Ask about this productRelated genes to: DKK1 protein
- 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 protein
Related articles to: DKK1 protein
- Mandibular reconstruction presents substantial clinical challenges due to the jaw's complex anatomical and functional requirements. This study investigated gene expression differences between tibial and mandibular periosteum to understand their distinct osteogenic properties and evaluate the therapeutic potential of tibial periosteum-derived stem cell (PSC) sheets for mandibular defect repair.Transcriptomic analysis revealed differential expression patterns: tibial periosteum demonstrated higher OPG expression, while mandibular periosteum exhibited increased RUNX2 and BMP-2 expression. KEGG enrichment analysis identified the Wnt signaling pathway as a key regulatory mechanism. To test this therapeutic approach, we cultured rat tibial PSCs into cell sheets and implanted them into mandibular defects, then assessed bone regeneration through micro-CT, histological examination, and immunohistochemistry.The results demonstrated that tibial PSC sheet implantation significantly enhanced bone volume, trabecular thickness, collagen deposition, and expression of osteogenic markers in mandibular defects. Notably, inhibition of Wnt signaling through DKK1 markedly suppressed mineralization and osteogenesis, confirming this pathway's critical role in the regenerative process.These findings establish that tibial PSC sheets promote mandibular bone repair through dual mechanisms: Wnt-mediated osteogenesis and OPG-driven anti-resorption activity. This combination provides sustained bone regeneration and represents a promising therapeutic strategy for mandibular reconstruction, demonstrating the feasibility of utilizing tibial periosteum-derived cells to overcome the inherent limitations of mandibular periosteum in bone repair applications. - Source: PubMed
Publication date: 2026/04/23
Huang LiangchongXie RongjuPu JiantongShao ShengjieWang Weihong - Rheumatoid arthritis (RA) is characterized by synovial inflammation leading to joint damage, periarticular bone loss, and systemic osteoporosis. While inflammation is a primary driver of structural damage, dysregulation of the Wnt signaling pathway, particularly through inhibitors such as Dickkopf-1 (Dkk1) and sclerostin, has been implicated in RA-associated bone loss. - Source: PubMed
Publication date: 2026/04/20
Pollastri FrancescoViapiana OmbrettaGatti DavideFassio AngeloBenini CamillaDartizio CarmelaGalvagni IsottaMessina ValeriaRossini MaurizioAdami Giovanni - Parathyroid hormone 1 receptor (PTH1R) signaling is critical for mineral ion homeostasis and skeletal development. Although its role in tooth root formation and eruption is established, its specific functions in adult periodontal tissues and craniofacial integrity remain incompletely defined. Here, we investigated the craniofacial and dentoalveolar phenotypes of mice with conditional deletion of PTH1R in DMP1-Cre-expressing cells. DMP1-Cre;PTH1R mutant mice exhibited craniofacial alterations, including reduced maxillary length and defects in the alveolar bone surrounding the molars, as revealed by micro-computed tomography and histological analysis. The mutant mice also displayed severe periodontal ligament (PDL) loss and extensive molar ankylosis, characterized by the direct fusion of alveolar bone to tooth roots, predominantly in regions of acellular cementum. In contrast, incisor development remained unaffected. PTH1R deficiency also resulted in pathological cementum overgrowth, disrupted PDL fiber organization, and decreased expression of key PDL matrix proteins, as evidenced by immunohistochemical and molecular analyses. Mechanistically, the loss of PTH1R enhanced Smad3 phosphorylation and upregulated Osterix, thereby promoting aberrant cementoblast differentiation and mineralization. Concurrently, Dkk1 expression was increased, leading to suppressed Wnt signaling. This evidence establishes PTH1R signaling in cementocytes as a central safeguard of cementum homeostasis and PDL integrity and demonstrates that its disruption induces pathological root-bone fusion and craniofacial abnormalities. These findings advance our understanding of the molecular mechanisms underlying adult periodontal tissue maintenance and open new opportunities for developing therapeutic strategies against ankylosis and related disorders by targeting PTH1R signaling. - Source: PubMed
Publication date: 2026/04/27
Turkkahraman HakanWalton Carson JosephZhu TianliAkel NisreenMarino SilviaYuan XueBellido Teresita M - Inflammation critically determines dental pulp regenerative outcomes, with dental pulp stem cells (DPSCs) orchestrating tissue homeostasis through differentiation, self-renewal and immunomodulation processes dynamically regulated by Wnt/β-catenin and NF-κB signaling crosstalk. Given the rising therapeutic potential of Wnt-targeted interventions in dental tissue engineering, elucidating these molecular interactions under pathological conditions is essential for developing regenerative therapeutics capable of simultaneously promoting reparative dentinogenesis while resolving inflammatory insults. - Source: PubMed
Publication date: 2026/04/24
Rajasekar VHuang MAbdalla M MNeelakantan PYiu C K Y - Recent advances in organ-on-a-chip (OOC) blood-brain barrier (BBB) models for oncology research have revealed key insights into the metastatic cascade. However, in most 3D BBB systems, type I collagen is commonly selected as the brain-side extracellular matrix (ECM) due to its ease of use and affordability. This selection overlooks the native ECM composition of the brain, which is primarily composed of hyaluronan/hyaluronic acid (HyA). Given that the ECM occupies approximately 20% of the brain volume and actively modulates tumor progression, substrate selection is an important yet frequently under-examined component in 3D BBB systems. Using our published blood-brain barrier niche (BBN), we compared HyA and type I collagen matrices to evaluate their impact on cancer cell phenotypes and the tumor microenvironment (TME) to establish which substrate affords the greatest versatility across different lines of investigation. Using a TA DHR-3 rheometer, we examined biophysical variations of these matrices in response to oscillatory shear. We then assessed phenotypic and migratory differences in human breast cancer cells, and their brain-seeking subclones in an ECM of HyA with media versus type I collagen, within our BBN device. Finally, ELISA analysis revealed significant matrix-dependent impact on key chemokine alterations, with collagen matrices promoting CXCL5 and DKK1 secretion across all conditions relative to HyA. We conclude that ECM selection to mimic the patient's brain microenvironment in OOC systems is a critical decision due to inherent substrate differences and either can be appropriate depending on the study goals. - Source: PubMed
Publication date: 2026/04/15
Dabaja Ali AHoque Apu EhsanulZhao VictorManimaran SivaniSlayton Mark DLi HuilingSerhan HabibBao LiweiMorikawa AkiLowenstein Pedro RCastro Maria GMerajver Sofia DOliver Christopher Ryan