ALPL Antibodies

Structure of ALPL

The tissue-specific alkaline phosphatase (TNAP) encoded by the ALPL gene is a glycoprotein with a molecular weight of approximately 86 kDa. Its precise molecular weight varies slightly depending on species and post-transcriptional modifications such as glycosylation. This protein is composed of 524 amino acids and forms a typical spherical structure. Its active center contains two zinc ions and one magnesium ion, which are crucial for catalyzing the hydrolysis of phosphate esters. The secondary structure of the ALPL protein is mainly composed of an α -helix and a β -fold, which jointly enclose the active pocket. Key residues such as histidine (His) and aspartic acid (Asp) are involved in metal ion coordination and substrate recognition. Their genetic variations can significantly affect enzyme activity and lead to hypophosphatase syndrome (HPP).

Fig. 1 ALPL - ATP signal axis regulation mechanism of angiogenesis.¹

Key structural properties of ALPL:

• Typical α/β hydrolase folding conformation
• The binuclear metal center (Zn²⁺/Mg²⁺) constitutes the catalytic active core
• Conserved aspartic acid residues are involved in substrate recognition and phosphate hydrolysis

Functions of ALPL

The main function of the ALPL gene-encoded protein (TNAP) is to catalyze the hydrolysis of phosphate esters and regulate the biomineralization process. In addition, it is also involved in a variety of physiological and pathological processes, including functions such as bone development, energy metabolism and nerve transmission.

The kinetic characteristics of this enzyme are characterized by broad-spectrum hydrolytic activity against various phosphate ester substrates, with an optimal pH of approximately 9-10. It relies on magnesium/zinc ions as cofactors, and its activity level directly reflects the metabolic and mineralization status of the tissue.

Applications of ALPL and ALPL Antibody in Literature

1. Mensali, Nadia, et al. "Supplementary information. ALPL-1 is a target for chimeric antigen receptor therapy in osteosarcoma." Nat Commun 14, 3375 (2023). https://doi.org/10.1038/s41467-023-39097-x

The article indicates that a specific CAR-T cell therapy has been developed for the osteosarcoma target ALPL-1. It can effectively target the primary and metastatic lesions in preclinical models without causing toxicity to healthy tissues, providing a basis for subsequent clinical applications.

2. Dong, Jiayi, et al. "ALPL regulates pro-angiogenic capacity of mesenchymal stem cells through ATP-P2X7 axis controlled exosomes secretion." Journal of Nanobiotechnology 22.1 (2024): 172. https://doi.org/10.1186/s12951-024-02396-6

Research has found that ALPL gene defects, by enhancing ATP release and activating the P2X7 receptor pathway, cause hBMMSCs to secrete excessive exosomes that inhibit angiogenesis, thereby impairs the angiogenesis capacity of bone tissue. Inhibiting P2X7 can reverse this process, providing a new target for the treatment of ALPL-related bone defects.

3. Seefried, Lothar, et al. "Whole genome sequencing in adults with clinical hallmarks of hypophosphatasia negative for ALPL variants." Molecular Biology Reports 51.1 (2024): 984. https://doi.org/10.1007/s11033-024-09906-7

The study found that through whole-genome sequencing of 16 patients clinically diagnosed with HPP and low ALP activity, no new pathogenic ALPL gene variations were discovered, nor were any other pathogenic gene patterns that could explain the HPP phenotype found. This indicates that the genetic mechanism of ALPL-negative HPP still needs further exploration.

4. Mao, aojian, et al. "Two novel mutations in the ALPL gene of unrelated Chinese children with Hypophosphatasia: case reports and literature review." BMC pediatrics 19.1 (2019): 456. https://doi.org/10.1186/s12887-019-1800-4

Study in four Chinese low phosphatase (HPP) found in patients with six ALPL gene mutations, two new mutations among c. 359 g & gt; C and c. 1017 dupg. The novel mutation c.359G>C is associated with severe infantile HPP, which can be fatal, highlighting the pathogenicity of the ALPL mutation in Chinese children.

5. Zhang, Liqiang, et al. "GSK3β rephosphorylation rescues ALPL deficiency-induced impairment of odontoblastic differentiation of DPSCs." Stem Cell Research & Therapy 12.1 (2021): 225. https://doi.org/10.1186/s13287-021-02235-7

Research has found that defects in the ALPL gene damage the differentiation of dental pulp stem cells into odontoblasts by inhibiting the phosphorylation of GSK3β, leading to abnormal tooth development in patients with hypophosphatase. Lithium chloride treatment can activate the GSK3β pathway and improve dental defects related to ALPL deficiency.

Creative Biolabs: ALPL Antibodies for Research

Creative Biolabs specializes in the production of high-quality ALPL antibodies for research and industrial applications. Our portfolio includes monoclonal antibodies tailored for ELISA, Flow Cytometry, Western blot, immunohistochemistry, and other diagnostic methodologies.

• Custom ALPL Antibody Development: Tailor-made solutions to meet specific research requirements.
• Bulk Production: Large-scale antibody manufacturing for industry partners.
• Technical Support: Expert consultation for protocol optimization and troubleshooting.
• Aliquoting Services: Conveniently sized aliquots for long-term storage and consistent experimental outcomes.

For more details on our ALPL antibodies, custom preparations, or technical support, contact us at email.