Linked Life Data

10095018

Source:http://linkedlifedata.com/resource/pubmed/id/10095018

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
1999-5-7
pubmed:databankReference
pubmed:abstractText
We have cloned and sequenced a full length rabbit GLUT 1 and partial rabbit GLUT 3 cDNAs. The derived rabbit GLUT 3 peptide revealed 84% homology to the mouse, 82% to the rat, human, dog, and sheep, and 69% to the chicken GLUT 3 peptides. Using Northern blot analysis, we investigated the tissue and brain cellular distribution of GLUT 1 and GLUT 3 expression. In addition, we examined the effect of development and hypoxic-ischemia upon brain GLUT 1 and GLUT 3 mRNA levels. While GLUT 1 mRNA was observed in most tissues, GLUT 3 was expressed predominantly in the brain, placenta, stomach, and lung with minor amounts in the heart, kidney and skeletal muscle. In the brain, both GLUT 1 and GLUT 3 were noted in neuron- and glial-enriched cultures. Both GLUT 1 and GLUT 3 mRNA levels demonstrated a similar developmental progression (p<0.05) secondary to post-transcriptional mechanisms. Further, while hypoxic-ischemia did not significantly affect brain GLUT 1 mRNA and protein, it altered GLUT 3 mRNA levels in a region-specific manner, with a three-fold increase in the cerebral cortex, a two-fold increase in the hippocampus, and a 50% increase in the caudate nucleus (p<0.05). We conclude, that the rabbit GLUT 3 peptide sequence exhibits 82-84% homology to that of other species in the coding region with a 62-89% sequence identity in the 3'-untranslated region. The tissue-specific expression of rabbit GLUT 3 mimics that of the human closely. Postnatal development and hypoxic-ischemia with reperfusion injury cause an increase in brain GLUT 3 expression, as a response to synaptogenesis and substrate deprivation, respectively.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0006-8993
pubmed:author
pubmed:copyrightInfo
Copyright 1999 Elsevier Science B.V.
pubmed:issnType
Print
pubmed:day
27
pubmed:volume
823
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
113-28
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:10095018-Aging, pubmed-meshheading:10095018-Amino Acid Sequence, pubmed-meshheading:10095018-Animals, pubmed-meshheading:10095018-Animals, Newborn, pubmed-meshheading:10095018-Anoxia, pubmed-meshheading:10095018-Base Sequence, pubmed-meshheading:10095018-Brain, pubmed-meshheading:10095018-Brain Ischemia, pubmed-meshheading:10095018-DNA, Complementary, pubmed-meshheading:10095018-Embryonic and Fetal Development, pubmed-meshheading:10095018-Fetus, pubmed-meshheading:10095018-Glucose Transporter Type 1, pubmed-meshheading:10095018-Glucose Transporter Type 3, pubmed-meshheading:10095018-Molecular Sequence Data, pubmed-meshheading:10095018-Monosaccharide Transport Proteins, pubmed-meshheading:10095018-Nerve Tissue Proteins, pubmed-meshheading:10095018-RNA, Messenger, pubmed-meshheading:10095018-Rabbits, pubmed-meshheading:10095018-Sequence Homology, Amino Acid
pubmed:year
1999
pubmed:articleTitle
Effect of development and hypoxic-ischemia upon rabbit brain glucose transporter expression.
pubmed:affiliation
Division of Neonatology and Developmental Biology, Department of Pediatrics, 300 Halket Street, University of Pittsburgh, Magee-Womens Research Institute, Pittsburgh, PA, 15213-3180, USA. sdevaskar@mail.magee.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.