pubmed-article:1842342 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:1842342 | lifeskim:mentions | umls-concept:C0018270 | lld:lifeskim |
pubmed-article:1842342 | lifeskim:mentions | umls-concept:C1155872 | lld:lifeskim |
pubmed-article:1842342 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:1842342 | pubmed:dateCreated | 1993-1-4 | lld:pubmed |
pubmed-article:1842342 | pubmed:abstractText | How does a quiescent cell decide to re-enter the cell cycle and start replicating its DNA? What controls cell proliferation? These are fundamental questions that have to be solved in order to understand the mechanisms of oncogenesis. Some recent data have provided clues about how signal transduction pathways may be connected to the cell cycle. A protein kinase cascade starting from the membrane growth factor receptor is thought to be involved in transducing extracellular stimuli to the master switches of the cell cycle control machinery. The recently identified extracellular-signal regulated kinases (ERKs) appear to play an important role in this pathway. Expression of cyclins, which are regulatory subunits of the universal cell cycle oscillator cdc2, may also be controlled through this kinase cascade. The products of tumor suppressor genes Rb and p53 also play an important role in regulating cell proliferation by interfering with the cell cycle pathway. Here, I will review and discuss the importance of these different new results. | lld:pubmed |
pubmed-article:1842342 | pubmed:language | eng | lld:pubmed |
pubmed-article:1842342 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1842342 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:1842342 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1842342 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1842342 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1842342 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1842342 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1842342 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:1842342 | pubmed:month | Aug | lld:pubmed |
pubmed-article:1842342 | pubmed:issn | 1043-4682 | lld:pubmed |
pubmed-article:1842342 | pubmed:author | pubmed-author:DucommunBB | lld:pubmed |
pubmed-article:1842342 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:1842342 | pubmed:volume | 2 | lld:pubmed |
pubmed-article:1842342 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:1842342 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:1842342 | pubmed:pagination | 233-41 | lld:pubmed |
pubmed-article:1842342 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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pubmed-article:1842342 | pubmed:year | 1991 | lld:pubmed |
pubmed-article:1842342 | pubmed:articleTitle | From growth to cell cycle control. | lld:pubmed |
pubmed-article:1842342 | pubmed:affiliation | E.M.B.L. Differentiation Programme, Heidelberg, Germany. | lld:pubmed |
pubmed-article:1842342 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:1842342 | pubmed:publicationType | Review | lld:pubmed |
http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:1842342 | lld:pubmed |