CXCL12 _ SDF1 (N_term)
- Known as:
- CXCL12 _ SDF1 (N_term)
- Catalog number:
- AP14571PU-N
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- CXCL12 _ SDF1 (N_term)
Related genes to: CXCL12 _ SDF1 (N_term)
- 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 (N_term)
Related articles to: CXCL12 _ SDF1 (N_term)
- Natural killer (NK) cells undergo stepwise differentiation from multipotent progenitors within secondary lymphoid tissues. Despite the central importance of the tissue microenvironment in their development, little is known about cell-cell interactions that regulate human NK cell trafficking and maturation. Here, we identify the chemokine receptor CXCR4 and its lig- and CXCL12 as regulators of stromal-NK cell interactions required for NK cell maturation. We demonstrate that CXCR4 is expressed throughout human NK cell development in peripheral blood and tonsil, and CXCL12 is enriched in stromal niches containing developing NK cells. Pharmacologic blockade or genetic disruption of CXCR4 resulted in diminished adhesion to integrin ligands and high-resolution imaging demonstrated crosstalk between CXCR4 and integrins, providing a mechanistic basis for chemokine-dependent modulation of adhesion. Further, CXCR4 blockade resulted in altered contact-dependent motility on stromal cells and integrin ligands, with decreased stable stromal engagement and increased cell speed. Consistent with a requirement for these interactions, treatment with the CXCR4 antagonist plerixafor (AMD3100) impaired NK cell generation from CD34 precursors. Analysis of NK cells from WHIM syndrome patients with CXCR4 gain-of-function mutations treated with plerixafor revealed similar defects in migration and adhesion, supporting the in-vivo relevance CXCR4-dependent regulation of NK cell adhesion and motility. - Source: PubMed
Publication date: 2026/03/15
Eisman Shira EGrossberg FrancescaKoenigsberg Batya SMcDermott David Hvan den Haak FrédériquePedroza Luis AHegewisch-Solloa EverardoMurphy Philip MMace Emily M - CXCR4 plays a pivotal role in liver fibrosis (LF) by mediating the activation of hepatic stellate cells (HSCs), which contribute to extracellular matrix (ECM) deposition and scar formation. The CXCR4/CXCL12 axis is essential in fibrogenesis, promoting HSCs activation, inflammation, and angiogenesis, which exacerbates fibrosis and creates an environment conducive to hepatocellular carcinoma (HCC) development. In HCC, CXCR4 signaling supports tumor cell proliferation, survival, and metastasis, linking chronic liver injury to cancer progression. Recent advancements in targeted drug delivery have facilitated the development of CXCR4-targeted therapies, improving treatment efficacy while minimizing systemic toxicity. This review examines the interactions between CXCR4 and its ligand CXCL12, the associated signaling pathways, and their role in LF and HCC. Furthermore, it explores CXCR4 as a therapeutic target, focusing on CXCR4 blockers, peptide inhibitors, and gene silencing/editing strategies. The review also highlights various CXCR4-targeted nano therapeutic strategies, such as liposomes, lipid NPs, microbubbles, polymeric NPs incorporating siRNA, miRNA, small molecules, peptides etc for the management of LF and HCC. Additionally, the review addresses the clinical progress of monoclonal antibodies, small molecules, and peptides targeting CXCR4 in both preclinical and clinical trials. Challenges and future directions of CXCR4-targeted nanotherapeutic are also discussed. In conclusion, this review emphasizes the therapeutic potential of CXCR4-targeted nanotherapeutic strategies for combating LF and HCC. - Source: PubMed
Publication date: 2026/04/22
Ullah AftabKhan MarinaZhang YibangShafiq MuhammadUllah MohsanAbbas AzarUllah KifayatXiangxiang XuChen GangDiao Yong - Atopic dermatitis (AD) is a heterogeneous inflammatory skin disease with known ethnic disparities in clinical presentation and treatment response. However, molecular data, particularly for Hispanic patients, remain limited. - Source: PubMed
Publication date: 2026/04/25
Liu DanielDel Duca EsterBrunner PatrickAvallone GianlucaBeaziz JessicaMetukuru RagasrutiLin XinyiEstrada YerielLau MeganLargen JosephUngar BenjaminGuttman-Yassky Emma - Skin diseases frequently coexist with other disorders, such as metabolic syndrome, diabetes mellitus, depression, psoriatic arthritis, and cardiovascular disease. Altered levels of distinct chemokines, like CCL5/RANTES, CXCL12/SDF-1a, CCL7/MCP-3, CCL2/MCP-1, CXCL1/GROa, and the eotaxin family, contribute to the development and/or exacerbation of inflammation, which is a common feature of numerous skin diseases as well as metabolic syndrome. The pathological and molecular connections between chronic inflammatory skin diseases and metabolic syndrome are increasingly recognized as being driven by shared inflammatory pathways, oxidative stress, and adipokine dysregulation. While systemic inflammation acts as a common thread, the precise mechanisms for some conditions remain partially understood. Nevertheless, the exact pathological and molecular connections between skin diseases (i.e., psoriasis, atopic dermatitis, pemphigus vulgaris, acute and chronic spontaneous urticaria, bullous pemphigoid, squamous cell carcinoma, alopecia areata, systemic sclerosis, discoid lupus erythematosus, diffuse large B-cell lymphoma) and metabolic syndrome are not yet fully understood. This narrative review summarizes the robust association between various chronic inflammatory skin diseases and metabolic syndrome in the context of pro-inflammatory chemokines. - Source: PubMed
Publication date: 2026/04/10
Matwiejuk MateuszMyśliwiec HannaMikłosz AgnieszkaChabowski AdrianFlisiak Iwona - This study aims to investigate how emodin, an active component of , regulates macrophage polarization through the HDAC4/NF-[Formula: see text]B/CXCL12 pathway and impacts the progression of hepatocellular carcinoma (HCC). The inhibitory effect of emodin on M2 polarization was assessed by collecting conditioned cell culture medium from HepG2 cells and treating macrophages with emodin. Network pharmacology and other experiments were used to identify HDAC4 as a key target, and this was further validated through molecular docking, surface plasmon resonance (SPR), and Western blot analysis. Additional validation of the HDAC4/NF-[Formula: see text]B(p65)/CXCL12 axis regarding HCC progression was conducted using single-cell RNA sequencing and an HCC model. The results demonstrate that macrophages with HepG2 supernatant after treating, including emodin, tetrahydroxy stilbene glucoside and physcion, were added to reduce macrophage M2 polarization and inhibit HepG2 invasion and migration. Network pharmacology and protein analysis were used to discover the role of HDAC4 as the target of three drugs in HCC. The feasibility of emodin as a drug target for HDAC4 was explored through molecular docking simulation and SPR, and then verified through Western blot and nuclear plasma separation analysis. Likewise, the HDAC4/NF-[Formula: see text]B (p65) pathway reduces M2 polarization and inhibits the invasion and migration of HepG2. By using a single-cell sequencing database to predict the high expression of chemokines in HCC, and verifying the effect of emodin's ability to reduce M2 polarization and inhibit HepG2 invasion and migration via the HDAC4/NF-[Formula: see text]B (p65)/CXCL12 pathway, the results were likewise validated . This study elucidates the novel role of emodin in HCC progression and macrophage polarization, and demonstrates how emodin-mediated HDAC4 inhibition effectively attenuates HCC invasion and migration. - Source: PubMed
Publication date: 2026/04/25
Zhang Yi-QiongXu Yong-JieLi Hai-ZhiWang ShuangLi Cheng-ChengHuang Chang-Yu-DongShi Ya-ChunLi XingZhao Shu-YunZhu Li-YingPan Wei