CXCL12 _ SDF1
- Known as:
- CXCL12 _ SDF1
- Catalog number:
- NBP1-19778
- Product Quantity:
- 0.1 mg
- 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
- High-grade serous ovarian cancer (HGSOC) is the most lethal histological subtype of ovarian cancer, exhibiting significant heterogeneity and limited therapeutic options. A comprehensive characterisation of proteomic landscape across disease stages is needed to identify actionable biomarkers and therapeutic targets. - Source: PubMed
Publication date: 2026/04/18
Tu MengyanTang SangsangZhang QiaoGuo TianchenCen YixuanXu XiaomengWu ShenglongChen XinLu WeiguoDing ChenXu Junfen - The chemokine CXCL12, as a pivotal immune regulator, plays a crucial role in teleost fish against bacterial infection, but current research on its specific mechanisms remains scarce. This study systematically identified two copies of the CXCL12 in turbot (Scophthalmus maximus) (SmCXCL12a and SmCXCL12b), investigated their expression patterns, and revealed their immune functions and antibacterial mechanisms. Firstly, phylogenetic and syntenic analyses indicated that the SmCXCL12a/b were relatively conserved and exhibited high homology with orthologs in other teleost fish, including Japanese flounder (Paralichthys olivaceus). Secondly, of the nine tissues examined in healthy fish, the highest expression level of SmCXCL12a was observed in the kidney, while the highest expression level of SmCXCL12b was detected in the skin. Following infection with Aeromonas salmonicida, significant differential expression of SmCXCL12a and SmCXCL12b was observed in the gills, intestines, and skin. Additionally, both rSmCXCL12a and rSmCXCL12b exhibited chemotactic activity toward kidney macrophages, splenic leukocytes, and peripheral blood leukocytes. Notably, the growth of Escherichia coli and Staphylococcus aureus was inhibited by rSmCXCL12a and rSmCXCL12b. In addition, rSmCXCL12a and rSmCXCL12b exhibited significant binding capacity to multiple Gram-positive and Gram-negative bacteria, with their binding patterns toward bacterial surface substances such as PGN, LPS, LTA, and Poly(I:C). Therefore, it was speculated that they might exert antibacterial functions by recognizing bacterial surface substances. Furthermore, the agglutination properties of rSmCXCL12a and rSmCXCL12b toward various bacteria suggested their capacity to engage with bacterial surface substances. Finally, it was observed that rSmCXCL12a/b could alter the permeability of bacterial cell membranes, resulting in propidium iodide (PI) influx. Meanwhile, changes in membrane potential were detected in DiOC(3) experiments. Hence, it was hypothesized that one of its antibacterial mechanisms could be membrane attack. To conclude, this research thoroughly elucidated the function of the two copies of SmCXCL12 in immune response and antibacterial mechanisms during bacterial infection, providing a theoretical basis for the application of chemokines in the prevention and control of bacterial fish diseases. - Source: PubMed
Publication date: 2026/04/16
Zhang XiaoxuWang BeibeiLiu YiyingZhang PeiChen ChonghuiLi ChaoFu Qiang - In colitis-associated colorectal cancer (CAC), chronic inflammation is the primary driver of tumorigenesis. A critical event in this process is the massive recruitment of neutrophils, which, while part of the host defense, can paradoxically fuel cancer progression. Excessive neutrophil infiltration contributes to sustained mucosal damage through the release of pro-inflammatory mediators and shapes a tumor-promoting microenvironment. Despite their recognized role, therapeutic strategies specifically targeting pathogenic neutrophil recruitment in CAC are limited. Thlaspi arvense (TA), a traditional medicinal plant, possesses purported anti-inflammatory properties, suggesting its potential utility against CAC. Therefore, this study was designed to evaluate the efficacy of TA in preventing CAC and to delineate its mechanism of action, particularly its impact on neutrophil-driven inflammation. - Source: PubMed
Publication date: 2026/04/17
Wang ZiweiWang WenkaiWang ChaoweiDong BijinSun YunchuanHe XinyingBi LingWang Yan - Microvessels within atherosclerotic plaques are crucially involved in disease progression. Here, we generated a transcriptomic atlas of human atherosclerosis at single-cell resolution, encompassing 17,367 vascular endothelial cells (VECs) from five scRNA-seq studies, and verified key morphological characteristics using histology. SULF1 arterial endothelial cells (ArtECs) represented the primary subcluster undergoing endothelial-to-mesenchymal transition (EndMT). Capillary-like endothelial cells (CapECs) were identified as primary mediators of angiogenesis, and a trajectory model illustrated the transition between tip and stalk cells, with subclusters of ArtECs and CapECs predominantly expressing CXCL12, thereby driving the CXCL12/CXCR4 signaling axis. The largest plaque EC cluster, exhibiting the most heterogeneity, was found among post-capillary venule endothelial cells (VenECs), particularly ACKR1NR2F2 VenECs, which displayed distinct inflammatory transcriptional signatures characterized by adhesion molecules and chemokines. Overall, this atlas of atherosclerosis underscores endothelial heterogeneity and identifies SULF1 ArtECs and VenECs as potential therapeutic targets for EndMT and leukocyte recruitment, respectively. - Source: PubMed
Publication date: 2026/04/17
Wu YanzhaoXue ZhiweiSun TaoYu YindaLiang XiangjunXing WenchenMu FeiyuZhang ZhihanLv MeilinLing LuHan MengtaoCheng LianGisterĂ¥ AntonWang Donghai - Pancreatic ductal adenocarcinoma (PDAC) diagnoses are often accompanied by a number of physical and psychological symptoms, including anxiety and depression. As a result, many patients are prescribed anxiolytics such as benzodiazepines that have unintended effects on the tumor. Previous work from our lab has highlighted that structural differences between benzodiazepine compounds may be responsible for different clinical outcomes influenced by their effects on cancer-associated fibroblasts (CAFs) within the PDAC tumor microenvironment (TME). Here, we demonstrate that the commonly prescribed N-substituted triazolobenzodiazepine alprazolam (ALP) abrogates the production of proinflammatory cytokines including CCL2, CXCL12, IL6, and IL8 in human CAFs. This phenotype is unique only to azole-containing benzodiazepines, including midazolam. The ability of ALP to regulate proinflammatory cytokine production is maintained in vivo, as ALP-treated mice bearing pancreatic tumors exhibited reductions in IL6 within the tumor interstitial fluid. Mechanistically, an unbiased phosphoproteomic approach revealed that ALP abrogates TLR4-mediated cytokine production in CAFs. These findings cumulatively support that ALP dampens CAF-mediated inflammatory signaling within the PDAC TME. - Source: PubMed
Publication date: 2026/04/17
Reavis Hunter DChaubey Aditi HSmythers Amanda LTisdale Arwen ATracz AmandaDimeck Alphonse NMaraszek Kathryn ECortes Gomez EduardoPaulo Joao ADasgupta SubhamoyGygi Steven PFeigin Michael E