CXCL12 _ SDF1
- Known as:
- CXCL12 _ SDF1
- Catalog number:
- GTX10395
- Product Quantity:
- 25 µg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- CXCL12 _ SDF1
Related genes to: CXCL12 _ SDF1
- Gene:
- CXCL12 NIH gene
- Name:
- C-X-C motif chemokine ligand 12
- Previous symbol:
- SDF1A, SDF1B, SDF1
- Synonyms:
- SCYB12, SDF-1a, SDF-1b, PBSF, TLSF-a, TLSF-b, TPAR1
- Chromosome:
- 10q11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1994-11-30
- Date modifiied:
- 2016-10-05
Related products to: CXCL12 _ SDF1
Anserine Stromal Cell Derived Factor 1 Elisa Kit (SDF1)Anserine anti - Stromal Cell Derived Factor 1 Elisa Kit (SDF1)anti-CXCL12(1F7)Anti-human CXCL12, Source: Monoclonal Murine, MABAnti-human SDF-1 alpha (CXCL12), bt, Source: Polyclonal bt. Rabbit, PABAnti-human SDF-1 alpha (CXCL12), bt, Source: Polyclonal bt. Rabbit, PABAnti-human SDF-1 alpha (CXCL12), bt, Source: Polyclonal bt. Rabbit, PABAnti-human SDF-1 alpha (CXCL12), Source: Polyclonal Rabbit, PABAnti-human SDF-1 alpha (CXCL12), Source: Polyclonal Rabbit, PABAnti-human SDF-1 alpha (CXCL12), Source: Polyclonal Rabbit, PABAnti-human SDF-1 beta (CXCL12), bt, Source: Polyclonal bt. Goat, PABAnti-human SDF-1 beta (CXCL12), bt, Source: Polyclonal bt. Goat, PABAnti-human SDF-1 beta (CXCL12), bt, Source: Polyclonal bt. Goat, PABAnti-human SDF-1 beta (CXCL12), Source: Polyclonal Goat, PABAnti-human SDF-1 beta (CXCL12), Source: Polyclonal Goat, PAB Related articles to: CXCL12 _ SDF1
- Bladder cancer therapy is frequently limited by inefficient drug retention and adaptive immune resistance within a hypoxic tumor microenvironment. Here, we report a CD44-targeted, fully synthetic nanocomposite (HPPZC) that converts chemotherapy into a mitochondria-associated therapeutic strategy accompanied by tumor immune remodeling. Rapid microwave-assisted assembly integrates hyaluronic acid (HA), polydopamine (PDA), protamine, zinc oxide (ZnO), and camptothecin (CPT) into a structurally integrated hybrid nanocomposite with tumor targeting, while the PDA/ZnO interface functions as a redox-active platform associated with mitochondrial dysfunction and redox modulation. HPPZC induces rapid mitochondrial depolarization, elevates oxidative stress, and is associated with PINK1/Parkin-related mitochondrial quality-control and autophagy-associated turnover signatures. In vivo, HPPZC treatment prolonged local intratumoral retention and produced tumor regression. The combination of chemotherapy with mitochondrial stress and tumor immune remodeling, suppressing CXCL12 and PD-L1, promoting M1-like marker profile, and increasing CD8⁺ T-cell infiltration. This work establishes a reproducibly fabricated redox-active nanotherapeutic associated with mitochondrial stress that couples targeted chemotherapy with immune microenvironment remodeling for antitumor efficacy. - Source: PubMed
Publication date: 2026/09/05
E-Y Chuang AndrewTung Szu-YuTzou Kai-YiCai Yao-EnHsu Hao-ChengTsui Ke-HungLin Wei-XuanRethi LekshmiDong Shao-WeiNguyen Hieu TrungLiu Chia-Hung - Coronary artery disease (CAD) is a leading cause of death worldwide. Evidence of genetic predisposition is derived mostly from studies of Europeans and East Asians. - Source: PubMed
Publication date: 2026/07/28
Mancini IlariaPagliari Maria TeresaSadeghian SaeedAbbasi Seyed HesameddinPoorhosseini HamidrezaBoroumand Mohammad AliLotfi-Tokaldany MasoumehPappalardo EmanuelaAgosti PasqualeRosendaal Frits RPeyvandi Flora - Colorectal cancer (CRC) develops within a mucosal ecosystem in which epithelial barrier function, colonizing microbes, inflammatory signaling, and immune cell composition are closely interdependent. Immune checkpoint inhibitors have significantly altered treatment outcomes in patients with mismatch repair-deficient or microsatellite instability-high (dMMR/MSI-H) CRC, but most microsatellite-stable (MSS) tumors still respond poorly, and this is not solely due to lower antigenicity. This article explains this gap mechanistically: gut microbiota dysbiosis weakens the mucosal barrier, promotes microbial translocation, amplifies cytokine and eicosanoid signaling, and remodels the tumor microenvironment into an immunosuppressive state dominated by myeloid cells. We focus on and enterotoxigenic , microbial metabolites, tight junction disruption, and the IL-6/STAT3, NF-κB, TNF-alpha, and COX-2/PGE2 pathways that link epithelial stress with innate immune remodeling. Downstream processes include tumor-associated macrophages, myeloid-derived suppressor cells, neutrophil polarization, dendritic cell dysfunction, regulatory T cells, cancer-associated fibroblasts, CXCL12-mediated T-cell exclusion, and hypoxia. These processes collectively create a spatially structured drug-resistance niche, preventing effector T cells from functioning effectively, rather than simply resulting in an immunologically "cold" tumor. We believe that integrating this microbiota-barrier-myeloid axis into biomarker development and mechanism-matched combination therapy design offers a more rational and promising approach to overcoming immunotherapy resistance in CRC, especially in MSS disease, compared to empirical drug combinations. - Source: PubMed
Publication date: 2026/08/21
Lu NaZhang LeiSun HanyuZhou YuwenshuHe PanliZhao ChangruiWang Yue - Resistance to anti-TNFα therapy (e.g., infliximab) in ulcerative colitis (UC) remains a significant clinical challenge, with the underlying cellular and spatial mechanisms poorly understood. - Source: PubMed
Publication date: 2026/08/20
Li PeihongZhang YikunZhao LiuqinWang YiwenHu HongyiGuo SiqingZhang TingtingLin ZhanchengLin JiangZeng KexinZhong LindaLiu ChangqinSun Boyun - Laryngeal squamous cell carcinoma (LSCC) remains a clinically challenging malignancy of the head and neck. Because organ preservation is a major therapeutic objective in LSCC, stromal biology is of particular clinical relevance. Stromal factors influence local disease control, functional outcomes, and treatment resistance. Cancer-associated fibroblasts (CAFs) are dynamic regulators of extracellular matrix remodeling, immune exclusion, angiogenesis, and therapeutic resistance. However, LSCC-specific evidence remains fragmented, and many mechanistic concepts are still extrapolated from head and neck squamous cell carcinoma (HNSCC) and hypopharyngeal squamous cell carcinoma (HPSCC). This review adopts an evidence-stratified framework that distinguishes direct LSCC evidence from translatable cross-site evidence and hypothesis-generating inferences. We propose a provisional five-state model for LSCC that includes myofibroblastic, inflammatory, antigen-presenting, extracellular matrix-remodeling, and putative immune-trapping CAF programs. Direct LSCC studies support the presence of early stromal activation along the leukoplakia-to-carcinoma continuum and the enrichment of -positive and -positive fibroblastic programs in metastatic disease. Associations involving stromal PD-L1 expression and altered CAF-derived exosomal microRNA cargo have also been reported. Translatable evidence from HNSCC implicates TGF-β- and CXCL12-dependent T-cell exclusion together with Gal9-mediated T-cell dysfunction. Additional mechanisms include IL-6/JAK/STAT3-driven myeloid skewing and NOX4-dependent stabilization of the myofibroblastic phenotype. We integrate these findings into a spatially informed conceptual framework encompassing the invasive front, the perivascular compartment, the cartilage interface, and the lymphovascular niche. We also discuss biomarker-guided therapeutic opportunities, including CAF normalization, -directed approaches, stromal signaling blockade, extracellular matrix-targeted strategies, and interference with extracellular vesicle-mediated signaling. This review thereby establishes an evidence-stratified framework for CAF heterogeneity in LSCC and clarifies the translational value and current limitations of stroma-targeted strategies. It further provides a structured foundation for hypothesis-driven clinical and experimental investigation in laryngeal cancer. - Source: PubMed
Publication date: 2026/08/20
Hong Wei-ZheHuang Guan-JiangLuo Qi-PingLu Biao-Qing