CXCR4 Antibody
- Known as:
- CXCR4 Antibody
- Catalog number:
- 1012
- 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
- Colorectal cancer (CRC) is one of the most common malignant tumors with the highest incidence and mortality rates worldwide. Immune checkpoint blockade (ICB) therapy has revolutionized the landscape of cancer treatment; however, most patients with CRC gain limited benefits from it. The immunosuppressive microenvironment of CRC is an important cause of tumor progression, metastasis, and immunotherapy resistance. This study aimed to reveal the key role of chemokine receptor 4 (CXCR4) in the immunosuppressive microenvironment and glutamine metabolism reprogramming using integrated single-cell transcriptomics and metabolomics analyses. The in vivo and in vitro experiments verified that CXCR4 mediated metabolic reprogramming in CRC cells by regulating the PI3K-Akt-SMAD4 pathway. Further co-culture experiments revealed that CXCR4 promoted the polarization of tumor-associated macrophages (TAMs) to M2 type through glutamine metabolic reprogramming and induced the exhaustion of CD8 T cells, thereby intensifying immune escape. The knockdown of CXCR4 significantly increased the infiltration of CD8 T cells and M1 TAMs, reduced the infiltration of M2 TAMs, effectively reshaped the immunosuppressive microenvironment of CRC-bearing mice, and significantly enhanced the immunotherapeutic effect against programmed cell death protein 1 (PD-1). This study discovered a novel mechanism by which CXCR4 drove CRC immune escape through the dual-axis regulation of the "glutamine metabolism-immune microenvironment." Targeting CXCR4 not only inhibits tumor metabolic adaptability but also reverses TAMs polarization and T cell exhaustion, thereby effectively sensitizing PD-1 inhibitors. This study provides an important theoretical basis and a highly promising new combined treatment strategy for overcoming ICB resistance in patients with CRC. - Source: PubMed
Publication date: 2026/05/04
Zhu ChengleLiu YutingXu ShaopengLi RuonanShi JiwenTang GuohuiRan RuorongPang BoChi ZixiangDing YongxingWang WenruiYang QinglingChen Changjie - Endothelial cells (ECs) damage serves as the initiating factor for acute cellular rejection after liver transplantation (LT). However, the origin and characteristics of post-transplant neonatal ECs remain controversial. We aim to uncover the mechanisms underlying cell-cell interaction of post-transplant ECs, and develop an EC-targeted strategy to alleviate transplant rejection. - Source: PubMed
Publication date: 2026/05/02
Chen RuihanLi XinqiangZhu PengweiYi XuewenWang TingChen HuiHuang XueyinYe GuoguoJiang JingyuOng MeichingJiang LiujunLi YaliZhong SiyiHe YangyanFan RongZhang BohuanLi HongjunCai JinzhenZheng ShusenXu QingboLing QiZhang Hongkun - Primary aldosteronism (PA) may present as either unilateral or bilateral disease. Differentiating unilateral forms-unilateral aldosterone- producing adenoma (APA) and unilateral adrenal hyperplasia-from bilateral forms-bilateral APA, bilateral adrenal hyperplasia (BAH)-is critical, as the management strategies differ. Currently, PA subtyping is performed using adrenal vein sampling (AVS) and computed tomography (CT). However, AVS is invasive and technically demanding, and CT has limited accuracy. CXCR4 (CXC chemokine receptor type 4) expression is higher in APAs than in normal adrenal tissue and non-functional tumors. Pentixafor, a CXCR4-specific ligand labelled with Ga, has shown potential for PA subtyping. - Source: PubMed
Publication date: 2026/01/05
Acharya Ashish KElangovan Indirani MuthukrishnanGauthaman Dinesh KumarSimon Shelley - Ovarian cancer (OC) remains a malignancy characterized by obscure risk factors and unfavorable prognosis. While 3-tert-butyl-4-hydroxyanisole (3-BHA) is suspected of exerting toxic effects on ovarian health, the precise molecular mechanisms underlying its impact remain elucidated. This study aims to systematically investigate the potential pathogenic mechanisms of 3-BHA in the progression of OC.Integrated transcriptomic data from the GEO database (GSE18520 and GSE40595) were analyzed. A synergistic computational framework was employed, incorporating Differentially Expressed Genes (DEGs) identification, Weighted Gene Co-expression Network Analysis (WGCNA), multiple machine learning algorithms, and SHapley Additive exPlanations (SHAP) analysis to achieve high-interpretability feature selection.Five hub genes-CXCR4, CCL7, CXCL8, CXCR2, and CX3CL1-were identified, all demonstrating robust diagnostic efficacy with AUC values of 0.911, 0.882, 0.823, 0.772, and 0.837, respectively. Prognostic profiling via GEPIA3 highlighted CXCR2 overexpression as a potential critical biomarker driving poor clinical outcomes in OC. Furthermore, molecular docking validated the strong binding affinity of 3-BHA with CX3CL1 and CXCR2. Subsequent 100 ns molecular dynamics simulations and thermodynamic stability assessments confirmed the structural stability of the 3-BHA-CXCR2 complex.By integrating bioinformatics and computational toxicology, this study deciphers the potential mechanistic landscape through which 3-BHA influences OC. These findings not only refine the toxicological understanding of 3-BHA but also provide novel candidates for early diagnosis and prognostic risk stratification in OC. - Source: PubMed
Publication date: 2026/05/03
Shi YifeiNiu DongJin Chunhui - Covalent Bruton tyrosine kinase (BTK) inhibitors have advanced the treatment of Waldenström macroglobulinaemia; however, the occurrence of progression, intolerance, and acquired resistance are not fully understood. We aim to report on the safety and activity of pirtobrutinib (a highly selective, non-covalent BTK inhibitor) in patients with relapsed or refractory Waldenström macroglobulinaemia, including those who received previous covalent BTK inhibitors as part of the phase 1/2 BRUIN trial. - Source: PubMed
Palomba M LiaPatel Manish REyre Toby AJurczak WojciechLewis DavidGastinne ThomasMa ShuoCohen Jonathon BPatel KrishBrown Jennifer RScarfò LydiaMunir TalhaLech-Maranda EwaHoffmann Marc SUjjani Chaitra SFakhri BitaWang Michael LIzutsu KojiNagai HirokazuTam Constantine SRhodes Joanna MVose JulieMcKinney MatthewGerson James NBarve Minal AKuss BryoneKoh YoungilBarrett AislingTreon Steven PCastillo Jorge JSeymour John FRuppert Amy SMcNeely Samuel CWalgren Richard ATsai Donald EBao KatherineNair BinojWoyach JenniferCheah Chan Y