Linked Life Data

11546675

Source:http://linkedlifedata.com/resource/pubmed/id/11546675

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2001-9-7
pubmed:abstractText
Glucose transporter isoform-1 (GLUT-1) expression is stimulated in response to stressful conditions. Here we examined the mechanisms mediating the enhanced expression of GLUT-1 by hyperosmolarity. GLUT-1 mRNA, GLUT-1 protein, and glucose transport increased after exposure of Clone 9 cells to 600 mosmol/l (produced by addition of mannitol). The stimulation of glucose transport was biphasic: in the early phase (0-6 h) a approximately 2.5-fold stimulation of glucose uptake was associated with no change in the content of GLUT-1 mRNA, GLUT-1 protein, or GLUT-1 in the plasma membrane, whereas the approximately 17-fold stimulation of glucose transport during the late phase (12-24 h) was associated with increases in both GLUT-1 mRNA (approximately 7.5-fold) and GLUT-1 protein content. Cell sorbitol increased after 3 h of exposure to hyperosmolarity. The increase in GLUT-1 mRNA content was associated with an increase in the half-life of the mRNA from 2 to 8 h. A 44-bp region in the proximal GLUT-1 promoter was necessary for basal activity and for the two- to threefold increases in expression by hyperosmolarity. It is concluded that the increase in GLUT-1 mRNA content is mediated by both enhanced transcription and stabilization of GLUT-1 mRNA and is associated with increases in GLUT-1 content and glucose transport activity.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0363-6143
pubmed:author
pubmed:issnType
Print
pubmed:volume
281
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
C1365-72
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Stimulation of GLUT-1 glucose transporter expression in response to hyperosmolarity.
pubmed:affiliation
Department of Physiology, Case Western Reserve University, Cleveland, Ohio 44106, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.