c- Src and its role in cystic fibrosis
- Autores
- Massip Copiz, María Macarena; Santa Coloma, Tomás Antonio
- Año de publicación
- 2016
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- 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-1β as intermediate signaling effectors between CFTR and c-Src.
Fil: Massip Copiz, María Macarena. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina
Fil: Santa Coloma, Tomás Antonio. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina - Materia
-
C-Src
Cystic-Fibrosis
Cftr
Intracellular-Chloride
Il-1β
Pp2
Il1rn - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
- Repositorio
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/47765
Ver los metadatos del registro completo
id |
CONICETDig_cd481d4bec65dfe7ce3b9747ce35f7d6 |
---|---|
oai_identifier_str |
oai:ri.conicet.gov.ar:11336/47765 |
network_acronym_str |
CONICETDig |
repository_id_str |
3498 |
network_name_str |
CONICET Digital (CONICET) |
spelling |
c- Src and its role in cystic fibrosisMassip Copiz, María MacarenaSanta Coloma, Tomás AntonioC-SrcCystic-FibrosisCftrIntracellular-ChlorideIl-1βPp2Il1rnhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Cystic 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-1β as intermediate signaling effectors between CFTR and c-Src.Fil: Massip Copiz, María Macarena. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; ArgentinaFil: Santa Coloma, Tomás Antonio. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; ArgentinaElsevier Gmbh2016-10info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/47765Massip Copiz, María Macarena; Santa Coloma, Tomás Antonio; c- Src and its role in cystic fibrosis; Elsevier Gmbh; European Journal Of Cell Biology; 95; 10; 10-2016; 401-4130171-9335CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1016/j.ejcb.2016.08.001info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0171933516300632info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-nd/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:56:34Zoai:ri.conicet.gov.ar:11336/47765instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-03 09:56:34.968CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
dc.title.none.fl_str_mv |
c- Src and its role in cystic fibrosis |
title |
c- Src and its role in cystic fibrosis |
spellingShingle |
c- Src and its role in cystic fibrosis Massip Copiz, María Macarena C-Src Cystic-Fibrosis Cftr Intracellular-Chloride Il-1β Pp2 Il1rn |
title_short |
c- Src and its role in cystic fibrosis |
title_full |
c- Src and its role in cystic fibrosis |
title_fullStr |
c- Src and its role in cystic fibrosis |
title_full_unstemmed |
c- Src and its role in cystic fibrosis |
title_sort |
c- Src and its role in cystic fibrosis |
dc.creator.none.fl_str_mv |
Massip Copiz, María Macarena Santa Coloma, Tomás Antonio |
author |
Massip Copiz, María Macarena |
author_facet |
Massip Copiz, María Macarena Santa Coloma, Tomás Antonio |
author_role |
author |
author2 |
Santa Coloma, Tomás Antonio |
author2_role |
author |
dc.subject.none.fl_str_mv |
C-Src Cystic-Fibrosis Cftr Intracellular-Chloride Il-1β Pp2 Il1rn |
topic |
C-Src Cystic-Fibrosis Cftr Intracellular-Chloride Il-1β Pp2 Il1rn |
purl_subject.fl_str_mv |
https://purl.org/becyt/ford/1.6 https://purl.org/becyt/ford/1 |
dc.description.none.fl_txt_mv |
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-1β as intermediate signaling effectors between CFTR and c-Src. Fil: Massip Copiz, María Macarena. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina Fil: Santa Coloma, Tomás Antonio. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina |
description |
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-1β as intermediate signaling effectors between CFTR and c-Src. |
publishDate |
2016 |
dc.date.none.fl_str_mv |
2016-10 |
dc.type.none.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion http://purl.org/coar/resource_type/c_6501 info:ar-repo/semantics/articulo |
format |
article |
status_str |
publishedVersion |
dc.identifier.none.fl_str_mv |
http://hdl.handle.net/11336/47765 Massip Copiz, María Macarena; Santa Coloma, Tomás Antonio; c- Src and its role in cystic fibrosis; Elsevier Gmbh; European Journal Of Cell Biology; 95; 10; 10-2016; 401-413 0171-9335 CONICET Digital CONICET |
url |
http://hdl.handle.net/11336/47765 |
identifier_str_mv |
Massip Copiz, María Macarena; Santa Coloma, Tomás Antonio; c- Src and its role in cystic fibrosis; Elsevier Gmbh; European Journal Of Cell Biology; 95; 10; 10-2016; 401-413 0171-9335 CONICET Digital CONICET |
dc.language.none.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
info:eu-repo/semantics/altIdentifier/doi/10.1016/j.ejcb.2016.08.001 info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0171933516300632 |
dc.rights.none.fl_str_mv |
info:eu-repo/semantics/openAccess https://creativecommons.org/licenses/by-nc-nd/2.5/ar/ |
eu_rights_str_mv |
openAccess |
rights_invalid_str_mv |
https://creativecommons.org/licenses/by-nc-nd/2.5/ar/ |
dc.format.none.fl_str_mv |
application/pdf application/pdf application/pdf |
dc.publisher.none.fl_str_mv |
Elsevier Gmbh |
publisher.none.fl_str_mv |
Elsevier Gmbh |
dc.source.none.fl_str_mv |
reponame:CONICET Digital (CONICET) instname:Consejo Nacional de Investigaciones Científicas y Técnicas |
reponame_str |
CONICET Digital (CONICET) |
collection |
CONICET Digital (CONICET) |
instname_str |
Consejo Nacional de Investigaciones Científicas y Técnicas |
repository.name.fl_str_mv |
CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas |
repository.mail.fl_str_mv |
dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar |
_version_ |
1842269410656518144 |
score |
13.13397 |