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Nat. Rev. Nephrol. doi:10.1038/nrneph.2017.60 Figure 1 Role of bone-specific alkaline phosphatase (BALP) in tissue mineralization Figure 1 | Role of bone-specific alkaline phosphatase (BALP) in tissue mineralization. The expression of alkaline phosphatase, tissue-nonspecific isozyme (TNALP) is stimulated by RUNX2, MSX2 and SOX9. TNALP is post-translationally modified (N-linked and O-linked glycosylations) in the endoplasmatic reticulum (ER) and Golgi apparatus under the influence of unknown regulators. Glycosylation produces numerous structural modifications, which increase the functional diversity of TNALP. Four bone-specific isoforms of TNALP exist (B/I, B1x, B1, and B2). These BALP isoforms are transported to the cell membrane and attached to the outer layer, where they act as ectoenzymes. In mineralizing cells, more BALP isoforms are transported to specific sections of the cell membrane, which then are released and form matrix vesicles that are rich in membrane-bound BALP isoforms and Sortillin (in vascular mesenchymal stem cells (MSCs)) but not Activin A or autophagy markers. BALP inactivates the mineralization inhibitors inorganic pyrophosphate (PPi) and osteopontin (by dephosphorylation) and thus substantially contributes to the generation of a pro-calcific extracellular milieu. BALP also binds directly to collagen type I, which forms a scaffold for the propagation of matrix mineralization. The functional role of collagen-bound BALP is not yet known. Pi, inorganic phosphate; VSMC, vascular smooth muscle cell. Haarhaus, M. et al. (2017) Alkaline phosphatase: a novel treatment target for cardiovascular disease in CKD Nat. Rev. Nephrol. doi:10.1038/nrneph.2017.60