pubmed-article:9708557 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:9708557 | lifeskim:mentions | umls-concept:C0005528 | lld:lifeskim |
pubmed-article:9708557 | lifeskim:mentions | umls-concept:C0007292 | lld:lifeskim |
pubmed-article:9708557 | lifeskim:mentions | umls-concept:C0011177 | lld:lifeskim |
pubmed-article:9708557 | lifeskim:mentions | umls-concept:C0017742 | lld:lifeskim |
pubmed-article:9708557 | lifeskim:mentions | umls-concept:C0039082 | lld:lifeskim |
pubmed-article:9708557 | lifeskim:mentions | umls-concept:C0011155 | lld:lifeskim |
pubmed-article:9708557 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:9708557 | pubmed:dateCreated | 1998-8-25 | lld:pubmed |
pubmed-article:9708557 | pubmed:abstractText | The glucose transporter protein syndrome (GTPS) is caused by defective transport of glucose across the blood-brain barrier via the glucose transporter GLUT1, resulting in hypoglycorrhachia, infantile seizures, and developmental delay. Recent reports indicated that GLUT1 is a multifunctional transporter. We investigated the transport of vitamin C in its oxidized form (dehydroascorbic acid) via GLUT1 into erythrocytes of 2 patients with GTPS. In both patients, uptake of oxidized vitamin C was 61% of the mothers' values. Our findings are consistent with recent observations that vitamin C is transported in its oxidized form via GLUT1. We speculate that impaired transport of this substrate and perhaps other substrates in GTPS might contribute to the pathophysiology of this condition. | lld:pubmed |
pubmed-article:9708557 | pubmed:language | eng | lld:pubmed |
pubmed-article:9708557 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9708557 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:9708557 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9708557 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9708557 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9708557 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:9708557 | pubmed:month | Aug | lld:pubmed |
pubmed-article:9708557 | pubmed:issn | 0364-5134 | lld:pubmed |
pubmed-article:9708557 | pubmed:author | pubmed-author:VeraJ CJC | lld:pubmed |
pubmed-article:9708557 | pubmed:author | pubmed-author:De VivoD CDC | lld:pubmed |
pubmed-article:9708557 | pubmed:author | pubmed-author:KlepperJJ | lld:pubmed |
pubmed-article:9708557 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:9708557 | pubmed:volume | 44 | lld:pubmed |
pubmed-article:9708557 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:9708557 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:9708557 | pubmed:pagination | 286-7 | lld:pubmed |
pubmed-article:9708557 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
pubmed-article:9708557 | pubmed:meshHeading | pubmed-meshheading:9708557-... | lld:pubmed |
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pubmed-article:9708557 | pubmed:meshHeading | pubmed-meshheading:9708557-... | lld:pubmed |
pubmed-article:9708557 | pubmed:meshHeading | pubmed-meshheading:9708557-... | lld:pubmed |
pubmed-article:9708557 | pubmed:meshHeading | pubmed-meshheading:9708557-... | lld:pubmed |
pubmed-article:9708557 | pubmed:meshHeading | pubmed-meshheading:9708557-... | lld:pubmed |
pubmed-article:9708557 | pubmed:year | 1998 | lld:pubmed |
pubmed-article:9708557 | pubmed:articleTitle | Deficient transport of dehydroascorbic acid in the glucose transporter protein syndrome. | lld:pubmed |
pubmed-article:9708557 | pubmed:affiliation | Neurological Institute, Columbia University, New York, NY 10032, USA. | lld:pubmed |
pubmed-article:9708557 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:9708557 | pubmed:publicationType | Clinical Trial | lld:pubmed |
pubmed-article:9708557 | pubmed:publicationType | Controlled Clinical Trial | lld:pubmed |
pubmed-article:9708557 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |