Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5054
pubmed:dateCreated
1992-5-20
pubmed:abstractText
Multidrug resistance in mammalian tumor cells is associated with the overexpression of mdr genes encoding P-glycoproteins, which function as drug efflux pumps. A yeast homolog of mdr, STE6, mediates export of a-factor mating peptide. Yeast MATa cells carrying a ste6 deletion produce no extracellular a-factor and therefore are defective in mating. Expression of a complementary DNA for the mouse mdr3 gene in a yeast ste6 deletion strain restored ability to export a-factor and to mate. A mutation (a serine to phenylalanine substitution at amino acid 939) known to affect the activity of the mdr3 gene product abolished its ability to complement the yeast ste6 deletion. Thus, functions of P-glycoproteins in normal mammalian cells may include the transmembrane export of endogenous peptides.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0036-8075
pubmed:author
pubmed:issnType
Print
pubmed:day
10
pubmed:volume
256
pubmed:geneSymbol
mdr
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
232-4
pubmed:dateRevised
2007-3-19
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
Functional complementation of yeast ste6 by a mammalian multidrug resistance mdr gene.
pubmed:affiliation
National Research Council of Canada, Biotechnology Research Institute, Montreal, Quebec.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't