| pubmed-article:12393009 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12393009 | lifeskim:mentions | umls-concept:C0007586 | lld:lifeskim |
| pubmed-article:12393009 | lifeskim:mentions | umls-concept:C1705165 | lld:lifeskim |
| pubmed-article:12393009 | lifeskim:mentions | umls-concept:C1707719 | lld:lifeskim |
| pubmed-article:12393009 | lifeskim:mentions | umls-concept:C2700061 | lld:lifeskim |
| pubmed-article:12393009 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:12393009 | pubmed:dateCreated | 2002-10-23 | lld:pubmed |
| pubmed-article:12393009 | pubmed:abstractText | CDK-cyclin complexes are the universal drivers of cell cycle transitions. Progression through G(1) and transition to S-phase, thereby initiating genome duplication, requires the concerted action of cyclin-dependent kinase (CDK)-cyclin complexes on specific targets. These targets belong to at least two major regulatory networks: the retinoblastoma-related (RBR)/E2F pathway and complexes that are responsible for the initiation of DNA replication. The G(1) phase is central to the integration of signals that regulate both the exit from the cell division cycle to differentiation and the reactivation of cell proliferation. Cellular factors that are involved in these pathways play a role in regulating cell size and number, and organogenesis. As a consequence, they are also involved in determining plant architecture. | lld:pubmed |
| pubmed-article:12393009 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12393009 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12393009 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:12393009 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12393009 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:12393009 | pubmed:issn | 1369-5266 | lld:pubmed |
| pubmed-article:12393009 | pubmed:author | pubmed-author:CastellanoM... | lld:pubmed |
| pubmed-article:12393009 | pubmed:author | pubmed-author:GutierrezCris... | lld:pubmed |
| pubmed-article:12393009 | pubmed:author | pubmed-author:Ramirez-Parra... | lld:pubmed |
| pubmed-article:12393009 | pubmed:author | pubmed-author:del PozoJ... | lld:pubmed |
| pubmed-article:12393009 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12393009 | pubmed:volume | 5 | lld:pubmed |
| pubmed-article:12393009 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12393009 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12393009 | pubmed:pagination | 480-6 | lld:pubmed |
| pubmed-article:12393009 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:12393009 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:12393009 | pubmed:articleTitle | G(1) to S transition: more than a cell cycle engine switch. | lld:pubmed |
| pubmed-article:12393009 | pubmed:affiliation | Centro de Biologia Molecular 'Severo Ochoa', Consejo Superior de Investigaciones Científicas and Universidad Autónoma de Madrid, Cantoblanco, 28049, Madrid, Spain. cgutierrez@cbm.uam.es | lld:pubmed |
| pubmed-article:12393009 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12393009 | pubmed:publicationType | Review | lld:pubmed |
| pubmed-article:12393009 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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