Linked Life Data

17451637

Source:http://linkedlifedata.com/resource/pubmed/id/17451637

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2007-6-12
pubmed:abstractText
N-Acetylglucosaminyltransferase-V (GnT-V) is a key enzyme in the processing of N-glycans during synthesis of glycoproteins. We have reported that down-regulating GnT-V could induce endoplasmic reticulum stress (ER stress) in 7721 cells, a human hepatocarcinoma cell line. In a search for mechanisms of ER stress, we found that there was a prominent decline of glucose uptake in antisense GnT-V transfectant, furthermore, a decrease of tri- or tetra-antannary sugar chain of glucose transporter 1 (GLUT1). However, distribution of GLUT1 in antisense GnT-V transfectant was not affected. Glucose deprivation has been known to activate ER stress in tumor cells. Therefore, the data presented in this study indicate that the glycosylation change and decrease of transport activity of GLUT1 may be one possible mechanism of ER stress induced by down-regulating GnT-V, and GnT-V may contribute to the regulation of glucose uptake by modifying glycosylation of GLUT1 in some tumor cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0003-9861
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
463
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
102-9
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Down-regulation of N-acetylglucosaminyltransferase-V induces ER stress by changing glycosylation and function of GLUT1.
pubmed:affiliation
Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, 130 Dong an Road, Shanghai 200032, China. li2sister@163.com
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't