Nucleostemin deletion reveals an essential mechanism that maintains the genomic stability of stem and progenitor cells

Proceedings of the National Academy of Sciences of the United States of America

Volumn 110, Issue 28, 2013, Pages 11415-11420

  Meng, Lingjun ^a   Lin, Tao ^a   Peng, Guang ^b   Hsu, Joseph K ^a   Lee, Sun ^a   Lin, Shiaw Yih ^b   Tsai, Robert Y L ^a  

^a UNIVERSITY OF TEXAS   (United States)

^b UNIVERSITY OF TEXAS MD ANDERSON CANCER CENTER   (United States)

Author keywords

Conditional knockout; DNA damage repair; Homologous recombination; Neural development; Replication fork stalling

Indexed keywords

CELL PROTEIN; HYDROXYUREA; NUCLEOSTEMIN; PROTEIN P53; RAD51 PROTEIN; UNCLASSIFIED DRUG;

ANIMAL CELL; ANIMAL TISSUE; ARTICLE; BRAIN DISEASE; CELL CYCLE ARREST; CELL DIVISION; CELL GROWTH; CELL PROTECTION; DNA DAMAGE; DNA REPLICATION; EMBRYO; FIBROBLAST; GENOMIC INSTABILITY; IN VIVO STUDY; MOUSE; NONHUMAN; NULL ALLELE; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEIN FUNCTION; RNA SYNTHESIS; STEM CELL;

CONDITIONAL KNOCKOUT; DNA DAMAGE REPAIR; HOMOLOGOUS RECOMBINATION; NEURAL DEVELOPMENT; REPLICATION FORK STALLING;

ALLELES; ANIMALS; DNA DAMAGE; DNA REPLICATION; FEMALE; GENOMIC INSTABILITY; MICE; MICE, INBRED C57BL; STEM CELLS;

EID: 84879910124     PISSN: 00278424     EISSN: 10916490     Source Type: Journal    
DOI: 10.1073/pnas.1301672110     Document Type: Article

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