PPBT_RAT Alpl ELISA tesk kit
- Known as:
- PPBT_RAT Alpl Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen17340
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- PPBT_RAT Alpl ELISA tesk kit
Ask about this productRelated genes to: PPBT_RAT Alpl ELISA tesk kit
- 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
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- 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 - Hypophosphatasia (HPP) is a rare inherited metabolic disorder characterized by deficient activity of serum alkaline phosphatase due to loss-of-function mutations in the ALPL gene. Diagnosis confirmation, management, and follow-up of HPP are challenging, and clinical guidance is scant due to the difficulty in gathering high-level evidence. Asfotase alfa is the first long-term enzyme replacement therapy indicated in patients with pediatric-onset HPP to treat the bone manifestations of the disease. In the absence of large clinical studies, sharing clinical observations is an important source of information and support for clinicians. This article presents three case studies. A woman affected by HPP with manifestations of the disease at pediatric age began asfotase alfa therapy at the age of 43 years, resulting in improvements in bone density and epilepsy management. A man diagnosed with HPP in childhood had a severely compromised quality of life. He experienced improvements in bone fragility, respiratory function, sleep quality, and physical function with asfotase alfa therapy. Finally, a woman with infantile-onset HPP, presenting with severe bone deformity, musculoskeletal pain, pseudofractures, and cardiovascular and neurological involvement, showed radiological and clinical improvements in bone health, reduced pain, and increased walking autonomy during asfotase alfa treatment. - Source: PubMed
Publication date: 2026/06/15
Pigliaru FrancescaNoto DavideBrandi Maria Luisa - Kawasaki disease (KD) is an acute self-limiting systemic vasculitis of unknown etiology, lacking specific diagnostic biomarkers. Neutrophils and their released extracellular traps play a central role in disease pathogenesis and coronary artery injury, making targeting this pathological process a key direction for exploring novel diagnostic and therapeutic strategies. Therefore, this study aimed to identify neutrophil-related genes associated with KD and to construct and validate a diagnostic model for improving the early and precise diagnosis of KD. - Source: PubMed
Publication date: 2026/04/23
Chen JingZhang Huan - Astrocytes regulate the assembly and functions of neural circuits, contribute to synaptic homeostasis, provide metabolic support to neurons, and control ion balance and blood-brain barrier integrity. These cells are morphologically and molecularly very heterogeneous and perform unique functions to accommodate the needs of subsets of neurons. In this study, we identified and characterized a subpopulation of cerebellar astrocytes expressing the transcription factor Olig2 (O2AST). We defined their molecular identity and transcriptional divergence from other well-established subpopulations of cerebellar astrocytes and cells of the oligodendrocyte lineage that also express Olig2. Specific deletion of Olig2 from astrocytes in vivo affects the locomotion of mice. We found that cerebellar O2AST are relatively abundant in the cerebellar nuclei but not in the cerebellar lobes. Cerebellar O2AST highly express a set of unique genes, including Slc6a11, Gpc5, Igsf1, Alpl, and Egfl6. Furthermore, we examined the regulatory influence of the transcription factor Yin Yang 1 (YY1), known to control maturation of cerebellar astrocytes, on O2AST differentiation and morphology. Specific deletion of Yy1 from astrocytes increases the number of O2AST in the cerebellar nuclei, affects O2AST differentiation, and cross-communication with the cells of oligodendrocyte lineage, diminishing differentiation of oligodendrocyte precursor cells (OPCs) to mature oligodendrocytes. In sum, our findings reveal a distinct, transcriptionally unique subpopulation of astrocytes expressing Olig2 in the cerebellum, uncovering novel regulatory mechanisms orchestrated by Yy1 during postnatal development. - Source: PubMed
Zarei-Kheirabadi MasoumehTyc Katarzyna MDain LaurenKheirabadi Maryam AshrafiHanco JenniferMockenhaupt KarliMunir SohaMcQuiston AdamSingh Sandeep KKordula Tomasz