| pubmed-article:10918589 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10918589 | lifeskim:mentions | umls-concept:C0086661 | lld:lifeskim |
| pubmed-article:10918589 | lifeskim:mentions | umls-concept:C0016030 | lld:lifeskim |
| pubmed-article:10918589 | lifeskim:mentions | umls-concept:C0017337 | lld:lifeskim |
| pubmed-article:10918589 | lifeskim:mentions | umls-concept:C0031437 | lld:lifeskim |
| pubmed-article:10918589 | lifeskim:mentions | umls-concept:C0813145 | lld:lifeskim |
| pubmed-article:10918589 | lifeskim:mentions | umls-concept:C0018270 | lld:lifeskim |
| pubmed-article:10918589 | lifeskim:mentions | umls-concept:C0439834 | lld:lifeskim |
| pubmed-article:10918589 | lifeskim:mentions | umls-concept:C0456148 | lld:lifeskim |
| pubmed-article:10918589 | pubmed:issue | 29 | lld:pubmed |
| pubmed-article:10918589 | pubmed:dateCreated | 2000-8-16 | lld:pubmed |
| pubmed-article:10918589 | pubmed:abstractText | The c-myc gene is frequently over-expressed in human cancers and is involved in regulation of proliferation, differentiation and apoptosis. c-Myc is a transcription factor that acts primarily by regulating the expression of other genes. However, it has been very difficult to identify bona fide c-Myc target genes that explain its diverse biological activities. The recent generation of c-myc deficient Rat1A fibroblasts with a profound and stable growth defect provides a new system to search for genes that can substitute for c-myc in proliferation. In this study, we have attempted to identify genes that rescue the slow growth phenotype of c-myc null cells through introduction of a series of potent cell cycle regulatory genes and several retroviral cDNA expression libraries. None of the candidate genes tested, including SV40 T-antigen and adenovirus E1A, caused reversal of the c-myc null growth defect. Furthermore, extensive screens with high-complexity retroviral cDNA libraries from three different tissue sources revealed that only c-myc and N-myc rescued the c-myc null slow-growth phenotype. Our data support the notion that there are no functional equivalents of the myc family of proto-oncogenes and also suggest that there are no c-Myc-activated genes that alone can substitute for c-Myc in control of cell proliferation. | lld:pubmed |
| pubmed-article:10918589 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10918589 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10918589 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10918589 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:10918589 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:10918589 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10918589 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10918589 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:10918589 | pubmed:issn | 0950-9232 | lld:pubmed |
| pubmed-article:10918589 | pubmed:author | pubmed-author:KonKK | lld:pubmed |
| pubmed-article:10918589 | pubmed:author | pubmed-author:BernardsRR | lld:pubmed |
| pubmed-article:10918589 | pubmed:author | pubmed-author:DaleyG QGQ | lld:pubmed |
| pubmed-article:10918589 | pubmed:author | pubmed-author:BerntJJ | lld:pubmed |
| pubmed-article:10918589 | pubmed:author | pubmed-author:HijmansE MEM | lld:pubmed |
| pubmed-article:10918589 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10918589 | pubmed:day | 6 | lld:pubmed |
| pubmed-article:10918589 | pubmed:volume | 19 | lld:pubmed |
| pubmed-article:10918589 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10918589 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10918589 | pubmed:pagination | 3330-4 | lld:pubmed |
| pubmed-article:10918589 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:10918589 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:10918589 | pubmed:articleTitle | A genetic screen to identify genes that rescue the slow growth phenotype of c-myc null fibroblasts. | lld:pubmed |
| pubmed-article:10918589 | pubmed:affiliation | Division of Molecular Carcinogenesis, and Center for Biomedical Genetics, The Netherlands Cancer Institute, Amsterdam. | lld:pubmed |
| pubmed-article:10918589 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10918589 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:10918589 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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