CXCR4 Antibody
- Known as:
- CXCR4 Antibody
- Catalog number:
- 1009
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- CXCR4 Antibody
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
- Neurodegenerative, cardiovascular, and regenerative disorders remain major causes of disability and mortality worldwide, necessitating the development of multimodal therapeutic strategies. Tanshinone IIA (Tan IIA), a bioactive diterpenoid isolated from Salvia miltiorrhiza, possesses potent antioxidant, anti-inflammatory, anti-apoptotic, and pro-angiogenic properties. Mesenchymal stem cells (MSCs) have emerged as promising regenerative therapeutics owing to their differentiation potential, immunomodulatory capacity, and paracrine effects. Growing evidence indicates that the combination of Tan IIA and MSCs exerts synergistic therapeutic effects by enhancing MSC survival, proliferation, migration, and regenerative function while mitigating oxidative stress and inflammatory injury. This review summarizes current evidence regarding the combined effects of Tan IIA and MSCs on neuroprotection, cardiovascular repair, tissue regeneration, muscle protein synthesis, and gut microbiota modulation across neurodegenerative, cardiovascular, and regenerative disease models. The underlying molecular mechanisms involve the regulation of PI3K/Akt, Wnt/β-catenin, TGF-β/Smad, and Nrf2 signaling pathways, together with improvements in angiogenesis, immune homeostasis, mitochondrial function, and cellular metabolism. Emerging evidence also suggests that modulation of the gut microbiota may contribute to enhanced systemic immune regulation and regenerative outcomes, whereas improvements in muscle protein synthesis may support tissue recovery and functional restoration. Although preclinical findings are promising, further mechanistic investigations and well-designed clinical trials are required to optimize treatment protocols and establish the efficacy, safety, and translational potential of this combinational therapeutic strategy. - Source: PubMed
Publication date: 2026/08/26
Wang WenzheGao HongyanWang Yuan - Chronic diabetic wounds persist in a hostile microenvironment that compromises the survival and reparative activity of transplanted stem cells. Here, we developed a structurally defined 3D-printed ordered porous chitosan methacrylate/gelatin methacryloyl (CSMA/GelMA) hydrogel scaffold platform to test whether topological order acts as a structurally relevant biomaterial cue for adipose-derived mesenchymal stem cell (ADSC) regulation. To enrich for topology-dependent effects, ordered and disordered scaffolds were fabricated from the same photocrosslinkable chitosan methacrylate/gelatin methacryloyl precursor system and subjected to the same crosslinking and lyophilization-rehydration workflow, while differing in spatial pore organization. Among the ordered architectures tested, the 200 μm scaffold showed the most favorable early biological performance and was selected for subsequent studies. Ordered topology induced ADSC polarization, directional F-actin organization, and nuclear elongation/alignment, indicating coordinated cytoskeletal-nuclear remodeling. Mechanistically, ordered scaffolds increased FAK phosphorylation and enhanced YAP nuclear localization, whereas pharmacological inhibition of FAK attenuated YAP-related responses and the reparative paracrine advantage conferred by ordered topology. On this basis, sustained SDF-1α presentation further enhanced the reparative secretory profile, at least partly through CXCR4-AKT/ERK-associated signaling. In an STZ-induced diabetic full-thickness skin wound model, the integrated ordered scaffold strategy improved wound closure, histological reconstruction, collagen deposition, and CD31- and CD206-associated reparative changes, with the greatest benefit observed when combined with ADSCs. These findings support a topology-mechanotransduction-function axis within this scaffold system and provide a rationale for biomaterial-guided stem-cell therapy in diabetic wound healing. - Source: PubMed
Tseng SongluXiang JieyuLi ZimingKang LinWang LiquanZhang ChiLi ZhujunYu NanzeHuang JiuzuoLong Xiao - Phthalates are ubiquitous endocrine-disrupting chemicals, but population-level evidence linking urinary phthalate burden with osteoporosis and the molecular context of these associations remains incomplete. - Source: PubMed
Publication date: 2026/09/08
Jiang JieChen GuanhouLi XinYan RanLi Shuai - Adult T-cell leukemia/lymphoma (ATLL) and peripheral T-cell lymphomas (PTCLs) are aggressive neoplasms of mature T cells with poor prognosis and limited therapies. ATLL originates from HTLV-1 infection, while PTCL comprises heterogeneous subtypes without a defined etiologic factor. Comparative molecular profiling of these malignancies remains limited. We conducted an integrative pooled transcriptomic analysis of publicly available Gene Expression Omnibus (GEO) microarray datasets to compare ATLL, PTCL, and normal T-cell samples. Differential expression, functional enrichment, and protein-protein interaction (PPI) network analyses were performed using STRING, Cytoscape, and Gephi. Key hub genes and functional modules were further analyzed through KEGG and Enrichr databases. Comparative analyses revealed upregulation of extracellular matrix (ECM) components (COL1A1, COL3A1, FN1, SPARC, THBS1) and immune-regulatory molecules (CD163, CXCL12-CXCR4, complement subunits). Shared pathways included ECM-receptor interaction, focal adhesion, and PI3K-Akt signaling. PTCL showed enrichment in coagulation and angiogenesis, while ATLL displayed distinct enrichment of cytoskeletal, chemokine, immune-regulatory, and signaling-associated pathways. PPI networks identified ECM and chemokine signaling as key hubs, with subtype-specific modules related to immune regulation, proliferation, and metabolism. This integrative approach uncovers common and distinct oncogenic programs in ATLL and PTCL, emphasizing ECM remodeling and immune modulation as shared hallmarks. Hub genes such as COL1A1, FN1, and CXCL12-CXCR4 may represent candidate molecular signatures that warrant validation in independent patient cohorts and functional studies before their clinical utility can be established. - Source: PubMed
Publication date: 2026/09/09
Akbarin Mohammad MehdiFarjami ZahraÁlvarez Hugo Ramírez - Idiopathic pulmonary fibrosis (IPF) is a fatal interstitial lung disease characterized by progressive scarring and respiratory failure. While T cells are elevated in IPF lungs, their contributions to fibrosis beyond inflammation remain poorly understood. Here, we performed multiplex imaging and single-cell RNA and protein profiling on about 90,000 CD3+ T cells from control and fibrotic lungs, revealing 11 distinct subsets of CD4+ and CD8+ T cells, including a rare CD56+ regulatory T cell. In addition to increased T cell numbers in severely fibrotic lungs compared with non-diseased controls, we observed CD4+ and CD8+ T cells localized near epithelial cells and in niches of abnormal epithelium. CXCR4/MIF signaling emerged as a central axis mediating T cell-epithelial interactions, while epidermal growth factor receptor (EGFR) and TGF-β pathways dominated in multiple T cell subsets. Our findings support the concept that T cells in IPF adopt nonclassical activation patterns that are driven by epithelial interactions within the fibrotic microenvironment. These studies provide a foundation for exploring alternative therapeutic strategies in IPF lungs by modulating T cell behavior and communication networks. - Source: PubMed
Publication date: 2026/09/08
Serezani Ana PmBazzano Julia MrPascoalino Bruno Dda Silva LudmillaDietrich Abigail JTaylor Chase JSherrill TaylorVannan AnnikaCalvi Carla LGonzalez-Ericsson Paula IWilfong Erin MBacchetta MatthewShaver Ciara MWare Lorraine BSalisbury Margaret LVan Kaer LucBanovich Nicholas EKropski Jonathan ABlackwell Timothy S