Human Polyclonal DKK1 Ab
- Known as:
- Human Polyclonal DKK1 Antibody
- Catalog number:
- a0567
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- ABclonal
- Gene target:
- Human Polyclonal DKK1
Related genes to: Human Polyclonal DKK1 Ab
- 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: Human Polyclonal DKK1 Ab
Related articles to: Human Polyclonal DKK1 Ab
- Pediatric B-cell acute lymphoblastic leukemia (B-ALL) is molecularly heterogeneous and influenced by the bone marrow microenvironment. Mesenchymal stromal cells (MSCs) provide critical niche signals, yet their transcriptomic remodeling in B-ALL is poorly defined. This study aims to define a compact gene signature that complements blast-centric diagnostics. - Source: PubMed
Publication date: 2026/06/26
Huang Zi-YiLi YunLuo RuiHan JuanQu PingYin Tian-TianCheng Yi-RenWang Jing-XuanFang KunZhou Fen - Combustion of composite solid propellants generates complex aerosols containing metallic nanoparticles (NPs) and acidic gases, raising concerns about inhalation toxicity. Here, we investigated the effects of alumina (Al₂O₃) NPs, alone or combined with hydrochloric acid (HCl), in a human alveolar-capillary barrier (ACB) model exposed at the air-liquid interface. The model consisted of hAELVi alveolar epithelial cells co-cultured with HPMEC-ST1.6 R pulmonary microvascular endothelial cells and exposed using a Vitrocell Cloud system under acute or repeated scenarios. Deposited Al₂O₃ NPs doses corresponding to low-to-high alveolar exposure scenarios were 0.007, 1.35 ± 0.1 and 2.3 ± 0.2 µg/cm², with or without HCl at 1.37 mM. Barrier integrity, viability, inflammatory and remodeling mediators, oxidative stress and DNA damage were assessed 24 h after the final exposure. The co-culture formed a tight functional barrier with high transepithelial electrical resistance, low permeability and organized junctional protein expression. Acute exposure to the highest Al₂O₃ NPs dose induced a compartment-specific inflammation-related response, based on the biomarkers investigated, with increased IL-1α, IL-8, IL-1β, CCL2, DKK1 and angiogenin, without cytotoxicity or barrier disruption. Repeated exposure shifted the response toward moderate cytotoxicity at the highest dose, with viability decreasing to 77% for Al₂O₃ NPs alone and 66% for Al₂O₃ NPs with HCl, while permeability remained unchanged. No significant oxidative stress or γ-H2AX-associated DNA damage was detected. HCl co-exposure did not enhance Al₂O₃ NPs toxicity. However, because HCl was administered in dissolved form prior to nebulization, the contribution of potential gas-particle interactions occurring in combustion plumes could not be evaluated and the results should not be interpreted as evidence for or against synergistic effects arising from gas-particle interactions occurring in combustion plumes. These findings show that exposure pattern critically shapes alveolar-capillary responses, supporting human air-liquid interface co-culture models for mechanistic inhalation toxicology. - Source: PubMed
Publication date: 2026/07/09
Cherriere MDe Araujo SOger MRival BFloreani MLe Coz CBarbier GValente MLacroix GFrançois SLoret TDekali S - Head and neck squamous cell carcinoma (HNSCC) is a common malignancy with high morbidity and mortality. Despite advances in immunotherapy, including the advent of immune checkpoint inhibitors (ICIs) targeting programmed cell death protein 1 (PD-1)/programmed cell death ligand 1 (PD-L1), only a subset of patients achieves significant benefit. This study aimed to evaluate the prognostic significance of Dickkopf-related protein 1 (DKK1), a potential modulator of the tumor immune microenvironment (TME), and to assess the therapeutic impact of combining DKK1 inhibition with ICIs. - Source: PubMed
Wang FeiYan MinzhuDong XuelinZhang ZhijunDong PinChen Xinwei - Periodontitis is traditionally regarded as an oral biofilm-driven inflammatory disease that leads to progressive loss of the tooth-supporting alveolar bone. However, accumulating evidence indicates that periodontal bone loss is more accurately understood as a state of pathological uncoupling of bone remodeling, in which exaggerated bone resorption coexists with inadequate bone formation response. In this review, we reposition periodontitis within the broader context of inflammatory skeletal diseases and synthesize current mechanistic insights from osteoimmunology, bone biology, and mechanobiology. We discuss how excessive osteoclastogenesis in periodontitis is sustained by receptor activator of nuclear factor kappa-B ligand (RANKL) dominance derived from osteocytes, osteoblast-lineage cells, stromal cells, monocytes/macrophages, B and T lymphocytes, and neutrophils within a cytokine-rich microenvironment characterized by tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and IL-17A signaling. Persistent activation of nuclear factor kappa-B (NF-κB) and mitogen-activated protein kinase (MAPK) pathways further enhance osteoclast differentiation, survival, and resorptive activity. At the same time, inflammatory mediators actively suppress osteoblast-lineage commitment by inhibiting Runx2 and Osterix, antagonizing canonical Wnt/β-catenin signaling through the upregulation of sclerostin and Dickkopf-1 (DKK1), and impairing bone matrix production and mineralization. We further examine how disruption of key osteoclast-osteoblast coupling mechanisms, including ephrinB2/EphB4 and semaphorin signaling, prevents the effective transition from resorption to formation, while osteocyte dysfunction amplifies the uncoupled phenotype by integrating inflammatory and mechanical signals. Comparisons with rheumatoid arthritis, inflammatory bowel disease-associated bone loss, and peri-implantitis reveal shared immune-driven mechanisms of remodeling imbalance, whereas the unique features of alveolar bone, including high turnover, continuous mechanical loading, and chronic microbial exposure, make it particularly susceptible to inflammatory uncoupling. Together, these concepts support a therapeutic shift toward restoring physiological coupling instead of solely inhibiting resorption and position periodontitis as a clinically accessible model for understanding and targeting inflammatory bone loss across skeletal diseases. - Source: PubMed
Publication date: 2026/07/06
de Molon Rafael ScafTetradis SotiriosVernal RolandoLeite Fabio Renato ManzolliVan Dyke Thomas E - Gallbladder cancer (GBC) is a highly lethal malignancy with limited experimental models to study disease biology or evaluate therapeutic responses. Although canonical Wnt activation is commonly used for patient-derived organoid (PDO) development and expansion, gallbladder PDOs have also been generated under Wnt-inhibitory conditions. No comparative assessments have determined how Wnt pathway modulation influences gallbladder PDO development, phenotype, or drug response. - Source: PubMed
Dutta AnkitaGuha PayelSelvarajan Akshaya VijayanChowdhury NanditaBanerjee PrithaGhosh Shrabanti SarkarShaw Archana KumariGanguli DebduttaSunderam UmaRoy Manas KumarBanerjee SudeepSrinivasan RajgopalRoy ParomitaSaha VaskarDutta AninditaGuhaSarkar Dwijit