CXCL12 _ SDF1
- Known as:
- CXCL12 _ SDF1
- Catalog number:
- GTX45118
- Product Quantity:
- 100 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
- Metastasis remains the major cause of mortality in colorectal cancer (CRC) despite continued advances in diagnosis and treatment. Increasing evidence identifies the CXCL12/CXCR4 chemokine axis as a critical driver of CRC progression and metastatic dissemination. Through dynamic interactions between tumor cells and the tumor microenvironment, this axis regulates multiple processes essential for metastasis, including driving migration and invasion, angiogenesis and lymphangiogenesis, and shaping the tumor immune microenvironment through recruitment of immunosuppressive populations, blockade of effector lymphocyte trafficking and function, and modulation of immunosuppressive cytokines including IL-10. In this review, we summarize the molecular mechanisms by which CXCL12/CXCR4 promotes CRC metastasis. These pleiotropic effects are mediated by crosstalk with PI3K/Akt, MAPK/ERK, and Wnt/β-catenin pathways, and are regulated at transcriptional, post-transcriptional, and post-translational levels. Preclinical studies demonstrate that CXCR4 antagonists (e.g., plerixafor, LY2510924) suppress metastasis and, when combined with immune checkpoint inhibitors, can reverse the "cold" immune phenotype of microsatellite-stable CRC. We also discuss recent advances in the regulation of CXCL12/CXCR4 expression, the role of related receptors such as CXCR7, and emerging strategies targeting this axis for therapeutic intervention. Collectively, current evidence supports the CXCL12/CXCR4 axis as a promising biomarker and therapeutic target in metastatic CRC, and further elucidation of its regulatory network may facilitate the development of more effective precision treatment strategies. - Source: PubMed
Publication date: 2026/04/23
Tian ShuanglinLiu JinruiYang XiulanGuo Jiawei - Adult mammals with spinal cord injury (SCI) face permanent disability from failed regeneration and scarring, while neonatal mice achieve scarless repair. We show neonatal mouse circulating blood-derived small extracellular vesicles (NCE) rejuvenate adult spinal cord microvascular endothelial cells (SCMECs), restoring lipid metabolism, easing immune imbalance, and supporting neuroaxonal regrowth. Post-SCI myelin debris triggers IRS1-mediated PI3K-Akt-mTOR overactivation in SCMECs, causing harmful lipid droplet buildup, organelle dysfunction, and endothelial-to-mesenchymal transition (EndoMT). It also increases CXCL12 secretion from SCMECs, which recruits CXCR4 macrophages. These macrophages release TNF-α and GDF15, promoting neuronal injury and EndoMT, and forming a destructive feedback loop. We create a "Microenvironment-Reprogramming Potent Hydrogel" - a high-adhesion GelNB hydrogel loaded with NCE - as an efficient delivery tool. NCE targetedly deliver miR-487b-3p to block IRS1 and CXCL12, breaking the vicious cycle. This remodels microvasculature, normalizes SCMEC lipid metabolism, reduces macrophage infiltration, promotes neuroregeneration, and achieves functional recovery. Our study uncovers an endothelium-immune crosstalk axis hindering SCI repair and highlights miR-487b-3p-rich sEVs as a promising therapy. - Source: PubMed
Publication date: 2026/05/06
Yuan FeifeiShi ChaoranLiang XisongXu JiaqiQin YimingXu ShengChen YongQin TianDing YingheHu ZhiyuLi ChengjunLu HongbinHu JianzhongCao Yong - Cancer-Associated Fibroblasts (CAFs) are key players in the tumor microenvironment (TME) of ovarian cancer, influencing progression and chemoresistance. Their heterogeneous subtypes contribute distinctly to immune evasion, extracellular matrix (ECM) remodelling, and drug resistance. - Source: PubMed
Publication date: 2026/05/05
Gopinath SambasivamBalakrishnan PavithraMuli YaminiRamasamy JubileePuniyakotti SaranyaVaradarajan NithyaVelmurugan Ramaiyan - Liberal transfusions of adult platelets increase preterm infant morbidity and mortality. This harm may be because of functional differences between neonatal and adult platelets. Preclinical murine models remain essential for investigating the underlying mechanisms. A prerequisite for developing and using these models is a cross-species comparison of developmentally regulated molecules in platelets. The objective of this study was to define proteins and biological pathways that differ between neonatal and adult platelets in mice and ascertain developmentally regulated molecules and pathways that are consistent across murine and human platelets. By comparing proteomes from resting murine and human platelets, we identified a consistent increase in inflammatory proteins in adult platelets across species, including β2M and CXCL12. Other markers for platelet function differed between species, including P-selectin, which was increased in adult murine platelets but did not differ with development in humans. To better elucidate developmentally regulated pathways across species, we used sparse principal component and machine learning-based approaches. These analyses revealed developmentally regulated growth factors, inflammatory signaling pathways, and metabolic changes that were consistent across species as well as some discrepant molecules and signaling pathways. Our results clarify molecular differences between neonatal and adult platelets with direct relevance for altered platelet reactivity and inflammatory functions. This approach helps bridge the gap between understanding animal models and human biology to investigate the impact of developmental differences in platelet biology on neonatal transfusion. These methods can be similarly used in other biological systems to improve the translatability of preclinical research. - Source: PubMed
Publication date: 2026/03/12
Thom Christopher SMa XinyueFeldman Henry AMcGrath Kathleen EMaurya PreetiFazelinia HosseinSpruce LynnO'Reilly DanielEl Nems AmaliaEscobar Jesselin RomeroPalis JamesMorrell Craig NSola-Visner MarthaMager Donald EDavenport Patricia E - Inhibiting hepatic stellate cells (HSCs) activation, which represents the initial step of liver fibrosis, is a key strategy for fibrosis treatment. Sorafenib has been repurposed as an antifibrotic agent; however, its reported effects largely rely on cytotoxic mechanisms. The antifibrotic mechanisms induced by minimally cytotoxic sorafenib remain unclear. We aimed to elucidate the dynamic changes in gene expression and lipid metabolites that occur during HSC inactivation using low-concentration sorafenib. - Source: PubMed
Publication date: 2026/04/29
Kim YeonseoHam BaknoonKim YeojinJung Byung HwaPark JinyoungLee Hyunbeom