Ask about this productRelated genes to: ALPL protein
- Gene:
- ALPL NIH gene
- Name:
- alkaline phosphatase, biomineralization associated
- Previous symbol:
- HOPS
- Synonyms:
- TNSALP, TNALP, TNAP
- Chromosome:
- 1p36.12
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2018-08-08
Related products to: ALPL protein
Related articles to: ALPL protein
- Bone regeneration requires tight coordination between mesenchymal stem cells (MSCs), immune signaling, and extracellular matrix remodeling. Yet, how atypical immune receptors contribute to this process remains unclear. Here, we identify Toll-like receptor 10 (TLR10) as a key regulator of osteogenic differentiation in human adipose-derived MSCs. Herein, ASC/TERT1 MSCs were engineered to overexpress or silence TLR10 using lentiviral vectors, and osteogenic differentiation (0-14 days) was assessed by metabolic assays-RT-qPCR of , and -Alizarin Red S staining, and quantitative mass spectrometry. Enhancing TLR10 expression promoted osteogenic gene programs, extracellular matrix organization, metabolic adaptation, and robust matrix mineralization, whereas TLR10 suppression maintained proliferative states and impaired osteoblast maturation. Proteomic analyses revealed that TLR10 selectively activates osteogenic, ECM-remodeling, and vitamin D-responsive pathways, while restraining programs antagonistic to differentiation. Notably, active vitamin D induced TLR10 expression and partially restored osteogenesis in TLR10-deficient cells, indicating that TLR10 is associated with vitamin D-driven bone formation. Together, beyond its established role in innate immunity, TLR10 emerges as a vitamin D-responsive regulator of mesenchymal stem cell osteogenesis, highlighting a potential therapeutic axis to enhance bone regeneration and osteogenic outcomes. - Source: PubMed
Publication date: 2026/04/15
Stierschneider AnnaNeuditschko BenjaminFischer IsabellaHellmann EstherZimmermann DanielProhaska KaterinaMilchram LisaHerzog FranzWiesner Christoph - Hypophosphatasia (HPP) is a rare metabolic bone disorder that can present with a wide spectrum of skeletal and extraskeletal signs and symptoms. Biochemically, HPP is characterized by a decreased activity of the tissue nonspecific alkaline phosphatase (TNSALP) and subsequent accumulation of inorganic pyrophosphate (PPi). Fractures in patients with HPP can show delayed healing or even progress to nonunion. In pediatric patients, fractures can be particularly debilitating, as children usually engage in high levels of physical activity. - Source: PubMed
Publication date: 2026/04/25
Windels OskarSimon AlexanderMuschol NicoleYorgan TimurBarvencik Florian - Hypophosphatasia (HPP) is a rare inborn error of metabolism caused by gene mutations, resulting in deficient tissue-nonspecific alkaline phosphatase (ALP) activity. We investigated genotype-phenotype correlations in a monozygotic female twin pair with infantile HPP. - Source: PubMed
Publication date: 2026/04/15
Hao LunaHuang NaTao YilunLi HuiZhuang JuyuLi XiaoyunHao ZekunZhao Feng - Critical sized craniomaxillofacial bone defects do not heal naturally and often exhibit chronic inflammatory responses that restrict regeneration. It is increasingly apparent that biomaterials must facilitate dynamic crosstalk between immune cells, such as macrophages, and osteoprogenitors to resolve inflammation and accelerate regeneration. Here, we evaluate interactions between macrophages in a neutral (M0) or pro-inflammatory (M1) state with mesenchymal stem cells (MSCs) in a basal or licensed state within a mineralized collagen scaffold. We reveal that MSC-macrophage crosstalk influences significant changes in osteoprogenitor cell differentiation and immune cell polarization. Notably, crosstalk between MSCs and macrophages drives an early-stage inflammatory response, which enhances the immunomodulatory activity of MSCs via secretion of IL-6, an effect that is heightened for already licensed MSCs. The presence of macrophages in the co-cultures upregulated osteogenic (, , , and ) and angiogenic genes () in basal MSC groups. Further, MSC-macrophage interactions subsequently drive increased M2-like macrophage polarization as early as 7 days of culture, as indicated by surface marker expression. These findings show that biomaterial scaffolds can be leveraged as mediators of MSC-mediated immunomodulation with an emphasis on achieving early-stage pro-inflammatory phenotypes that drive subsequent macrophage polarization and markers of increased regenerative potency. - Source: PubMed
Publication date: 2026/03/12
Kolliopoulos VasilikiPolanek MaxwellGamage Hashni E VidanaLing Melisande Wong YanTiffany AleczandriaNelson Erik RSpiller Kara LHarley Brendan A C - Acute respiratory exacerbations in bronchiectasis are important as they impair quality of life and are associated with accelerated lung function decline. Yet, no validated methods exist to identify children at increased risk of exacerbations. We therefore determined if peripheral blood gene expression (GE) signatures can identify those at risk of an impending exacerbation. Thirty-one children with bronchiectasis had RNA extracted from peripheral blood collected whilst they were clinically stable, with 22 having an exacerbation during the next 3 months. Microarray assays using the HumanHT-12 v4.0 Expression BeadChip identified differentially expressed genes (p value ≤ 0.05, fold change > 1.5). The top targets were verified using real-time quantitative polymerase chain reaction (rt-qPCR) assays, and receiver operating characteristics and area under the curve (AUC) were assessed. Functional analysis of these genes was performed using Ingenuity Pathway Analysis. Overall, 647 entities were significantly dysregulated (p < 0.05) in the exacerbation group (n = 22), and pathway analysis identified neutrophil degranulation as the dominant affected pathway, which was also significantly inhibited (p < 0.001). Forty entities (32 genes) were associated with a future exacerbation (p ≤ 0.05, fold change ≥ 1.5) and six genes (ANXA3, ALAS2, DEFA1, ALPL, SNCA, PROK2) were verified using RT-qPCR (all p < 0.04) as the most discriminatory. DEFA1 and ANXA3 had the highest AUC (0.92, 95% confidence interval [CI] 0.82-1.00, and 0.87, 95% CI 0.73-1.00, respectively). We identified neutrophil-associated genes from peripheral blood that could be potential biomarkers for children with bronchiectasis at increased risk of exacerbations during the next 3 months. These GE signatures warrant further investigation and validation in larger, independent cohorts. KEY MESSAGES: Exacerbations in paediatric bronchiectasis are important. Peripheral blood gene expression may help identify children at risk of exacerbations. Six neutrophil-associated genes were associated with a future exacerbation. Identifying predictive gene expression signatures warrants further investigation. - Source: PubMed
Publication date: 2026/04/01
O'Farrell Hannah EGoyal VikasChang Anne BGrimwood KeithCheng MichaelYerkovich Stephanie TBaines Katherine J