| pubmed-article:3517865 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:3517865 | lifeskim:mentions | umls-concept:C1510411 | lld:lifeskim |
| pubmed-article:3517865 | lifeskim:mentions | umls-concept:C0009221 | lld:lifeskim |
| pubmed-article:3517865 | lifeskim:mentions | umls-concept:C0034677 | lld:lifeskim |
| pubmed-article:3517865 | lifeskim:mentions | umls-concept:C0596988 | lld:lifeskim |
| pubmed-article:3517865 | lifeskim:mentions | umls-concept:C1706395 | lld:lifeskim |
| pubmed-article:3517865 | lifeskim:mentions | umls-concept:C0015295 | lld:lifeskim |
| pubmed-article:3517865 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:3517865 | pubmed:issue | 8 | lld:pubmed |
| pubmed-article:3517865 | pubmed:dateCreated | 1986-5-23 | lld:pubmed |
| pubmed-article:3517865 | pubmed:abstractText | The hypothesis is tested that the ras gene of Harvey sarcoma virus (Ha-SV) and the proto-ras DNAs from certain tumor cells derive transforming function from specific codons in which they differ from normal proto-ras genes. Molecularly cloned Harvey proviral vectors carrying viral ras, normal rat proto-ras, and recombinant ras genes in which the virus-specific ras codons 12 and 59 were replaced by proto-ras equivalents each transformed aneuploid mouse 3T3 cells after latent periods that ranged from 4 to 10 days. Viruses with or without virus-specific ras codons all transformed diploid rat cells in 3-5 days equally well. However, in the absence of virus replication, mutant codons were beneficial for transforming function. Deletion of non-ras regions of Ha-SV did not affect transforming function. We conclude that specific ras codons are not necessary for transforming function. Comparisons of the ras sequences of Ha-SV, BALB SV, and Rasheed SV with sequences of proto-ras genes from rat and man revealed an upstream proto-ras exon, termed exon -1. The 3' end of this exon is present in all three viruses and in a ras pseudogene of the rat. Since ras genes transform without mutation and since exon -1 is truncated in viral ras genes and all transforming proto-ras DNAs of the Harvey and the Kirsten ras family, we propose that ras genes are activated by truncation of exon -1 either via viral transduction or artificially via cloning and transfection. The proposal implies that untruncated proto-ras genes with point mutations may not be cellular cancer genes. | lld:pubmed |
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| pubmed-article:3517865 | pubmed:language | eng | lld:pubmed |
| pubmed-article:3517865 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:3517865 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:3517865 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:3517865 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:3517865 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:3517865 | pubmed:author | pubmed-author:DuesbergP HPH | lld:pubmed |
| pubmed-article:3517865 | pubmed:author | pubmed-author:CichutekKK | lld:pubmed |
| pubmed-article:3517865 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:3517865 | pubmed:volume | 83 | lld:pubmed |
| pubmed-article:3517865 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:3517865 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:3517865 | pubmed:pagination | 2340-4 | lld:pubmed |
| pubmed-article:3517865 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:3517865 | pubmed:year | 1986 | lld:pubmed |
| pubmed-article:3517865 | pubmed:articleTitle | Harvey ras genes transform without mutant codons, apparently activated by truncation of a 5' exon (exon -1). | lld:pubmed |
| pubmed-article:3517865 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:3517865 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:3517865 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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