Tissue-nonspecific Alkaline Phosphatase Regulates Purinergic Transmission in the Central Nervous System During Development and Disease
Computational and Structural Biotechnology Journal, ISSN: 2001-0370, Vol: 13, Page: 95-100
2015
- 54Citations
- 88Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations54
- Citation Indexes54
- 54
- CrossRef52
- Captures88
- Readers88
- 88
Review Description
Tissue-nonspecific alkaline phosphatase (TNAP) is one of the four isozymes in humans and mice that have the capacity to hydrolyze phosphate groups from a wide spectrum of physiological substrates. Among these, TNAP degrades substrates implicated in neurotransmission. Transgenic mice lacking TNAP activity display the characteristic skeletal and dental phenotype of infantile hypophosphatasia, as well as spontaneous epileptic seizures and die around 10 days after birth. This physiopathology, linked to the expression pattern of TNAP in the central nervous system (CNS) during embryonic stages, suggests an important role for TNAP in neuronal development and synaptic function, situating it as a good target to be explored for the treatment of neurological diseases. In this review, we will focus mainly on the role that TNAP plays as an ectonucleotidase in CNS regulating the levels of extracellular ATP and consequently purinergic signaling.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S2001037014000543; http://dx.doi.org/10.1016/j.csbj.2014.12.004; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84948739379&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/25709758; https://linkinghub.elsevier.com/retrieve/pii/S2001037014000543; http://linkinghub.elsevier.com/retrieve/pii/S2001037014000543
Elsevier BV
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