أعرض تسجيلة المادة بشكل مبسط
| 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 |
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| 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). |
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| 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). |
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| dc.description |
[Conclusions] These data suggest that -838A is associated with reduced p27kip1 promoter activity and increased risk of myocardial infarction. |
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| 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 |
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| dc.type |
Artículo |
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أعرض تسجيلة المادة بشكل مبسط