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Título : | c- Src and its role in cystic fibrosis | Autor : | Massip Copiz, María Macarena Santa Coloma, Tomás Antonio |
Palabras clave : | FIBROSIS QUISTICA; GENES; CLORURO INTRACELULAR; REGULADOR DE CONDUCTANCIA DE TRANSMEMBRANA DE FIBROSIS QUISTICA | Fecha de publicación : | 2016 | Editorial : | Elsevier | Cita : | Massip Copiz, M. M., Santa Coloma, T. A. c- Src and its role in cystic fibrosis [en línea]. European Journal of Cell Biology. 2016, 95 (10). doi: https://doi.org/10.1016/j.ejcb.2016.08.001. Disponible en: https://repositorio.uca.edu.ar/handle/123456789/14562 | Resumen : | Abstract: Cystic fibrosis (CF) is a lethal inherited disease produced by mutations in the gene encoding the CFTR chloride channel. Loss of function in the CFTR gene is associated with a not much noticed increased expression and activity of the non-receptor protein-tyrosine kinase c-Src. CF is therefore the result from the loss of CFTR chloride transport function and its consequences, including a chronic and excessive c-Src signaling. On the other hand, c-Src, encoded by the SRC gene, is involved in diverse signaling mechanisms that regulate key cellular functions such as cell proliferation, apoptosis, oxidative stress, inflammation, and innate immunity. These c-Src-regulated cellular functions are also affected in CF; however, studies exploring a direct role of c-Src in the regulation of these cellular functions in CF are yet scarce and often controversial. Here we describe the c-Src regulation and functions, with emphasis in those altered in CF, and describe the role of CFTR as a “signaling molecule” that negatively modulates c-Src expression and activity. It is also discussed the emerging role of intracellular Cl− and IL-1 as intermediate signaling effectors between CFTR and c-Src. | URI : | https://repositorio.uca.edu.ar/handle/123456789/14562 | ISSN : | 0070-2463 (online) 0171-9335 |
Disciplina: | MEDICINA | DOI: | 10.1016/j.ejcb.2016.08.001 | Derechos: | Acceso abierto |
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