DKK-1, human
- Known as:
- DKK-1, H. sapiens
- Catalog number:
- P705-100
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- 101 Bio.
- Gene target:
- DKK-1 human
Related genes to: DKK-1, human
- 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: DKK-1, human
Related articles to: DKK-1, human
- Stromal nerves regulate the sensory functions of the cornea, which can be disrupted by surgical, traumatic, or chemical injuries. Corneal Schwann cells (cSCs) ensheath axons to provide trophic support, but their role in axonal regeneration is still unexplored. We utilized the proteolipid protein 1-enhanced green fluorescent protein (Plp1-eGFP) reporter mice to investigate cSCs in two models of corneal nerve injury: the corneal micropocket injury (CMI) model, which causes focal stromal axonal severance, and acute exposure to nitrogen mustard (NM), which results in blunt damage across the entire cornea and limbal tissue. After CMI, the cSC network declined rapidly over 7 days post-injury (dpi) but recovered to levels of uninjured controls by 14 dpi with sprouting at both the injury and collateral areas. Axons remained significantly lower than cSCs, compromising mechanosensory functions. The NM injury led to a sustained cSC and axonal deficit with persistent mechanosensory loss through 14 dpi. Previously, we identified Dickkopf-related protein 1 (DKK1) as a novel candidate gene expressed in cSCs. In this study, we developed a micellar formulation RM4404 incorporating a small-molecule DKK1 inhibitor for topical application and tested the therapeutic potential of this drug in both injury models. Application of RM4404 during the cSC regenerative phase (7-14 dpi) enhanced cSC repair and significantly improved axonal regeneration with restoration of mechanosensory function in both injury paradigms. These findings identify a promising DKK1-targeted therapy that promotes cSC repair, enhances corneal nerve regeneration, and restores sensory function in models of corneal injury. - Source: PubMed
Li MichaelTallo Christian AEddy Mary KatherineKolli AarushParamo RickyBargagna-Mohan PaolaMohan Royce - Odontogenic differentiation of stem cells from apical papilla (SCAPs) is critical for pulp regeneration therapy. Protein arginine methyltransferase 6 (PRMT6) plays an important role in stem cell differentiation, but the specific functions and mechanisms remain unclear. This study aimed to explore the role of PRMT6 nuclear localization sequence (NLS) in regulating SCAPs osteogenic and odontogenic differentiation and its underlying mechanism. - Source: PubMed
Publication date: 2026/06/13
Yan WanhaoGuo XiaoliZhao BingqiLi YongkangShen ZheShi RuitangZhang Chen - ARHGEF3 (also known as XPLN) is a Rho guanine nucleotide exchange factor that activates RhoA/B. Variants in the ARHGEF3 gene are associated with hip and spine BMD and fracture risk, suggesting ARHGEF3 may play key role in maintaining bone mass. However, the extent to which ARHGEF3 facilitates the anabolic and catabolic effects of RhoA are unclear alongside the down-stream impact on bone mass. We report using knockout mice that ARHGEF3 deletion leads to significant gains in cortical area and moment of inertia, driven by increased periosteal bone formation. Increased periosteal bone formation was attributed to osteocytes' down-regulation of sclerostin and Dkk1 combined with increased Wnt3a and Wnt5a expression. In contrast, endocortical bone formation was reduced in KO mice and attributed to deficits in mineralization despite gains in osteoblast viability and alkaline phosphatase activity. ARHGEF3 deletion also suppressed bone resorption despite no direct effect on osteoclastogenesis. Instead, the decrease in osteoclast numbers and bone resorption in the absence of ARHGEF3 is attributed to decreased M-CSF levels among osteoblasts and osteoblast precursors. Collectively, our findings demonstrate that ARHGEF3 deletion has pro-anabolic and anti-catabolic effects that increase bone mass and may offer a novel target for preventing bone loss in an aging population. - Source: PubMed
Publication date: 2026/06/11
Chougule AmitZhang ChunbinDenbow JordanVinokurov NickolasGardinier Joseph - Annexin A6 (AnxA6) is a predominantly intracellular calcium-dependent membrane-binding multifunctional protein that is also detected extracellularly and in small extracellular vesicles (exosomes). We previously demonstrated that lapatinib resistance in triple-negative breast cancer (TNBC) cells is associated with AnxA6 upregulation and accumulation of cholesterol in late endosomes. Here, we investigated the fate of AnxA6 and cholesterol in lapatinib-resistant (LAP-R) cells and whether extracellular AnxA6 influences TNBC cell survival. We demonstrate that reduced expression of AnxA6 in LAP-R cells decreased the secretion of MCP-1/CCL2, CCL8/IL-8, DKK1, TSP-1, and OPN by antibody arrays. The secretion of exosomes was also markedly reduced in AnxA6-depleted LAP-R cells, while AnxA6 upregulation stimulated the release of MCP-1 and exosomes. Compared to the respective controls, exosome-associated AnxA6, Rab7, and cholesterol levels were increased in exosomes isolated from AnxA6-expressing LAP-R cells. Mechanistically, we demonstrated by co-immunoprecipitation, GST pulldown, and proximity ligation assays that AnxA6 interacts with SNAP23, a component of the membrane fusion machinery. Finally, blocking extracellular AnxA6 with neutralizing antibodies reduced the viability of AnxA6-low TNBC cells but had little effect on AnxA6-high cells. These findings suggest that extracellular AnxA6 is critical for the survival of highly proliferative AnxA6-low basal-like breast cancer cells and that AnxA6 influences TNBC progression by facilitating the secretion of pro-inflammatory cytokines and cholesterol-enriched exosomes. - Source: PubMed
Publication date: 2026/05/31
Sakwe Nobelle IKorolkova Olga YVuong Ngoc BEdwards Alayjha DBlack Perrin JBall Destiny DMcIntosh Antonisha RThomas Portia LWhalen Melvin Diva SBeasley Heather KHinton Antentor OOchieng JosiahSakwe Amos M - This study aimed to evaluate periosteum-derived mesenchymal stem cells (P-MSCs) cultured under simulated microgravity (SMG) conditions. P-MSCs were induced toward osteogenic differentiation and then exposed to SMG for up to 48 h. As a control, P-MSCs were maintained under identical conditions but without SMG exposure. Cell viability, osteogenesis-related analytes, and gene expression were analyzed at 3, 24 and 48 h. Cell viability under SMG was lower after 3 h but was significantly higher after 24 h, with no difference at 48 h. There was a higher expression of pathways associated with inflammation at 3 h, which was attenuated by 24 h and neutralized at 48 h. P-MSCs under SMG demonstrated three characteristics in at least one timepoint, which supports a pro-osteogenic signaling response: (1) higher osteoprotegerin levels; (2) lower DKK1 and TNF levels; (3) upregulation of genes related to osteogenesis. Our data suggest that P-MSCs exhibit enhanced pro-osteogenic regulatory modulation in SMG. - Source: PubMed
Publication date: 2026/05/28
Canal RaulMartinez Elizabeth FFoster Jamie SBombaldi de Souza Fernanda CarlaBombaldi de Souza Renata FrancielleMorales Marcelo MarcosPontes Marcos Cesarda Rocha Daniel NHolliday Lexie SYu FahongSilva Anderson TadeuFanganiello Roberto DFerreira José Ricardo MPelegrine André A