ArticleScientific reports2017
PiT2 regulates neuronal outgrowth through interaction with microtubule-associated protein 1B.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Article
- A Novel Frameshift Mutation inBiomedicines · 2026Article
- Slc20a1 and Slc20a2 regulate neuronal plasticity and cognition independently of their phosphate transport ability.Cell death & disease · 2024Article
- The Pathology of Primary Familial Brain Calcification: Implications for Treatment.Neuroscience bulletin · 2023Review
- Mechanisms of PiT2-loop7 Missense Mutations Induced Pi Dyshomeostasis.Neuroscience bulletin · 2023Article
- PiT2 deficiency prevents increase of bone marrow adipose tissue during skeletal maturation but not in OVX-induced osteoporosis.Frontiers in endocrinology · 2022Article
- Article
- Partial reduced Pi transport function of PiT-2 might not be sufficient to induce brain calcification of idiopathic basal ganglia calcification.Scientific reports · 2019Article
- Phosphate-dependent FGF23 secretion is modulated by PiT2/Slc20a2.Molecular metabolism · 2018Article
Corrections and comments
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Authors and funding
20 authors.
Funding
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Abstract
PiT2 is a member of the inorganic phosphate transporter family, and is extensively expressed in the nervous system. It was found that loop7 domain of PiT2 is not required for retroviral recognition and transport function. The exact functions of loop7 remain poorly understood. Here we show that loop7 of PiT2 is necessary for the transport of PiT2 protein to the cell surface. Further, loop7 is also related to the outgrowth of neurite in Neuro2A cells interacts with the light chain 1 of microtubule-associated protein 1B (MAP1B). PiT2 with mutated MAP1B binding sites affect neurite outgrowth whereas Pi transport function deficient mutants of PiT2 do not. We also show that Drosophila dPiT interacts with microtubule-associated protein Futsch, and dPiT is crucial for the normal development of neuromuscular junctions (NMJs). These results indicate that PiT2 might participate in the regulation of neuronal outgrowth by interacting with MAP1B and independently of its Pi transport function in the nervous system.
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