c- Src and its role in cystic fibrosis
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 the...
Guardado en:
| Autores principales: | , |
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| Formato: | Artículo |
| Lenguaje: | Inglés |
| Publicado: |
Elsevier
2022
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| Materias: | |
| Acceso en línea: | https://repositorio.uca.edu.ar/handle/123456789/14562 |
| Aporte de: |
| Sumario: | 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. |
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