Ask about this productRelated genes to: DKK1 antibody
- 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: DKK1 antibody
Related articles to: DKK1 antibody
- : Thyroid hormones influence bone metabolism, and autoimmune thyroid diseases may further impact skeletal homeostasis. Wnt signaling inhibitors, including Dickkopf-1 (DKK-1) and sclerostin (SOST), as well as osteoprotegerin (OPG), play key roles in regulating bone formation and resorption. This study aimed to evaluate circulating DKK-1, SOST, and OPG in women with newly diagnosed overt thyroid dysfunction. : This cross-sectional study included 62 women with newly diagnosed, untreated overt thyroid dysfunction (35 hypothyroid and 27 hyperthyroid) and 33 age- and BMI-matched healthy controls. Serum levels of DKK-1, sclerostin, and OPG were measured using ELISA. Thyroid function and autoantibodies were assessed using automated immunoassays. Correlation analysis was performed to evaluate associations between variables. : Serum DKK-1 levels were significantly elevated in both hypothyroid and hyperthyroid women compared with controls ( < 0.001). Sclerostin levels showed a non-significant trend toward higher values. OPG levels were significantly increased in hyperthyroid patients and moderately elevated in hypothyroid patients. Significant positive correlations were observed between OPG and FT3 (r = 0.42, = 0.001) and FT4 (r = 0.43, = 0.001). In hypothyroid patients, OPG correlated positively with TgAb (r = 0.46, = 0.007). A strong positive correlation was found between DKK-1 and SOST ( < 0.001), while DKK-1 was negatively associated with age ( < 0.05). : Overt thyroid dysfunction is associated with significant alterations in circulating Wnt signaling inhibitors and OPG. These findings suggest a potential role of Wnt signaling and immune-bone interactions in thyroid-related changes in bone metabolism. - Source: PubMed
Publication date: 2026/04/30
Miteva Mariya ZhivkovaOrbetzova Maria MitkovaNonchev Boyan IvanovDavcheva Delyana MitevaGigov Kostadin - Head and Neck Squamous Cell Carcinoma (HNSCC) diagnosis remains a challenge for clinicians, with human papillomavirus (HPV) status long associated with HNSCC prognosis and response to therapy. Small non-coding molecules, such as microRNAs (miRNAs), significantly alter gene expression, particularly of immune-modulatory genes. In the current study, an effort to map the interaction patterns between miRNAs and their target genes was carried out using diverse computational tools. A microarray-based study was retrieved and analysed using GEO2R to identify ubiquitously expressed miRNAs in HPV-associated HNSCC samples, with HPV-negative samples used as controls. Seven miRNAs were identified, namely hsa-miR-150-5p, hsa-miR-142-5p, hsa-miR-142-3p, hsa-miR-1-3p, hsa-miR-133b, hsa-miR-206, and hsa-miR-1260b. Functional annotation using miRNet identified numerous significant signalling pathways dysregulated by the aforementioned miRNAs. miRDB was used to map miRNA target genes, which were visualised in Cytoscape; among these, key immune-modulatory genes were analysed in a comprehensive meta-analysis. Furthermore, the GEPIA2 tool was used to perform survival analysis and generate Kaplan-Meier plots correlating survival percentages in HNSCC patients with gene expression patterns. The viral infectious cycle was dysregulated by miR-1260b expression. DKK1, STC2, SPOCK1, and TP53 were among the genes whose aberrant expression was associated with a significant reduction in survival in HNSCC-affected individuals. This report elucidates the pivotal role of miRNAs in modulating the expression of key immune-modulatory genes, thereby influencing the prognosis of HNSCC and HPV infection. - Source: PubMed
Publication date: 2026/03/31
Datta AnkurMuthu Meenakshi MDaniels SusannaVarshaa BC George Priya Doss - Alveolar bone defects following tooth extraction in severe periodontitis pose significant clinical challenges. This study evaluates the synergistic osteogenic effect of Er, Cr: YSGG laser combined with guided bone regeneration (GBR) in rat extraction sockets and explores the underlying Wnt/β-catenin pathway mechanism. Fifty Sprague-Dawley rats were randomized into five groups (n = 10/group): Control (extraction only), Laser (Er, Cr: YSGG laser irradiation only), GBR (Bio-Oss bone graft + barrier membrane), Laser+Bone Graft (laser irradiation + Bio-Oss without membrane), and Laser + GBR (laser irradiation + Bio-Oss + barrier membrane). At 4 and 8 weeks post-operation, CBCT quantified bone volume fraction (BV/TV) and bone mineral density (BMD). Histological staining was used to evaluate new bone formation. ELISA and qPCR analyzed osteogenic markers (β-catenin, Runx2, BMP-2) and the Wnt pathway inhibitor (DKK-1). MSD assays quantified β-catenin nuclear translocation and the p-GSK-3β/GSK-3β ratio to assess pathway activation. The Laser + GBR group demonstrated the highest BV/TV and BMD at 8 weeks, with complete scaffold degradation, dense trabeculae, and minimal inflammatory infiltration on histology. ELISA and qPCR confirmed the highest expression of β-catenin, Runx2, and BMP-2 alongside the lowest DKK-1 levels in this group at both time points. MSD detection revealed the highest β-catenin nuclear translocation rate and the lowest p-GSK-3β/GSK-3β ratio, indicating robust Wnt/β-catenin pathway activation. Er, Cr: YSGG laser synergizes with GBR to enhance alveolar bone regeneration, likely by suppressing DKK-1, inhibiting GSK-3β activity, and promoting β-catenin nuclear translocation, thereby activating the Wnt/β-catenin pathway and upregulating downstream osteogenic genes. This combination represents a promising strategy for post-extraction bone defect repair.Clinical Trial Number: Not applicable. - Source: PubMed
Publication date: 2026/05/23
Guo YanweiWang YongmanZhang GuangdeKong LingbinYang Shimao - Following the publication of the above article, a concerned reader drew to the authors' attention that the immunohistochemical data shown for the 'Collagen I/Control' panel in Fig. 5B on p. 1104, and the 'β‑catenin/DKK' panel for the immunofluorescence data shown in Fig. 7B on p. 1106, subsequently appeared in a pair of later publications by the same research group. In addition, in Fig. 5B, the 'Vimentin/ALI' and 'Vimentin/ALI+MSC‑GFP' data panels were found to contain an overlapping section, such that data which were intended to show the results of differently performed experiments had apparently been derived from the same original source. Furthermore, upon performing an independent analysis of the data in this paper in the Editorial Office, it also came to light that the 'α‑SMA/ALI+MSC‑CXCR4' data panel in Fig. 5B had subsequently reappeared in an article by the same research group; the Control panel for the 'MSC (GFP+)' experiment in Fig. 3A on p. 1102 was matching with the Control panel shown in Fig. 6A on p. 1105; certain of the β‑actin and MMP2 protein bands shown for the ALI+MSC‑CXCR4 and ALI+MSC‑GFP experiments in Fig. 7A appeared to be identical in the two sets of western gels; and finally, in Fig. 5A, two sets of data [namely, the data for the IL‑6 and TNF‑α blots for the ALI+MSC‑GFP experiments (central panel of blots), and the pair of Con and 3d 18S blots for the ALI experiments and the 7d and 14d 18S blots for the ALI+MSC‑GFP experiments], bore strikingly resemblances to each other. On re‑examining their original data, the authors realized that they had inadvertently included some of the data incorrectly in Figs. 5, 6 and 7. The revised versions of these three figures, now featuring the correct data for Fig. 5A (the PCR analysis results of TNF‑α and 18S in the ALI+MSC‑GFP group), Fig. 5B (vimentin antibody immunohistochemical staining of the ALI+MSC‑GFP group, α‑SMA antibody immunohistochemical staining of the ALI+MSC‑CXCR4 group, and Collagen Ⅰ antibody immunohistochemical staining of the Control group); Fig. 6A (α‑SMA immunofluorescence staining), Fig. 6C (IgG immunofluorescence staining), Fig. 7A (western blotting results of β‑catenin in the ALI group, MMP2 and β‑actin in the ALI+MSC‑CXCR4 group, and MMP2 and β‑actin in the ALI+MSC‑GFP group) and Fig. 7B (β‑catenin antibody immunofluorescence staining of the DKK1 group), are shown on the subsequent three pages. The image duplications were caused by accidental mix‑up of the files during figure sorting and final manuscript preparation. The authors regret that they did not perform more rigorous cross‑checking of the figures before submission. The corrected figures are consistent with the original experimental data; moreover, there are now no overlaps with any of the group's previously published work, Notably, the overall experimental results and scientific conclusions of the article remain entirely unchanged following the correction of these figures. All the authors agree with the publication of this corrigendum, and they are grateful to the Editor of for granting them the opportunity to publish this; furthermore, they apologize to the readership for any inconvenience caused. [International Journal of Molecular Medicine 33: 1097‑1109, 2014; DOI: 10.3892/ijmm.2014.1672]. - Source: PubMed
Publication date: 2026/05/22
Sun ZhaoruiWang CongShi ChaowenSun FangfangXu XiaomengQian WeipingNie ShinanHan Xiaodong - Spondyloarthritis (SpA) comprises a heterogeneous group of chronic inflammatory rheumatic diseases affecting the axial skeleton, peripheral joints, and entheses. It is uniquely characterized by the coexistence of inflammation and pathological new bone formation, ultimately leading to ankylosis. Although the precise pathogenic sequence remains incompletely defined, experimental animal models have provided essential mechanistic insights by reproducing key immunological and structural features of the disease. This narrative review synthesizes current knowledge on SpA pathophysiology derived from these models. Rodent models have demonstrated the central role of the IL-23/IL-17 axis. The HLA-B27 transgenic rat and the SKG mouse illustrate how dysregulated type 3 immunity, often amplified by intestinal dysbiosis, drives sustained entheseal inflammation. Non-HLA-B27 inflammatory models, such as proteoglycan-induced arthritis and spontaneous arthritis in DBA/1 mice, have clarified the contribution of osteogenic pathways, particularly Wnt and BMP/TGF-β signaling, in the transition from inflammation to pathological bone formation. Other models highlight the continuum between inflammatory, destructive, and anabolic processes. In transmembrane TNF transgenic mice, severe ossification occurs independently of major erosions. The TNF^ΔARE (TNFTg197) model has been instrumental in establishing a mechanistic link between impaired Wnt inhibition and ankylosis, as pharmacological blockade of Dkk-1 shifts the phenotype from erosive sacroiliitis to complete joint fusion. Together, these models have elucidated the interplay between immune activation, the microbiota, and osteogenic pathways in SpA. They remain indispensable for mechanistic research and therapeutic development and are increasingly integrated with OMICS-based approaches. - Source: PubMed
Publication date: 2026/05/14
Hilliquin StéphaneRosine NicolasLories RikMiceli-Richard Corinne