CXCL12 _ SDF1
- Known as:
- CXCL12 _ SDF1
- Catalog number:
- AVARP07031_P050
- Product Quantity:
- 50 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
- The regenerative capacity of adult bone relies on the rapid activation and lineage engagement of skeletal stromal and progenitor cells (SSPCs). While signaling pathways that regulate these processes have been extensively studied, the epigenetic mechanisms that constrain progenitor activation and lineage permissiveness during adult bone repair remain poorly defined. Disruptor of telomeric silencing 1 like (Dot1L), the sole histone methyltransferase responsible for H3K79 methylation, is essential for skeletal development, yet its function in adult skeletal regeneration has not been established. Here, we identify Dot1L as a key epigenetic regulator that limits the early regenerative response to bone injury. Genetic reduction of Dot1L activity in the Prrx1 mesenchymal lineage enhances stromal progenitor activation, proliferative engagement, and differentiation capacity, revealing a previously unrecognized role for Dot1L in restraining progenitor responsiveness in adult bone. Notably, acute pharmacologic inhibition of Dot1L using the selective H3K79 methyltransferase inhibitor EPZ-5676 similarly enhances early progenitor activation, indicating that reduced Dot1L enzymatic activity is sufficient to modulate regenerative engagement. At the cellular level, reduced Dot1L activity expands injury-responsive Cxcl12 stromal populations and increases osteogenic progenitor abundance following injury. Consistent with these cellular changes, Dot1L reduction is associated with accelerated early bone formation Collectively, these findings position Dot1L as an epigenetic gatekeeper that constrains early progenitor activation during the initial phase of adult skeletal repair. - Source: PubMed
Publication date: 2026/04/09
Stetsiv MartaDauphinee DrewAbdulsalam SakinahPrabhu ShagunTress AlexanderCobb KerrySanjay ArchanaGuzzo Rosa M - Successful pregnancy requires exquisite balance: the placenta must invade just enough to access maternal blood but not so deep it remains attached at birth. Disrupting this balance causes life-threatening pregnancy complications, for which treatments remain limited. Animal models are desperately needed to discover mechanisms underlying balanced uteroplacental development and how pregnancy complications arise, but this is hampered by the view that mouse placentation lacks human characteristics such as extensive trophoblast invasion and targeting of uterine spiral arteries. Here, we utilize 3D imaging, mouse genetics, and pharmacological perturbations to demonstrate that: (1) The mouse placenta invades more extensively than previously recognized with most spiral arteries heavily enveloped by fetal trophoblasts, (2) This process is disrupted without CXCL12-CXCR4 signaling specifically during early pregnancy, and (3) Disrupting early uteroplacental development ultimately results in excessively deep trophoblast invasion, closely mimicking the pregnancy complication placenta accreta. Mechanistically, uterine epithelium, stroma, and arteries activate CXCR4 signaling in early pregnancy, and inhibition causes decidualization failure, followed by dissolution of spiral artery development. Trophoblasts consequently migrate deep into uterine muscle and its arteries, reproducing hallmarks of human accreta. Thus, with 3D imaging, the mouse more effectively models human uteroplacental development and defines an early etiological window for intervention. - Source: PubMed
Publication date: 2026/04/09
Zwierzynski James BMoufarrej Mira NRed-Horse Kristy - Osteoarthritis (OA) is a degenerative joint disease involving multiple cell types, yet the role of osteoblast (OB)-immune cell interactions remains poorly understood. - Source: PubMed
Publication date: 2026/04/11
Liu KunLi Jia-LiChen YanLi Yu-XinDeng Jeffrey DGong YunCao ChongZeng QinXiao Zheng-WuWen Kai-ZhiQu Xiao-ChaoChen Xiang-DingDeng YunDeng Hong-WenTan Li-Jun - Cancer-associated fibroblasts (CAFs) play important roles in breast cancer (BC) progression and metastasis. Here we investigated whether CAFs from indolent vs. aggressive BCs differ in gene expression profiles and how they impact metastasis. - Source: PubMed
Publication date: 2026/04/17
Miller Philip CSharma UtsavTao JiaXiangSun JunMedina-Saenz KelsiePicon-Ruiz ManuelMorata-Tarifa CynthiaBare Susan MSlingerland Joyce MEl-Ashry DorrayaLippman Marc E - Pancreatic ductal adenocarcinoma (PDAC) is among the most aggressive and metastatic malignancies worldwide. Migrating cancer stem cells (miCSCs), marked by CD133⁺CXCR4⁺ expression is a key driver of PDAC progression, which currently lack effective therapeutic targets. Activated pancreatic stellate cells (PSCs) within the tumor microenvironment secrete CXCL12, the ligand for CXCR4, thereby promoting stemness, epithelial-to-mesenchymal transition (EMT), and chemoresistance in miCSCs. Despite advances in understanding PDAC biology, clinically effective strategies that target CXCR4⁺ CSC populations remain limited. In order to investigate the molecular mechanisms sustaining miCSCs, we performed protein-protein interaction network analysis, which identified the transcription factor BMI1 as a key downstream effector of the CXCL12/CXCR4 axis. Functional studies using shRNA-mediated knockdown of CXCR4 and BMI1 were conducted to assess their roles in miCSC migration, EMT, and self-renewal. We further evaluated the therapeutic potential of the endogenous CXCR4 antagonist EPI-X4 and its optimized derivative JM#21 in PDAC cell lines. We addressed the peptide stability by encapsulating JM#21 into mesoporous silica nanoparticles (MSNs) designed for improved half-life and sustained release under physiological conditions. BMI1 was confirmed as a critical mediator of CXCL12/CXCR4-driven stemness and EMT. Knockdown of CXCR4 or BMI1 significantly impaired miCSC maintenance and migration towards CXCL12. Both EPI-X4 and JM#21 potently inhibited CXCL12-mediated signaling, reduced EMT and stemness markers, and suppressed miCSC migratory potential. JM#21 displayed superior efficacy and re-sensitized previously resistant PDAC cell lines to gemcitabine and paclitaxel. Functional assays demonstrated that nanoparticle-loaded JM#21 more effectively suppressed EMT markers and self-renewal than the free peptide, highlighting the advantage of nanoparticle delivery in therapeutic applications. Given their biocompatibility and modularity, silica nanoparticles offer a promising platform for stabilizing peptide drugs. Our findings reveal that tumor-stroma crosstalk via the CXCL12/CXCR4/BMI1 axis plays a central role in sustaining miCSC-driven metastasis and therapy resistance in PDAC. Targeting this signaling pathway with nanoparticle-stabilized JM#21 represents a novel and clinically promising therapeutic strategy to disrupt PDAC progression and improve the efficacy of existing combination treatments. - Source: PubMed
Publication date: 2026/04/16
Tiwary KanishkaLahusen AntonInaas SyedaBeitzinger BastianSchmid RomanHarms MirjaHauff StefanieArnold FrankWalter KarolinAlcala SoniaHahn StephanHeßmann ElisabethKleger AlexanderAzoitei NinelSeufferlein ThomasSainz BrunoMünch JanLindén MikaHermann Patrick C