Linked Life Data

3358773

Source:http://linkedlifedata.com/resource/pubmed/id/3358773

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1988-5-24
pubmed:abstractText
Phorbol-12-myristate-13-acetate (PMA) inhibited growth of human mammary carcinoma cell lines and increased mainly the phosphorylation of two cytosolic phosphoproteins (pp) of 27 kD with isoelectric points of 5.5 (pp27a) and 5.0 (pp27b). The time course of pp27 phosphorylation closely paralleled the rapid PMA-induced subcellular redistribution of protein kinase C (PKC) activity and its subsequent down regulation. Addition of phospholipase C and fetal calf serum to intact cells or purified PKC to a cell free system enhanced the phosphorylation of both pp27 suggesting that the two polypeptides are specific substrates for PKC. Exposure of human mammary carcinoma cells to stress inducers such as arsenite or cadmium increased the 32P incorporation of both pp27 to an extent comparable to PMA. The increased phosphorus content following stress was rather due to a higher rate of synthesis of both pp27 than to a higher phosphorylation state of these polypeptides as determined by [3H]-leucine labeling. These results indicate that the major substrates of PKC, phosphorylated during the PMA-induced growth inhibition of human mammary carcinoma cells, are members of the stress protein family, suggesting a new possible function for these proteins.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0006-291X
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
152
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
62-8
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1988
pubmed:articleTitle
The 27,000 daltons stress proteins are phosphorylated by protein kinase C during the tumor promoter-mediated growth inhibition of human mammary carcinoma cells.
pubmed:affiliation
Department of Research, University Clinic Medical School, Basel, Switzerland.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't