Linked Life Data

19375851

Source:http://linkedlifedata.com/resource/pubmed/id/19375851

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2009-8-4
pubmed:abstractText
RLIP76 is a stress-responsive glutathione-electrophile-conjugates (GS-E) and drugs transporter which is over-expressed in different types of cancers. Cdc2 is a cell-cycle check point control kinase which has been shown to bind to RLIP76 during mitosis, such that endocytosis is inhibited. In present studies, we have purified cdc2 and examined its effect on the transport activity of RLIP76 reconstituted into artificial liposomes. Both doxorubicin (DOX) and dinitro-phenyl S-glutathione (DNP-SG) transport were inhibited by cdc2 in a concentration dependent manner. Liposomal delivery of cdc2 to H358 cells caused apoptosis, resulted in an increased intracellular doxorubicin-accumulation and decreased rate of efflux from the cells. In the present communication, we propose that the accumulation-deficient drug-resistance mediated by RLIP76 can be modulated by inhibition of RLIP76 transport activity by cdc2.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1872-7980
pubmed:author
pubmed:issnType
Electronic
pubmed:day
8
pubmed:volume
283
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
152-8
pubmed:dateRevised
2011-5-3
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Increased expression of cdc2 inhibits transport function of RLIP76 and promotes apoptosis.
pubmed:affiliation
Department of Molecular Biology and Immunology, 3500 Camp Bowie Blvd., University of North Texas Health Science Center, Fort Worth, TX 76107-2699, United States. ssinghal@hsc.unt.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't