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| DC Field | Value | Language |
|---|---|---|
| dc.creator | González, Pelayo | - |
| dc.creator | Díez-Juan, Antonio | - |
| dc.creator | Coto, Eliecer | - |
| dc.creator | Victoria, Álvarez | - |
| dc.creator | Reguero, Julian R. | - |
| dc.creator | Batalla, Alberto | - |
| dc.creator | Andrés, Vicente | - |
| dc.date | 2007-05-08T15:59:36Z | - |
| dc.date | 2007-05-08T15:59:36Z | - |
| dc.date | 2004-04-02 | - |
| dc.date.accessioned | 2017-01-31T00:57:12Z | - |
| dc.date.available | 2017-01-31T00:57:12Z | - |
| dc.identifier | BMC Biology 2004, 2:5 | - |
| dc.identifier | 1741-7007 | - |
| dc.identifier | http://hdl.handle.net/10261/1441 | - |
| dc.identifier.uri | http://dspace.mediu.edu.my:8181/xmlui/handle/10261/1441 | - |
| dc.description | This article is available from: http://www.biomedcentral.com/1741-7007/2/5 | - |
| dc.description | [Background] Excessive proliferation of vascular smooth muscle cells and leukocytes within the artery wall is a major event in the development of atherosclerosis. The growth suppressor p27kip1 associates with several cyclin-dependent kinase/cyclin complexes, thereby abrogating their capacity to induce progression through the cell cycle. Recent studies have implicated p27kip1 in the control of neointimal hyperplasia. For instance, p27kip1 ablation in apolipoprotein-E-null mice enhanced arterial cell proliferation and accelerated atherogenesis induced by dietary cholesterol. Therefore, p27kip1 is a candidate gene to modify the risk of developing atherosclerosis and associated ischaemic events (i.e., myocardial infarction and stroke). | - |
| dc.description | [Results] In this study we found three common single-nucleotide polymorphisms in the human p27kip1 gene (+326T>G [V109G], -79C>T, and -838C>A). The frequency of -838A carriers was significantly increased in myocardial infarction patients compared to healthy controls (odds ratio [OR] = 1.73, 95% confidence interval [95%CI] = 1.12–2.70). In addition, luciferase reporter constructs driven by the human p27kip1 gene promoter containing A at position -838 had decreased basal transcriptional activity when transiently transfected in Jurkat cells, compared with constructs bearing C in -838 (P = 0.04). | - |
| dc.description | [Conclusions] These data suggest that -838A is associated with reduced p27kip1 promoter activity and increased risk of myocardial infarction. | - |
| dc.description | PG was the recipient of a fellowship from the Fundación para el Fomento en Asturias de la Investigación Científica Aplicada y Tecnológica (FICYT, BP 01-082). AD-J received salary support from Fondo Social Europeo (CSICPrograma I3P). This work was supported by grants from the Spanish Fondo de Investigaciones Sanitarias to EC (FIS 03/05) and from the Spanish Ministry of Science and Technology and Fondo Europeo de Desarrollo Regional to VAndrés (SAF2002-1443). | - |
| dc.description | Peer reviewed | - |
| dc.language | eng | - |
| dc.publisher | BioMed Central | - |
| dc.relation | Publisher’s version | - |
| dc.rights | openAccess | - |
| dc.title | A single-nucleotide polymorphism in the human p27kip1 gene (-838C>A) affects basal promoter activity and the risk of myocardial infarction | - |
| dc.type | Artículo | - |
| Appears in Collections: | Digital Csic | |
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