Atm-null mice exhibit enhanced radiation-induced birth defects and a hybrid form of embryonic programmed cell death indicating a teratological suppressor function for ATM.

The FASEB journal : official publication of the Federation of American Societies for Experimental Biology

Volumn 18, Issue 7, 2004, Pages 896-898

  Laposa, Rebecca R ^a   Henderson, Jeffrey T ^a   Xu, Elaine ^a   Wells, Peter G ^a  

^a UNIVERSITY OF TORONTO   (Canada)

Author keywords

[No Author keywords available]

Indexed keywords

DNA;

ANIMAL; APOPTOSIS; ARTICLE; CELL DEATH; CELL DIVISION; COMPARATIVE STUDY; CONGENITAL MALFORMATION; DNA DAMAGE; DNA REPAIR; EMBRYO; EPITHELIUM CELL; FEMALE; FETUS RESORPTION; GENETICS; GENOTYPE; GESTATIONAL AGE; MALE; MOUSE; MOUSE MUTANT; NECROSIS; NERVE CELL; PATHOLOGY; PREGNANCY; PRENATAL DEVELOPMENT; RADIATION DOSE; RADIATION EXPOSURE; RADIATION RESPONSE; TAIL; TELENCEPHALON; TUMOR SUPPRESSOR GENE;

ABNORMALITIES, RADIATION-INDUCED; ANIMALS; APOPTOSIS; CELL DEATH; CELL DIVISION; DNA; DNA DAMAGE; DNA REPAIR; DOSE-RESPONSE RELATIONSHIP, RADIATION; EMBRYO; EMBRYONIC AND FETAL DEVELOPMENT; EPITHELIAL CELLS; FEMALE; FETAL RESORPTION; GENES, P53; GENOTYPE; GESTATIONAL AGE; MALE; MICE; MICE, KNOCKOUT; NECROSIS; NEURONS; PREGNANCY; RADIATION TOLERANCE; TAIL; TELENCEPHALON;

MLCS; MLOWN;

EID: 3543035181     PISSN: None     EISSN: 15306860     Source Type: Journal    
DOI: 10.1096/fj.03-0903fje     Document Type: Article

References (0)