Depósito Digital de Documentos de la UAB Encontrados 4 registros  La búsqueda tardó 0.02 segundos. 
1.
11 p, 1.0 MB Cardiomyocyte hypertrophy induced by Endonuclease G deficiency requires reactive oxygen radicals accumulation and is inhibitable by the micropeptide humanin / Blasco, Natividad (Cell Signaling and Apoptosis group, Universitat de Lleida - IRBLleida, Lleida, Spain) ; Cámara, Yolanda (Research Group on Neuromuscular and Mitochondrial Diseases, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona and CIBERER, Barcelona, Spain) ; Núñez, Estefanía (Cardiovascular Proteomics group, Spanish National Center for Cardiovascular Research (CNIC) and CIBERCV Madrid, Spain) ; Beà, Aida (Cell Signaling and Apoptosis group, Universitat de Lleida - IRBLleida, Lleida, Spain) ; Barés, Gisel (Cell Signaling and Apoptosis group, Universitat de Lleida - IRBLleida, Lleida, Spain) ; Forné, Carles (Biostatistics Unit, IRBLleida, Universitat de Lleida, Lleida, Spain) ; Ruíz-Meana, Marisol (Cardiovascular Diseases Research Group, VHIR and CIBERCV, Barcelona, Spain) ; Girón, Cristina (Cell Signaling and Apoptosis group, Universitat de Lleida - IRBLleida, Lleida, Spain) ; Barba, Ignasi (Cardiovascular Diseases Research Group, VHIR and CIBERCV, Barcelona, Spain) ; García-Arumí, Elena (Research Group on Neuromuscular and Mitochondrial Diseases, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona and CIBERER, Barcelona, Spain) ; García Dorado, David (Cardiovascular Diseases Research Group, VHIR and CIBERCV, Barcelona, Spain) ; Vázquez, Jesús (Cardiovascular Proteomics group, Spanish National Center for Cardiovascular Research (CNIC) and CIBERCV Madrid, Spain) ; Martí, Ramon (Research Group on Neuromuscular and Mitochondrial Diseases, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona and CIBERER, Barcelona, Spain) ; Llovera, Marta (Cell Signaling and Apoptosis group, Universitat de Lleida - IRBLleida, Lleida, Spain) ; Sanchis, Daniel (Cell Signaling and Apoptosis group, Universitat de Lleida - IRBLleida, Lleida, Spain)
The endonuclease G gene (Endog), which codes for a mitochondrial nuclease, was identified as a determinant of cardiac hypertrophy. How ENDOG controls cardiomyocyte growth is still unknown. Thus, we aimed at finding the link between ENDOG activity and cardiomyocyte growth. [...]
2018 - 10.1016/j.redox.2018.02.021
Redox Biology, Vol. 16 (march 2018) , p. 146-156  
2.
16 p, 2.3 MB Iron-loaded transferrin (Tf) is detrimental whereas iron-free Tf confers protection against brain ischemia by modifying blood Tf saturation and subsequent neuronal damage / Gregorio-Rocasolano Barbany, Núria de (Institut Germans Trias i Pujol) ; Martí Sistac, Octavi (Universitat Autònoma de Barcelona) ; Ponce, Jovita (Institut Germans Trias i Pujol) ; Castelló Ruiz, María (Institut d'Investigació Sanitària La Fe) ; Millán Torné, Mònica (Hospital Universitari Germans Trias i Pujol. Departament de Neurocències) ; Guirao, Verónica (Institut Germans Trias i Pujol) ; García Yébenes, Isaac (Universidad Complutense de Madrid. Departamento de Farmacología) ; Salom, Juan B. (Institut d'Investigació Sanitària La Fe) ; Ramos Cabrer, Pedro (Hospital Clínico Universitario de Santiago. Departamento de Neurología) ; Alborch, Enrique (Institut d'Investigació Sanitària La Fe) ; Lizasoain, Ignacio (Universidad Complutense de Madrid. Departamento de Farmacología) ; Castillo, José (Hospital Clínico Universitario de Santiago. Departamento de Neurología) ; Dávalos, Antoni (Hospital Universitari Germans Trias i Pujol. Departament de Neurocències) ; Gasull Dalmau, Teresa (Institut Germans Trias i Pujol)
Despite transferrin being the main circulating carrier of iron in body fluids, and iron overload conditions being known to worsen stroke outcome through reactive oxygen species (ROS)-induced damage, the contribution of blood transferrin saturation (TSAT) to stroke brain damage is unknown. [...]
2018 - 10.1016/j.redox.2017.11.026
Redox biology, Vol. 15 (May 2018) , p. 143-158  
3.
10 p, 1.2 MB A single cysteine post-translational oxidation suffices to compromise globular proteins kinetic stability and promote amyloid formation / Marinelli, Patrizia (Institut de Biotecnologia i de Biomedicina "Vicent Villar Palasí") ; Navarro, Susanna (Universitat Autònoma de Barcelona. Departament de Bioquímica i Biologia Molecular) ; Graña Montes, Ricardo (Institut de Biotecnologia i de Biomedicina "Vicent Villar Palasí") ; Bañó-Polo, Manuel (Institut de Biotecnologia i de Biomedicina "Vicent Villar Palasí") ; Fernández Gallegos, Ma. Rosario (María Rosario) (Institut de Biotecnologia i de Biomedicina "Vicent Villar Palasí") ; Papaleo, Elena (Kræftens Bekæmpelse) ; Ventura i Zamora, Salvador (Institut de Biotecnologia i de Biomedicina "Vicent Villar Palasí")
Oxidatively modified forms of proteins accumulate during aging. Oxidized protein conformers might act as intermediates in the formation of amyloids in age-related disorders. However, it is not known whether this amyloidogenic conversion requires an extensive protein oxidative damage or it can be promoted just by a discrete, localized post-translational modification of certain residues. [...]
2017 - 10.1016/j.redox.2017.10.022
Redox Biology, Vol. 14 (April 2018) , p. 566-575  
4.
13 p, 1.1 MB Protein aggregation into insoluble deposits protects from oxidative stress / Carija, Anita (Institut de Biotecnologia i de Biomedicina "Vicent Villar Palasí") ; Navarro, Susanna (Universitat Autònoma de Barcelona. Departament de Bioquímica i Biomedicina Molecular) ; Sánchez de Groot, Natalia (Centre de Regulació Genòmica) ; Ventura i Zamora, Salvador (Institut de Biotecnologia i de Biomedicina "Vicent Villar Palasí")
Protein misfolding and aggregation have been associated with the onset of neurodegenerative disorders. Recent studies demonstrate that the aggregation process can result in a high diversity of protein conformational states, however the identity of the specific species responsible for the cellular damage is still unclear. [...]
2017 - 10.1016/j.redox.2017.03.027
Redox Biology, Vol. 12 (Aug. 2017) , p. 699-711  

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