Induction of p19INK4d in response to ultraviolet light improves DNA repair and confers resistance to apoptosis in neuroblastoma cells

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The genetic instability driving tumorigenesis is fuelled by DNA damage and by errors made by the DNA replication. Upon DNA damage the cell organizes an integrated response not only by the classical DNA repair mechanisms but also involving mechanisms of replication, transcription, chromatin structure...

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Detalles Bibliográficos
Autores principales: Ceruti, J.M., Scassa, M.E., Flo, J.M., Varone, C.L., Cánepa, E.T.
Formato: Artículo publishedVersion
Lenguaje:Inglés
Publicado: 2005
Materias:
Apoptosis
CDK4/6
DNA repair
INK4
Neuroblastoma
UV
caspase 3
DNA
DNA fragment
RNA
animal cell
apoptosis
article
cell cycle
cell strain BHK
chromatin structure
controlled study
DNA damage
DNA replication
DNA synthesis
enzyme activity
human
human cell
immunofluorescence
immunoprecipitation
neuroblastoma cell
nonhuman
Northern blotting
polyacrylamide gel electrophoresis
priority journal
protein expression
ultraviolet radiation
Western blotting
Animals
Cell Cycle
Cell Cycle Proteins
Cell Line, Tumor
Cyclin-Dependent Kinase Inhibitor p19
DNA Damage
DNA Repair
DNA Replication
G1 Phase
Humans
Kinetics
Mice
Protein Transport
RNA, Messenger
RNA, Neoplasm
Ultraviolet Rays
Acceso en línea:http://hdl.handle.net/20.500.12110/paper_09509232_v24_n25_p4065_Ceruti
Aporte de:
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires

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