Cargando…
DNA damage-induced cellular senescence is sufficient to suppress tumorigenesis: a mouse model
Tumor suppressor p53-dependent apoptosis is critical in suppressing tumorigenesis. Previously, we reported that DNA double-strand breaks (DSBs) at the V(D)J recombination loci induced genomic instability in the developing lymphocytes of nonhomologous end-joining (NHEJ)–deficient, p53-deficient mice,...
Autores principales: | Van Nguyen, Thang, Puebla-Osorio, Nahum, Pang, Hui, Dujka, Melanie E., Zhu, Chengming |
---|---|
Formato: | Texto |
Lenguaje: | English |
Publicado: |
The Rockefeller University Press
2007
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2118600/ https://www.ncbi.nlm.nih.gov/pubmed/17535972 http://dx.doi.org/10.1084/jem.20062453 |
Ejemplares similares
-
The Yin-Yang of DNA Damage Response: Roles in Tumorigenesis and Cellular Senescence
por: Li, Xiaoman, et al.
Publicado: (2013) -
Absence of p53-Dependent Apoptosis Combined With Nonhomologous End-Joining Deficiency Leads to a Severe Diabetic Phenotype in Mice
por: Tavana, Omid, et al.
Publicado: (2010) -
Cellular Plasticity: A Route to Senescence Exit and Tumorigenesis
por: De Blander, Hadrien, et al.
Publicado: (2021) -
DNA Damage, Cellular Senescence in Health and Disease
por: Neidernhofer, Laura
Publicado: (2020) -
Ku70 Functions in Addition to Nonhomologous End Joining in Pancreatic β-Cells: A Connection to β-Catenin Regulation
por: Tavana, Omid, et al.
Publicado: (2013)