| pubmed-article:1496380 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1496380 | lifeskim:mentions | umls-concept:C1257739 | lld:lifeskim |
| pubmed-article:1496380 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
| pubmed-article:1496380 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
| pubmed-article:1496380 | lifeskim:mentions | umls-concept:C1879746 | lld:lifeskim |
| pubmed-article:1496380 | lifeskim:mentions | umls-concept:C1547011 | lld:lifeskim |
| pubmed-article:1496380 | lifeskim:mentions | umls-concept:C0598002 | lld:lifeskim |
| pubmed-article:1496380 | pubmed:issue | 5070 | lld:pubmed |
| pubmed-article:1496380 | pubmed:dateCreated | 1992-9-4 | lld:pubmed |
| pubmed-article:1496380 | pubmed:abstractText | Serum and growth factors can increase the proportion of Ras in the active guanosine triphosphate (GTP)-bound form. Growth factors might stimulate guanine nucleotide exchange or decrease the activity of the guanosine triphosphatase-activating proteins GAP and neurofibromin (NF1). In NIH 3T3 cells that overexpress the mutant Ras protein His116, which releases bound guanine nucleotide at a constitutively high rate and retains sensitivity to GAP and NF1, the proportion of GTP bound to the His116 protein was not altered by serum or platelet-derived growth factor. However, these mitogens increased the proportion of Ras in the GTP-bound form in cells that overexpressed control Ras proteins with a normal intrinsic rate of guanine nucleotide release. The amount of GTP-bound His116 or control Ras proteins was higher in cells at low density than in cells at high density, which have more GAP-like activity. The lower proportion of GTP-bound Ras in NIH 3T3 cells at high density may result from increased GAP-like activity. By contrast, serum and platelet-derived growth factors appear to stimulate guanine nucleotide exchange. | lld:pubmed |
| pubmed-article:1496380 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:1496380 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:1496380 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1496380 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:1496380 | pubmed:issn | 0036-8075 | lld:pubmed |
| pubmed-article:1496380 | pubmed:author | pubmed-author:LowyD RDR | lld:pubmed |
| pubmed-article:1496380 | pubmed:author | pubmed-author:PapageorgeA... | lld:pubmed |
| pubmed-article:1496380 | pubmed:author | pubmed-author:ZhangKK | lld:pubmed |
| pubmed-article:1496380 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1496380 | pubmed:day | 31 | lld:pubmed |
| pubmed-article:1496380 | pubmed:volume | 257 | lld:pubmed |
| pubmed-article:1496380 | pubmed:geneSymbol | c-ras | lld:pubmed |
| pubmed-article:1496380 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1496380 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1496380 | pubmed:pagination | 671-4 | lld:pubmed |
| pubmed-article:1496380 | pubmed:dateRevised | 2007-3-19 | lld:pubmed |
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| pubmed-article:1496380 | pubmed:year | 1992 | lld:pubmed |
| pubmed-article:1496380 | pubmed:articleTitle | Mechanistic aspects of signaling through Ras in NIH 3T3 cells. | lld:pubmed |
| pubmed-article:1496380 | pubmed:affiliation | Laboratory of Cellular Oncology, National Cancer Institute, Bethesda, MD 20892. | lld:pubmed |
| pubmed-article:1496380 | pubmed:publicationType | Journal Article | lld:pubmed |
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