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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
1993-1-27
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pubmed:abstractText |
The carboxy-terminal part of the Saccharomyces cerevisiae SDC25 gene product (SDC25 C domain) can elicit activation of mammalian Ras proteins. Specifically, SDC25 C domain functions as an exchange factor for cellular Ras proteins in CHO cells. In this study, we used the dominant inhibitory Ha-Ras Asn-17 mutant and SDC25 C domain to further investigate the interaction between cellular Ras proteins and their putative endogenous guanine nucleotide-releasing factors. Transcription from the polyomavirus thymidine kinase gene (Py tk) promoter is strongly inhibited by the expression of Ha-Ras Asn-17 in NIH 3T3 cells. Coexpression of SDC25 C domain overcomes the negative effect of the Ras mutant on the Py tk promoter. On the other hand, transactivation of the Ras-responsive element of the Py tk promoter induced by SDC25 C domain is lost upon coexpression of increasing amounts of Ha-Ras Asn-17. In addition, coexpression of SDC25 C domain overcomes the inhibition of proliferation of NIH 3T3 cells caused by Ha-Ras Asn-17. These results are consistent with the idea that the Ha-Ras Asn-17 mutant functions by titrating an upstream activator of cellular Ras proteins.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-1312392,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-1312393,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-1317056,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-1372395,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-1376246,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-1379346,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-1386920,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-1553544,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-1608472,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-1631150,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-1689011,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-1826565,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-1901951,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-1907371,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-1922022,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-2000228,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-2022184,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-2072908,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-2118993,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-2118994,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-2121370,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-2121371,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-2122974,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-2181667,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-2188363,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-2188736,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-2198577,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-2201921,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-2403524,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-2480526,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-2545538,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-2550807,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-2651897,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-2821624,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-2833702,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-2833817,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-3043178,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-3145408,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8380225-3545497
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0270-7306
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
13
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pubmed:geneSymbol |
SDC25
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
39-43
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:8380225-3T3 Cells,
pubmed-meshheading:8380225-Animals,
pubmed-meshheading:8380225-Cell Division,
pubmed-meshheading:8380225-Enhancer Elements, Genetic,
pubmed-meshheading:8380225-Fungal Proteins,
pubmed-meshheading:8380225-GTP-Binding Proteins,
pubmed-meshheading:8380225-Gene Expression Regulation,
pubmed-meshheading:8380225-Genes, Dominant,
pubmed-meshheading:8380225-Genes, ras,
pubmed-meshheading:8380225-Guanine Nucleotides,
pubmed-meshheading:8380225-Mice,
pubmed-meshheading:8380225-Polyomavirus,
pubmed-meshheading:8380225-Proto-Oncogene Proteins p21(ras),
pubmed-meshheading:8380225-Recombinant Proteins,
pubmed-meshheading:8380225-Saccharomyces cerevisiae,
pubmed-meshheading:8380225-Structure-Activity Relationship,
pubmed-meshheading:8380225-Transcription, Genetic,
pubmed-meshheading:8380225-Transfection,
pubmed-meshheading:8380225-rap GTP-Binding Proteins
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pubmed:year |
1993
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pubmed:articleTitle |
The Saccharomyces cerevisiae SDC25 C-domain gene product overcomes the dominant inhibitory activity of Ha-Ras Asn-17.
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pubmed:affiliation |
Dana-Farber Cancer Institute, Boston, Massachusetts.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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