RAD51 foci formation in response to DNA damage is modulated by TIP49

International Journal of Biochemistry and Cell Biology

Volumn 41, Issue 4, 2009, Pages 925-933

  Gospodinov, Anastas ^a   Tsaneva, Irina ^b   Anachkova, Boyka ^a  

^a INSTITUTE OF MOLECULAR BIOLOGY   (Bulgaria)

^b UNIVERSITY COLLEGE LONDON   (United Kingdom)

Author keywords

H2AX; Histone acetylation; Homologous recombination; Mammalian cells; RAD51; TIP49

Indexed keywords

ADENOSINE TRIPHOSPHATASE; BUTYRIC ACID; DNA; HISTONE DEACETYLASE INHIBITOR; HISTONE H2AX; PROTEIN; PROTEIN TIP49; RAD51 PROTEIN; SMALL INTERFERING RNA; UNCLASSIFIED DRUG;

ARTICLE; CHROMATIN; CONTROLLED STUDY; DNA CROSS LINKING; DNA DAMAGE; DNA REPAIR; DOUBLE STRANDED DNA BREAK; EMBRYO; GENE SILENCING; HOMOLOGOUS RECOMBINATION; HUMAN; HUMAN CELL; MALE; PROTEIN DEPLETION; PROTEIN FUNCTION; PROTEIN LOCALIZATION; PROTEIN PHOSPHORYLATION; RNA INTERFERENCE; SIGNAL TRANSDUCTION;

CARRIER PROTEINS; CELL CYCLE; CELL LINE, TUMOR; DNA DAMAGE; DNA HELICASES; DNA REPAIR; GENE KNOCKDOWN TECHNIQUES; GENE SILENCING; HUMANS; PHOSPHORYLATION; RAD51 RECOMBINASE; RNA INTERFERENCE;

MAMMALIA;

EID: 59849088152     PISSN: 13572725     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.biocel.2008.09.004     Document Type: Article

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