Mouse Dickkopf 1,DKK1 ELISA Kit
- Known as:
- Mouse Dickkopf 1,DKK1 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- E0948Mo
- Product Quantity:
- 48T
- Category:
- Elisa Kits
- Supplier:
- Sunlog
- Gene target:
- Mouse Dickkopf 1 DKK1 ELISA Kit
Related genes to: Mouse Dickkopf 1,DKK1 ELISA Kit
- Gene:
- DKK1 NIH gene
- Name:
- dickkopf WNT signaling pathway inhibitor 1
- Previous symbol:
- -
- Synonyms:
- SK, DKK-1
- Chromosome:
- 10q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2000-09-01
- Date modifiied:
- 2018-06-28
Related products to: Mouse Dickkopf 1,DKK1 ELISA Kit
Related articles to: Mouse Dickkopf 1,DKK1 ELISA Kit
- Osteosarcoma (OS) is an aggressive primary bone malignancy that predominantly affects children and adolescents. Although surgery and chemotherapy have improved survival, therapeutic progress has remained limited over recent decades. Aberrant fatty acid metabolism has been increasingly implicated in OS progression, yet its distribution across different cellular compartments of the tumor microenvironment remains unclear. In this study, we integrated single-cell RNA-sequencing data from 140,562 cells across 17 OS patients and characterized the metabolic heterogeneity of tumor microenvironment. Two fatty acid metabolism-associated populations were identified: IBSP+ malignant osteosarcoma cells and SPARC+ macrophages. IBSP+ malignant cells showed preferential activation of fatty acid degradation and occupied an intermediate state along the pseudo-time trajectory. Lipid uptake and cholesterol efflux programs reached their highest activity near this state, indicating substantial lipid metabolic remodeling along the inferred transition among malignant-cell states. By contrast, SPARC macrophages exhibited a lipid-adapted, immunosuppressive phenotype accompanied by elevated fatty acid degradation activity. Cell-cell communication analysis further identified IBSP malignant cells as a major source of APOE- and SPP1-related signals directed toward SPARC+ macrophages, suggesting coordinated metabolic communication between these populations. To evaluate its clinical relevance, we applied transcriptomic deconvolution to independent OS cohorts. Concurrent enrichment of IBSP+ malignant cells and SPARC+ macrophages was associated with significantly shorter overall survival. Comparison of the double-high and double-low groups subsequently identified DKK1 as a candidate effector linked to this adverse metabolic niche. Consistent with this observation, DKK1 silencing in MG-63 cells reduced proliferation, colony formation, migration, and invasion. Collectively, these findings characterize fatty acid metabolism-associated cellular heterogeneity and a clinically relevant association between IBSP malignant cells and SPARC macrophages in OS, while identifying DKK1 as a candidate prognostic and therapeutic factor associated with the double-high phenotype. - Source: PubMed
Publication date: 2026/09/07
Wang LifangGao MeiyanLiang Zhizhong - Osteoporosis is characterized by reduced bone mineral density (BMD) and an increased risk of fractures, but the relationships between plasma proteins and site-specific BMD phenotypes remain unclear. We aimed to investigate the potential causal associations of plasma proteins on BMD using a Mendelian randomization (MR). - Source: PubMed
Publication date: 2026/09/21
Lv KuiFang JialiuWang ShengyouXing XingZhu Rui - Immune checkpoint blockade has transformed treatment in selected gastrointestinal (GI) cancers, yet primary resistance, incomplete responses and acquired resistance remain common. This heterogeneity is not explained by tumour-cell genomics alone; extracellular signalling programmes within the tumour microenvironment can determine immune recruitment, access and adaptation to therapy. The tumour secretome-including cytokines, chemokines, growth factors, complement components, matricellular proteins, soluble checkpoint molecules and extracellular-vesicle-associated cargo-regulates immune-cell recruitment, exclusion, suppression, tertiary lymphoid structure formation and exhaustion across anatomical and molecular contexts. Across gastric and esophageal cancers, colorectal cancer, pancreatic ductal adenocarcinoma, hepatocellular carcinoma and biliary tract cancers, recurrent suppressive circuits include TGF-β, VEGF, CXCL12-CXCR4, CXCL8/IL-8-CXCR1/2, CCL2-CCR2, CSF1-CSF1R, IL-6-family cytokines, SPP1/osteopontin, periostin, galectins, DKK1, MIF, complement and soluble or vesicular PD-L1. Conversely, CXCL9/10/11-CXCR3 signalling and CXCL13-associated tertiary lymphoid structures characterise immune-permissive states that can support checkpoint responsiveness. We organise these circuits into four overlapping functional modules-myeloid-enriched, fibroblast-driven exclusion, angiogenic-immunosuppressive and immune-permissive-and apply a four-level evidence hierarchy that separates clinical validation from mechanistic inference. Clinically useful secretome biomarkers will therefore need to integrate cellular source, spatial localisation, receptor context, temporal dynamics and linkage to actionable immune-state transitions. - Source: PubMed
Publication date: 2026/09/11
Li KexunQian ZilongMao JieHan YongtaoLeng Xuefeng - Osteoporosis remains a major global health challenge, and current single-pathway therapies often fail to achieve coordinated bone remodeling. Dickkopf-1 (DKK-1) is a potent inhibitor of the Wnt/β-catenin signaling pathway and plays a critical role in osteoporotic bone loss. Neutralization of DKK-1 represents a promising therapeutic strategy to promote bone formation while simultaneously inhibiting bone resorption. - Source: PubMed
Publication date: 2026/08/27
Hou ShengGao TianyuWu YimeiWang HaoZhang DapengGuo QingchengXu JinGuo HuaizuQian Weizhu - Oral squamous cell carcinoma (OSCC) is a malignant tumor arising from the oral mucosa and is highly prevalent in Southeast Asia and the Pacific region. Recurrence and metastasis significantly contribute to poor clinical outcomes, highlighting the importance of understanding the underlying molecular mechanisms. Circular RNAs (circRNAs), a class of covalently closed non-coding RNAs, have emerged as key regulators of tumor development and progression. However, their roles in OSCC remain largely unexplored. In this study, we identified for the first time that circRHBDD1(4,5) (hsa_circ_0058493, a 656-nt circRNA generated by back-splicing of exons 4 and 5 of the RHBDD1 gene) is markedly upregulated in OSCC and promotes tumor cell proliferation, invasion, and metastasis. Mechanistically, circRHBDD1(4,5) functions as a molecular scaffold that brings IGF2BP2 and DKK1 mRNA into close proximity, thereby facilitating the mA-dependent recognition of DKK1 mRNA by IGF2BP2, which is mediated by WTAP. This interaction enhances DKK1 mRNA stability, leading to increased DKK1 expression and subsequent activation of the PI3K-AKT signaling pathway, thereby driving the malignant progression in OSCC. Collectively, our findings highlight the critical role of the circRHBDD1(4,5)/IGF2BP2/DKK1 axis in OSCC pathogenesis and provide a potential foundation for developing novel targeted therapeutic strategies. - Source: PubMed
Publication date: 2026/09/11
Ren DaixiZhang JiarongHuang MaoWu JieYang MeiLiu YixuanXiang PingjuanQu HongkeWang DanGe JunshangYan QijiaShi LeiXiang BoXiong WeiLi GuiyuanFan ChunmeiZeng Zhaoyang