CXCL12 _ SDF1
- Known as:
- CXCL12 _ SDF1
- Catalog number:
- NB120-10395
- Product Quantity:
- 0.025 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
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- 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 - Nao-Xin-Tong Capsule (NXT), a modern formulation derived from the classical qi-invigorating and blood-activating prescription Buyang Huanwu Decoction, has been clinically applied for ischemic stroke (IS) management over three decades with established safety. Its multi-component composition targets the core pathogenesis of cerebral no-reflow phenomenon-qi deficiency and blood stasis-by restoring microcirculatory perfusion. - Source: PubMed
Publication date: 2026/04/24
Shang JinfengWei WantingWang BohongWei RanCui YiranWang JingjuanLiu Xin - Leukaemic stem cells (LSCs) reside in protective bone marrow (BM) niches that promote therapeutic resistance and relapse. Here we characterized longitudinal BM niches supporting LSC survival, distinguishing the metaphysis from the central marrow. Quiescent LSCs preferentially localized to the metaphysis and exhibited reduced stemness and aggressiveness upon mobilization to the central marrow. Targeting DPP4 in acute myeloid leukaemia (AML) cells altered CXCL12 gradients at three spatial scales. Systemically, reversal of the BM-peripheral blood CXCL12 gradient confined AML cells within the BM. At the BM level, disruption of the metaphysis-central marrow gradient displaced LSCs from their protective niche. At the microscale, loss of the CXCL12 gradient between N-cadherin stromal cells and the surrounding matrix impaired LSC recruitment. These effects arise from the CXCL12-DPP4-GPC3 axis, in which DPP4 truncates and inactivates CXCL12, whereas stromal GPC3 restrains DPP4 activity. Modulating this axis disrupts niche protection and enhances therapeutic vulnerability in AML. - Source: PubMed
Publication date: 2026/04/24
Wang ChenPan YiDong RuochenZhou WenxuanMeng XiaduoKang XiNistala RaviHammer Richard DLi LinhengKang XunLei - A significant population of chronic stroke patients urgently requires more effective therapies because of functional plateaus and limited intervention options. Intermittent theta-burst stimulation (iTBS) has been increasingly adopted in chronic-phase ischemic stroke management. However, the efficacy decreases over time. Mesenchymal stem cells (MSCs) have emerged as a promising therapeutic strategy for chronic stroke management through multiple mechanisms. Whether combined MSC transplantation and iTBS confers superior synergistic efficacy warrants further investigation. In this study, human umbilical cord-derived MSCs were stereotactically injected into the penumbra of the brain parenchyma adjacent to infarct sites in cynomolgus monkeys with chronic-stage middle cerebral artery occlusion (MCAO)-induced ischemic stroke. iTBS commenced at 1 week post-transplantation (5 sessions/week until week 17). Behavioral tests, electrophysiological recordings, functional magnetic resonance imaging (fMRI), magnetic resonance spectroscopy (MRS), and plasma proteomic analysis were conducted longitudinally, with terminal histological and spatial proteomic analysis at week 17. The results indicated that combined MSC/iTBS therapy enhanced motor function, reduced cortical excitation thresholds, shortened motor-evoked potential (MEP) latency, increased neural activity intensity/synchronization, strengthened functional connectivity, and optimized motor cortex metabolism. In addition to the commonly attributed therapeutic mechanisms of MSCs and iTBS, the combined therapy additionally triggered neurogenesis and stem cell chemotaxis, which was potentially mediated by iTBS-enhanced CXCL12 secretion from MSCs. Therefore, MSC/iTBS combination therapy can effectively treat chronic stroke through multiple mechanisms, particularly involving the activation of endogenous neural stem cells (NSCs), representing a promising interdisciplinary treatment strategy. - Source: PubMed
Publication date: 2026/04/24
Ma Yuan-HuanChen Geng-BinWu Man-FengLi GeZhang YuLv Jian-PingWen MinCai LeiZhang Cai-LingJiang Jun-BoZhang KeZhang Ke-JunLiu YingLiu ZhouChen Jia-LinLin TuoWang Li-XinXu Guang-QingZeng XiangLan Yue