CXCL12 _ SDF1
- Known as:
- CXCL12 _ SDF1
- Catalog number:
- GTX10395
- Product Quantity:
- 25 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
- Myelofibrosis (MF) is a myeloproliferative neoplasm characterized by clonal hematopoietic dysregulation, amplification of chronic inflammation, and progressive remodeling of the bone marrow fibrotic niche, clinically manifesting as bone marrow failure, splenomegaly, and systemic inflammatory symptoms. Although Janus kinase (JAK) inhibitors can alleviate symptom burden and reduce spleen size, they have limited capacity to eradicate malignant clones or reverse fibrosis. Allogeneic hematopoietic stem cell transplantation remains the only potentially curative option; however, its application is constrained by advanced age, comorbidities, unavailable donor, and transplant-related risks. Therefore, the development of disease-modifying therapeutic strategies has become a central focus in MF research. Chimeric antigen receptor T (CAR-T)-cell therapy has demonstrated robust efficacy across various hematologic malignancies. Its application in MF holds the potential not only to selectively eliminate malignant hematopoietic clones but also to modulate the immunosuppressive and profibrotic microenvironment through advanced cellular engineering, thereby enabling a dual therapeutic paradigm involving both clonal control and microenvironmental reprogramming. In this context, potential targets and pathways include CD123, myeloproliferative leukemia protein (MPL), fibroblast activation protein (FAP), the TGF-β signaling axis, the CXCR4-CXCL12 niche-regulatory axis, and molecules associated with myeloid-derived suppressor cells (MDSCs) and tumor-associated macrophages (TAMs). Future strategies may optimize both efficacy and safety through combinatorial approaches, including integration with JAK inhibitors, development of armored CAR-T constructs, and bridging to hematopoietic stem cell transplantation. Collectively, CAR-T-cell therapy offers a promising avenue for shifting MF management from symptomatic control toward true disease modification. - Source: PubMed
Publication date: 2026/05/06
Kong LuluFu ChunlingSong LiangguiWang WenxiaoJi MengchuLi FeiShi XiaofengChen Wei - Chronic pain, a complex multidimensional disorder, remains a major healthcare issue and a therapeutic challenge. Neuropathic pain is a chronic pain condition that results from damage or dysfunction in the nervous system. While mechanisms of neuropathic pain at the peripheral and spinal cord level have been extensively studied, pain mechanisms in the brain remain underexplored. The amygdala, a limbic brain region, has emerged as a critical brain area for the emotional-affective dimension of pain and pain modulation. Amygdala neuroplasticity has been associated with pain states, but the exact molecular and cellular mechanisms underlying these states and the transition from acute to chronic pain are not well understood. Here, we used the spinal nerve ligation (SNL) model of neuropathic pain in male rats to investigate changes in gene expression in the amygdala at the chronic pain stage using RNA sequencing (RNA-Seq). Two amygdala nuclei, the basolateral (BLA) and central (CeA), were investigated in a hemisphere-dependent manner. We used an integrative approach that focuses on functional significance and cell-type specificity of differentially expressed genes (DEGs) to nominate mechanistic targets for central regulation of chronic pain. Our integrative transcriptomic and bioinformatic analyses identified individual genes (e.g., , , , , , , , , and ), molecular pathways (e.g., cytokine-mediated signaling pathway), biological processes (e.g., myelination, synaptic transmission), and specific cell types (e.g., oligodendrocytes, glutamatergic, and GABAergic neurons) affected by chronic pain. Our results also provide some evidence for the emerging concept of hemispheric lateralization of pain processing in the amygdala. Overall, our study proposes oligodendrocyte dysfunction in the amygdala, neuroimmune signaling in the CeA, and glutamatergic neurotransmission in the BLA as key processes and potential therapeutic targets for the management of chronic neuropathic pain. - Source: PubMed
Publication date: 2026/04/25
Presto PeytonCardenas JulianBustamante ChristianKisby Brent RJi GuangchenPonomareva OlgaNeugebauer VolkerPonomarev Igor - Chemokines and their cognate receptors are central orchestrators of the immune response to Mycobacterium tuberculosis (Mtb) infection. While their overall significance in tuberculosis (TB) is well-established, this review synthesizes recent advances to clarify the distinct roles of CC and CXC chemokines in differentiating active disease, latent infection, and the often overlooked subclinical TB state. We evaluate the potential of specific chemokine signatures as emerging diagnostic biomarkers compared to conventional standards and assess their promise as novel therapeutic targets in personalized clinical settings. Furthermore, we examine paradoxical findings in the field, including how certain chemokines (such as CCL5, CXCL12, and CXCL16) can simultaneously support host defense and facilitate pathogen evasion. By integrating these complex narratives, we offer a renewed perspective on chemokine dynamics in TB immunity, bridge important gaps between bench research and clinical application, and establish a strong foundation for developing precision diagnostics and host-directed therapies. - Source: PubMed
Publication date: 2026/05/12
Yin XuyingXiao DangshengYang Jiezuan - HIV-1 entry into susceptible cells requires the dynamic interaction of its envelope (Env) glycoprotein with the host cell receptor CD4 and a co-receptor, either CCR5 or CXCR4. While the core molecular mechanisms driving Env-receptor interactions and subsequent membrane fusion are well characterized, the precise nanoscale spatial reorganization of these co-receptors at the viral binding site remains poorly defined. In this study, we employed single-particle tracking total internal reflection fluorescence (SPT-TIRF) microscopy to quantitatively analyze nanoscale organizational changes of CXCR4 on the surface of human CD4 T cells following binding by X4-tropic HIV-1. Our data reveal that both recombinant X4-gp120 and virus-like particles expressing physiological levels of X4 Env proteins (gp120 and gp41) promote CXCR4 clustering, a phenomenon linked to cell infection. Furthermore, these ligands induced oligomerization of CXCR4, a naturally occurring mutant associated with WHIM syndrome that supports HIV-1 infection, but fails to oligomerize in response to CXCL12. Our findings establish a link between CXCR4 clustering and HIV-1 infection, enhancing our understanding of the initial events in viral attachment and entry. These results further suggest that HIV-1 depends on a specific spatial arrangement of co-receptors, distinct from that induced by their natural chemokine ligands, highlighting the critical role of cell-surface receptor spatial organization in dictating cellular function. - Source: PubMed
Publication date: 2026/05/12
Quijada-Freire AdrianaSantiago César AGarcía-Cuesta Eva MSoler Palacios BlancaAyala-Bueno RosaGardeta Sofia RSan Sebastian EnaraArmendariz-Burgoa EvaPuertas Maria CarmenVillares RicardoGaraigorta UrtziGonzález-Granado Luis IgnacioRodriguez Frade Jose MiguelChojnacki JakubMartinez-Picado JavierMellado Mario - 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