期刊
EUROPEAN JOURNAL OF CELL BIOLOGY
卷 95, 期 10, 页码 401-413出版社
ELSEVIER GMBH
DOI: 10.1016/j.ejcb.2016.08.001
关键词
c-Src; Cystic fibrosis; CFTR; Intracellular chloride; IL-1 beta; PP2; IL1RN
类别
资金
- National Agency for the Promotion of Science and Technology (ANPCYT) [PICT 2012-1278]
- National Research Council for Science and Technology of Argentina (CONICET) [PIP 2012-0685]
- Pontifical Catholic University of Argentina
- National Research Council of Argentina (CONICET)
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 beta as intermediate signaling effectors between CFTR and c-Src. (C) 2016 Elsevier GmbH. All rights reserved.
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