Defective enamel and bone development in sodium-dependent citrate transporter (NaCT) Slc13a5 deficient mice.

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Defective enamel and bone development in sodium-dependent citrate transporter (NaCT) Slc13a5 deficient mice.

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2017 nî lūn-bûn

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2017 թուականի Ապրիլին հրատարակուած գիտական յօդուած

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2017 թվականի ապրիլին հրատարակված գիտական հոդված

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2017年の論文

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2017年論文

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2017年論文

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2017年論文

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2017年論文

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2017年論文

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2017年论文

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Defective enamel and bone deve ...... (NaCT) Slc13a5 deficient mice.

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Defective enamel and bone deve ...... (NaCT) Slc13a5 deficient mice.

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Defective enamel and bone development in sodium-dependent citrate transporter

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Item

label

Defective enamel and bone deve ...... (NaCT) Slc13a5 deficient mice.

@ast

Defective enamel and bone deve ...... (NaCT) Slc13a5 deficient mice.

@en

Defective enamel and bone development in sodium-dependent citrate transporter

@nl

prefLabel

Defective enamel and bone deve ...... (NaCT) Slc13a5 deficient mice.

@ast

Defective enamel and bone deve ...... (NaCT) Slc13a5 deficient mice.

@en

Defective enamel and bone development in sodium-dependent citrate transporter

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P1476

Defective enamel and bone deve ...... (NaCT) Slc13a5 deficient mice.

@en

P2093

Armando R Irizarry

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Guirui Yan

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Jonathan Lucchesi

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Matthew J Hamang

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Qingqiang Zeng

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Yanfei L Ma

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P2860

Strongly bound citrate stabilizes the apatite nanocrystals in bone

The SLC13 gene family of sodium sulphate/carboxylate cotransporters

Structure, function, and expression pattern of a novel sodium-coupled citrate transporter (NaCT) cloned from mammalian brain

Functional features and genomic organization of mouse NaCT, a sodium-coupled transporter for tricarboxylic acid cycle intermediates

Human Na+ -coupled citrate transporter: primary structure, genomic organization, and transport function

The developmental clock of dental enamel: a test for the periodicity of prism cross-striations in modern humans and an evaluation of the most likely sources of error in histological studies of this kind

Mutations in the Na(+)/citrate cotransporter NaCT (SLC13A5) in pediatric patients with epilepsy and developmental delay

Recessive mutations in SLC13A5 result in a loss of citrate transport and cause neonatal epilepsy, developmental delay and teeth hypoplasia.

Teriparatide [rhPTH (1-34)], but not strontium ranelate, demonstrated bone anabolic efficacy in mature, osteopenic, ovariectomized rats.

Mutations in SLC13A5 cause autosomal-recessive epileptic encephalopathy with seizure onset in the first days of life.

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e0175465

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scholarly article

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10.1371/JOURNAL.PONE.0175465

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English

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P478

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James Xiaojun Rong

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2017-04-13T00:00:00Z

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28406943

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5391028

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