| pubmed-article:12086860 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12086860 | lifeskim:mentions | umls-concept:C0033684 | lld:lifeskim |
| pubmed-article:12086860 | lifeskim:mentions | umls-concept:C0021467 | lld:lifeskim |
| pubmed-article:12086860 | lifeskim:mentions | umls-concept:C1519692 | lld:lifeskim |
| pubmed-article:12086860 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:12086860 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:12086860 | pubmed:dateCreated | 2002-6-27 | lld:pubmed |
| pubmed-article:12086860 | pubmed:abstractText | Inactivation of the von Hippel-Lindau tumor suppressor gene is linked to the development of hereditary (VHL Disease-associated) and sporadic clear cell carcinoma of the kidney. The VHL gene product, pVHL, targets the heterodimeric transcription factor HIF for polyubiquitination, and restoration of pVHL function in VHL(-/-) renal carcinoma cells suppresses their ability to form tumors in nude mice. Here we show that tumor suppression by pVHL can be overridden by a HIF variant that escapes pVHL control. These studies prove that HIF is a critical downstream target of pVHL and establish that activation of HIF target genes can promote tumorigenesis in vivo. | lld:pubmed |
| pubmed-article:12086860 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12086860 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:12086860 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:12086860 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12086860 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:12086860 | pubmed:issn | 1535-6108 | lld:pubmed |
| pubmed-article:12086860 | pubmed:author | pubmed-author:KondoKeiichiK | lld:pubmed |
| pubmed-article:12086860 | pubmed:author | pubmed-author:KaelinWilliam... | lld:pubmed |
| pubmed-article:12086860 | pubmed:author | pubmed-author:NakamuraEijir... | lld:pubmed |
| pubmed-article:12086860 | pubmed:author | pubmed-author:KlcoJeffJ | lld:pubmed |
| pubmed-article:12086860 | pubmed:author | pubmed-author:LechpammerMir... | lld:pubmed |
| pubmed-article:12086860 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12086860 | pubmed:volume | 1 | lld:pubmed |
| pubmed-article:12086860 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12086860 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12086860 | pubmed:pagination | 237-46 | lld:pubmed |
| pubmed-article:12086860 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:12086860 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:12086860 | pubmed:articleTitle | Inhibition of HIF is necessary for tumor suppression by the von Hippel-Lindau protein. | lld:pubmed |
| pubmed-article:12086860 | pubmed:affiliation | Department of Adult Oncology, Dana-Farber Cancer Institute and Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. | lld:pubmed |
| pubmed-article:12086860 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12086860 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:12086860 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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