Linked Life Data

10764208

Source:http://linkedlifedata.com/resource/pubmed/id/10764208

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2000-5-25
pubmed:abstractText
We test the hypothesis that lysinuric protein intolerance (LPI), a rare autosomal recessive defect of cationic amino acid transport, results from the absence of the recently described y+L amino acid transporter. We compare fluxes of lysine (1 microM) into erythrocytes of normal subjects with those of patients homozygous for the LPI mutation. No significant differences in fluxes through system y+L in normal or LPI cells were found, excluding the possibility that system y+L cannot be expressed in patients with LPI. Reasons for supposing that there may be tissue-specific processing of two recently described genes encoding the y+L transporter are discussed. Polymerase chain reaction measurement of expression of these two genes in an erythroleukemic cell line suggests that alternatively there may be an as-yet-unidentified additional member of this gene family.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0031-6768
pubmed:author
pubmed:issnType
Print
pubmed:volume
439
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
513-6
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Cationic amino acid transport through system y+L in erythrocytes of patients with lysinuric protein intolerance.
pubmed:affiliation
Department of Human Anatomy and Genetics, University of Oxford, UK. richard.boyd@human-anatomy.ox.ac.uk
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't