TY  - JOUR
AU  - Murga, Matilde
AU  - Bunting, Samuel
AU  - Montaña, Maria F
AU  - Soria, Rebeca
AU  - Mulero, Francisca
AU  - Cañamero, Marta
AU  - Lee, Youngsoo
AU  - McKinnon, Peter J
AU  - Nussenzweig, Andre
AU  - Fernandez-Capetillo, Oscar
PY  - 2009
DO  - 10.1038/ng.420
UR  - http://hdl.handle.net/20.500.12105/17685
AB  - Although DNA damage is considered a driving force for aging, the nature of the damage that arises endogenously remains unclear. Replicative stress, a source of endogenous DNA damage, is prevented primarily by the ATR kinase. We have developed a mouse...
LA  - eng
PB  - Nature Publishing Group
KW  - DNA Replication
KW  - Stress, Physiological
KW  - Abnormalities, Multiple
KW  - Aging
KW  - Alleles
KW  - Animals
KW  - Apoptosis
KW  - Ataxia Telangiectasia Mutated Proteins
KW  - Brain
KW  - Cell Cycle Proteins
KW  - DNA Damage
KW  - DNA Repair
KW  - DNA-Activated Protein Kinase
KW  - DNA-Binding Proteins
KW  - Disease Models, Animal
KW  - Embryo, Mammalian
KW  - Fibroblasts
KW  - Humans
KW  - Mice
KW  - Nuclear Proteins
KW  - Phenotype
KW  - Progeria
KW  - Protein Kinase Inhibitors
KW  - Protein Serine-Threonine Kinases
KW  - Syndrome
KW  - Tumor Suppressor Protein p53
TI  - A mouse model of ATR-Seckel shows embryonic replicative stress and accelerated aging.
TY  - journal article
ER  -