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Experimental & Molecular Medicine ; : 495-504, 2008.
Artículo en Inglés | WPRIM | ID: wpr-84653

RESUMEN

Exposure to light can induce photoreceptor cell death and exacerbate retinal degeneration. In this study, mice with genetic knockout of several genes, including rhodopsin kinase (Rhok-/-), arrestin (Sag-/-), transducin (Gnat1-/-), c-Fos (c-Fos-/-) and arrestin/transducin (Sag-/-/Gnat1-/-), were examined. We measured the expression levels of thousands of genes in order to investigate their roles in phototransduction signaling in light-induced retinal degeneration using DNA microarray technology and then further explored the gene network using pathway analysis tools. Several cascades of gene components were induced or inhibited as a result of corresponding gene knockout under specific light conditions. Transducin deletion blocked the apoptotic signaling induced by exposure to low light conditions, and it did not require c-Fos/AP-1. Deletion of c-Fos blocked the apoptotic signaling induced by exposure to high intensity light. In the present study, we identified many gene transcripts that are essential for the initiation of light-induced rod degeneration and proposed several important networks that are involved in pro- and anti-apoptotic signaling. We also demonstrated the different cascades of gene components that participate in apoptotic signaling under specific light conditions.


Asunto(s)
Animales , Ratones , Apoptosis/efectos de la radiación , Quinasa 1 del Receptor Acoplado a Proteína-G/genética , Subunidades alfa de la Proteína de Unión al GTP/genética , Perfilación de la Expresión Génica , Genes fos/genética , Luz/efectos adversos , Fototransducción/genética , Ratones Noqueados , Análisis de Secuencia por Matrices de Oligonucleótidos , Retina/metabolismo , Degeneración Retiniana/etiología , Transducina/genética
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