ALPL
- Known as:
- ALPL
- Catalog number:
- PA1004
- Product Quantity:
- 100μg
- Category:
- -
- Supplier:
- SDlabs
- Gene target:
- ALPL
Related genes to: ALPL
- 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
Related articles to: ALPL
- Pyle disease is a rare metaphyseal dysplasia caused by loss-of-function variants in SFRP4, leading to abnormal cortical modeling with relative preservation of trabecular bone. The mechanisms involved in severe and persistent bone pain in adult patients remain incompletely understood. - Source: PubMed
Publication date: 2026/06/16
Lizcano FernandoAvilés ElianaLópez CristianMaradei-Anaya SilviaBallesteros-García Maria CamilaBustamante LizethLuna FredyO'Meara MiguelValenzuela Alex - Odonto-hypophosphatasia (odonto-HPP) is a mild form of hypophosphatasia (HPP) characterised by premature exfoliation of primary and/or permanent teeth accompanied by low serum alkaline phosphatase (ALP) activity levels, without abnormalities of the skeletal system. Tooth agenesis (TA) is a common developmental anomaly characterised by the absence of one or more teeth due to the failure of tooth formation. In this study, the present authors report on a family simultaneously affected by odonto-HPP and TA for the first time. Comprehensive genetic analysis identified two novel missense variants (c.103G>A and c.247G>A) in the ALPL gene associated with odonto-HPP and no pathogenic variants in the reported TA genes, which may expand the genetic spectrum of odonto-HPP and imply an unforeseen additional dental abnormality associated with HPP. - Source: PubMed
Xu Tao YunGuo Xin YueZhang Bai ZeDuan Xiao Hong - Hypophosphatasia (HPP) is a metabolic disorder characterized by deficient alkaline phosphatase (ALP) activity, defective mineralization of bones and teeth, and non-skeletal manifestations. We compared disease burden between patients with skeletal and non-skeletal manifestations. - Source: PubMed
Publication date: 2026/06/28
Kishnani Priya SIng StevenHoover-Fong JuliePallais J CarlVoskopoja AngieFang ShonaMowrey William RRush EricDahir Kathryn - The selective EP4 receptor (PTGER4) agonist KMN-159 stimulates osteoblast function and may support applications in dental bone tissue regeneration and tissue engineering. The goal of this study was to further validate stimulation of osteogenic differentiation ex vivo and in vivo by KMN-159. We tested KMN-159 in cultured human bone marrow-derived mesenchymal stem/stromal cells (BM-MSCs) and rat BM-MSCs grown in a three-dimensional deproteinized bone explant culture model. The effects of KMN-159 treatment in vivo were also investigated in two different alveolar bone repair models (i.e., male rat tooth socket model with and without a dental implant), as well as in a pilot study with a dental repair model in which human implants were insert into the mandibles of male minipigs. Our results show that KMN-159 promotes osteogenic differentiation of human BM-MSCs, (e.g., ALPL enzyme and mineralization) and the temporal expression of osteoblast markers (e.g., RUNX2, SP7, BMP2, TNFRSF11B) and extracellular matrix (ECM) proteins (e.g., BGLAP). KMN-159 also stimulates osteogenesis in rat BM-MSCs in bone-derived 3D scaffolds by accelerating proliferation and modulating expression of osteoblast phenotype markers. In the in vivo studies of bone repair KMN-159 increases bone volume in the tooth socket or around the coronal aspect of the implant in the rat maxillary extraction models. Similar results were obtained in the porcine dental implant repair model. We conclude that KMN-159 is a viable pharmacotherapeutic candidate to promote bone mass accrual or to support bone tissue engineering in dental, craniofacial and skeletal applications. - Source: PubMed
Publication date: 2026/06/17
Owen Thomas ARzeczycki PhillipLeguizamon Natalia Da PonteJin QimingPatel ChandniWei ShanqiaoBarrett Stephen Dvan Wijnen Andre JMorano María Inés - Circadian disruption promotes tumor progression and therapy resistance, but its prognostic value and impact on the tumor immune microenvironment in lung squamous cell carcinoma (LUSC) remain unclear. This study aimed to develop a circadian-immune-related gene signature to improve LUSC risk stratification and therapy guidance. - Source: PubMed
Publication date: 2026/05/15
Lu YihengLi HuiWang SiyaoYang FanXiao ShuyanLiu YiningLiu QiaoweiHan XiaoHu Yi