Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1995-10-24
pubmed:abstractText
Nucleocytoplasmic shuttling of glucocorticoid receptors (GRs) is disrupted in v-mos-transformed cells leading to the redistribution of hormone-bound receptors from the nuclear to cytoplasmic compartments. We show here that GRs from v-mos-transformed cells are hyperphosphorylated on a specific peptide and maintain hormone-induced phosphorylations upon a prolonged hormone treatment that is associated with disruptions in its nucleocytoplasmic shuttling. Since similar effects on GR nucleocytoplasmic shuttling and phosphorylation were exerted upon treatment of nontransformed cells with the protein phosphatase inhibitor okadaic acid, we examined whether hyperphosphorylation of GRs in v-mos-transformed cells resulted from inhibition of receptor dephosphorylation. Protein phosphatase activity, measured using various substrates in vitro, was identical in cell-free extracts prepared from v-mos-transformed and nontransformed cells. Analysis of phosphate turnover in vivo from either the sum of all GR phosphorylation sites or from individual sites using pulse-chase analysis, did not reveal any significant difference between v-mos-transformed cells versus nontransformed cells. Thus, hyperphosphorylation of GR in v-mos-transformed cells does not appear to result from inhibition of GR dephosphorylation, but rather from stimulation of GR phosphorylation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0039-128X
pubmed:author
pubmed:issnType
Print
pubmed:volume
60
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
375-82
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Glucocorticoid receptor phosphorylation in v-mos-transformed cells.
pubmed:affiliation
Department of Biological Sciences, University of Pittsburgh, Pennsylvania 15260, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't