellular traps (NETs) are increasingly recognized as key drivers of vascular inflammation and aneurysm progression, the transcriptomic landscape of NETs-related genes (NRGs) in AAA remains inadequately characterized. This study aimed to identify reliable diagnostic biomarkers and explore the immune heterogeneity of AAA to facilitate early risk stratification. We integrated transcriptomic datasets from the Gene Expression Omnibus to elucidate the role of dysregulated NRGs. A comprehensive bioinformatics pipeline was employed, combining weighted gene co-expression network analysis with differential expression profiling to screen for AAA-specific NRGs. Rigorous feature selection was conducted through the intersection of 3 machine learning algorithms - least absolute shrinkage and selection operator, support vector machine-recursive feature elimination, and random forest - to derive a diagnostic signature. The model was constructed using the GSE232911 cohort and validated in an independent external cohort. A robust 4-gene diagnostic signature comprising CXCR4, GZMB, ITGA6, and CD47 was identified. This signature demonstrated a favorable diagnostic performance, achieving an area under the curve of 0.920 in the training cohort. The model maintained consistent discriminatory ability in the external validation cohort, primarily driven by the high discriminative ability of CXCR4 and GZMB. Consensus clustering based on these hub genes revealed 2 distinct molecular subtypes, with Cluster 2 characterized by significant enrichment of neutrophils and innate immune pathways, suggesting intense NETosis activity. Furthermore, drug prediction analyses identified candidate therapeutic compounds, including Eugenol and Tretinoin, offering potential avenues for targeting the NETs-associated molecular landscape. Our findings underscore the pivotal role of NETs-mediated inflammation in AAA pathogenesis and validate a robust 4-gene signature for early diagnosis. By delineating immune-related molecular subtypes and identifying potential drug candidates, this study provides a foundational framework for precision risk stratification and the development of targeted nonsurgical therapies for aneurysm management. - Source: PubMed
Jiang FengLv JiamingZheng ZhenDong Mengmeng - Breast milk not only is the most optimal source of nutrition for newborns but also provides crucial immune support. While there is extensive evidence highlighting the health benefits of breastfeeding, the scientific understanding behind many of these advantages remains limited. The immune cell fraction of breast milk has been poorly studied, and characterization of this essential component may be crucial to shed light on the subject. Here, we investigate the population of neutrophils in breast milk to unveil their phenotype and functions. - Source: PubMed
Publication date: 2026/05/22
Gomez-Casado GemaSaldaña-García NataliaCantarero-Cuenca AntonioGonzalez-Jimenez AndrésPaz-López GuillermoGarcia-Hurtado PatriciaTinahones Francisco JGonzález-Mesa ErnestoOrtega-Gomez Almudena - Immunotherapies remain ineffective in triple-negative breast cancer (TNBC), underscoring the need to define drivers of immune suppression. Natural killer (NK) cells are crucial for eliminating disseminated tumor cells (DTCs) through NK cell cytotoxicity (NKCC), but this is impaired in metastasis. While tumor cell-intrinsic mechanisms of NK cell evasion are known, the role of other cells in the tumor microenvironment remains unclear. Using the Cherry-niche labeling system, we profiled early TNBC lung micrometastases and identified bone marrow-derived monocytes to be highly enriched and capable of suppressing NK cells within metastatic niches. Functional studies revealed that monocyte-derived macrophage migration inhibitory factor (MIF) suppresses NKCC against TNBC cells via CXCR4. MIF inhibition restored NK cell activatory receptors, cytotoxic mediators, and tumor cell killing in vitro, while reducing metastatic outgrowth and increasing NK cell activatory receptors in vivo. These findings reveal MIF as a potential target to enhance NK cell function in TNBC metastasis. - Source: PubMed
Publication date: 2026/05/21
Ermogenous ChristosBrucoli MartiPerini AlessandraYunda de Miguel AdrianaKumar RithuBarcelo JaumeBoardman MaddyGrover MahimaBeattie GordonKafka AikateriniOmbrato Luigi - Immunogenic cell death (ICD) is an important regulatory form of cell death, which can trigger anti-tumor immune responses and plays a crucial role in the development of cancer. Gastric cancer (GC) is a highly malignant tumor with poor prognosis. Currently, there is still a need to explore effective prognostic markers for clinical risk stratification. Therefore, this study aims to identify key prognostic genes related to ICD and construct a novel prognostic signature for the prognosis assessment of GC. - Source: PubMed
Publication date: 2026/02/26
Wan QianZhang LingZheng XiaQian Jun - Following the publication of the above article, a concerned reader drew to the authors' attention that the immunohistochemical data shown for the 'Collagen I/Control' panel in Fig. 5B on p. 1104, and the 'β‑catenin/DKK' panel for the immunofluorescence data shown in Fig. 7B on p. 1106, subsequently appeared in a pair of later publications by the same research group. In addition, in Fig. 5B, the 'Vimentin/ALI' and 'Vimentin/ALI+MSC‑GFP' data panels were found to contain an overlapping section, such that data which were intended to show the results of differently performed experiments had apparently been derived from the same original source. Furthermore, upon performing an independent analysis of the data in this paper in the Editorial Office, it also came to light that the 'α‑SMA/ALI+MSC‑CXCR4' data panel in Fig. 5B had subsequently reappeared in an article by the same research group; the Control panel for the 'MSC (GFP+)' experiment in Fig. 3A on p. 1102 was matching with the Control panel shown in Fig. 6A on p. 1105; certain of the β‑actin and MMP2 protein bands shown for the ALI+MSC‑CXCR4 and ALI+MSC‑GFP experiments in Fig. 7A appeared to be identical in the two sets of western gels; and finally, in Fig. 5A, two sets of data [namely, the data for the IL‑6 and TNF‑α blots for the ALI+MSC‑GFP experiments (central panel of blots), and the pair of Con and 3d 18S blots for the ALI experiments and the 7d and 14d 18S blots for the ALI+MSC‑GFP experiments], bore strikingly resemblances to each other. On re‑examining their original data, the authors realized that they had inadvertently included some of the data incorrectly in Figs. 5, 6 and 7. The revised versions of these three figures, now featuring the correct data for Fig. 5A (the PCR analysis results of TNF‑α and 18S in the ALI+MSC‑GFP group), Fig. 5B (vimentin antibody immunohistochemical staining of the ALI+MSC‑GFP group, α‑SMA antibody immunohistochemical staining of the ALI+MSC‑CXCR4 group, and Collagen Ⅰ antibody immunohistochemical staining of the Control group); Fig. 6A (α‑SMA immunofluorescence staining), Fig. 6C (IgG immunofluorescence staining), Fig. 7A (western blotting results of β‑catenin in the ALI group, MMP2 and β‑actin in the ALI+MSC‑CXCR4 group, and MMP2 and β‑actin in the ALI+MSC‑GFP group) and Fig. 7B (β‑catenin antibody immunofluorescence staining of the DKK1 group), are shown on the subsequent three pages. The image duplications were caused by accidental mix‑up of the files during figure sorting and final manuscript preparation. The authors regret that they did not perform more rigorous cross‑checking of the figures before submission. The corrected figures are consistent with the original experimental data; moreover, there are now no overlaps with any of the group's previously published work, Notably, the overall experimental results and scientific conclusions of the article remain entirely unchanged following the correction of these figures. All the authors agree with the publication of this corrigendum, and they are grateful to the Editor of for granting them the opportunity to publish this; furthermore, they apologize to the readership for any inconvenience caused. [International Journal of Molecular Medicine 33: 1097‑1109, 2014; DOI: 10.3892/ijmm.2014.1672]. - Source: PubMed
Publication date: 2026/05/22
Sun ZhaoruiWang CongShi ChaowenSun FangfangXu XiaomengQian WeipingNie ShinanHan Xiaodong