| pubmed-article:3099298 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:3099298 | lifeskim:mentions | umls-concept:C0029016 | lld:lifeskim |
| pubmed-article:3099298 | lifeskim:mentions | umls-concept:C1257739 | lld:lifeskim |
| pubmed-article:3099298 | lifeskim:mentions | umls-concept:C0018270 | lld:lifeskim |
| pubmed-article:3099298 | lifeskim:mentions | umls-concept:C1149838 | lld:lifeskim |
| pubmed-article:3099298 | lifeskim:mentions | umls-concept:C1517945 | lld:lifeskim |
| pubmed-article:3099298 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:3099298 | pubmed:dateCreated | 1987-2-19 | lld:pubmed |
| pubmed-article:3099298 | pubmed:abstractText | Data indicating that the 21-kDa protein (p21) Harvey-ras gene product shares sequence homology with guanine nucleotide-binding proteins (G proteins) has stimulated research on the influence(s) of p21 on G-protein-regulated systems in vertebrate cells. Our previous work demonstrated that NIH-3T3 mouse cells expressing high levels of the cellular ras oncogene isolated from the EJ human bladder carcinoma (EJ-ras) exhibited reduced hormone-stimulated adenylate cyclase activity. We now report that in these cells another enzyme system thought to be regulated by G proteins is inhibited, namely phospholipases A2 and C. NIH-3T3 cells incubated in plasma-derived serum release significant levels of prostaglandin E2 (PGE2) as determined by radioimmunoassay when exposed to platelet-derived growth factor (PDGF) at 2 units/ml; the levels of PGE2 released from EJ-ras-transfected cells are only 3% those of controls despite a similar basal (unstimulated) release from control and EJ-ras-transfected cells. The lack of PDGF-stimulated PGE2 release from EJ-ras-transfected cells is not due to a defect in the prostaglandin cyclooxygenase enzyme, since incubation of control cells and EJ-ras-transfected cells in 0.33, 3.3, or 33 microM arachidonate resulted in identical levels of PGE2 release. The lack of PDGF-stimulated PGE2 release from EJ-ras-transfected cells also does not result from the loss of functional PDGF receptors. EJ-ras-transformed cells bind 70% as much 125I-labeled PDGF as control cells and are stimulated to incorporate [3H]thymidine and to proliferate after exposure to PDGF. Moreover, this inhibition is not likely the result of a secondary cellular effect related to the transformed phenotype, since NIH-3T3 cells transformed by v-src released PGE2 at wild-type levels after exposure to PDGF. Determination of total water-soluble inositolphospholipids and changes in the specific activities of phosphatidylcholine in control and EJ-ras-transfected cells demonstrated that PDGF-stimulated phospholipase C and A2 activities are inhibited in the EJ-ras-transfected cells. | lld:pubmed |
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| pubmed-article:3099298 | pubmed:language | eng | lld:pubmed |
| pubmed-article:3099298 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:3099298 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:3099298 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:3099298 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:3099298 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:3099298 | pubmed:author | pubmed-author:GormanR RRR | lld:pubmed |
| pubmed-article:3099298 | pubmed:author | pubmed-author:TarpleyW GWG | lld:pubmed |
| pubmed-article:3099298 | pubmed:author | pubmed-author:BenjaminC WCW | lld:pubmed |
| pubmed-article:3099298 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:3099298 | pubmed:volume | 84 | lld:pubmed |
| pubmed-article:3099298 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:3099298 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:3099298 | pubmed:pagination | 546-50 | lld:pubmed |
| pubmed-article:3099298 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:3099298 | pubmed:year | 1987 | lld:pubmed |
| pubmed-article:3099298 | pubmed:articleTitle | Loss of platelet-derived growth factor-stimulated phospholipase activity in NIH-3T3 cells expressing the EJ-ras oncogene. | lld:pubmed |
| pubmed-article:3099298 | pubmed:publicationType | Journal Article | lld:pubmed |
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