P53 directly transactivates Δ133p53α, regulating cell fate outcome in response to DNA damage

Cell Death and Differentiation

Volumn 18, Issue 2, 2011, Pages 248-258

  Aoubala, M ^a   Murray Zmijewski, F ^a   Khoury, M P ^a,b   Fernandes, K ^a   Perrier, S ^a   Bernard, H ^a,b   Prats, A C ^b   Lane, D P ^a   Bourdon, J C ^a,b  

^a UNIVERSITY OF DUNDEE   (United Kingdom)

^b INSERM   (France)

Author keywords

apoptosis; cancer; cell cycle; DNA damage; p53 isoforms; splice

Indexed keywords

DELTA133P53ALPHA PROTEIN; DOXORUBICIN; ISOPROTEIN; PROTEIN P53; UNCLASSIFIED DRUG;

APOPTOSIS; ARTICLE; CELL CYCLE ARREST; CELL CYCLE G1 PHASE; CELL CYCLE G2 PHASE; CELL FATE; COMPLEX FORMATION; CONTROLLED STUDY; DNA DAMAGE; EXON; GENE EXPRESSION; HUMAN; HUMAN CELL; INTRON; NUCLEOTIDE SEQUENCE; PRIORITY JOURNAL; PROMOTER REGION; PROTEIN EXPRESSION; PROTEIN FUNCTION; REGULATORY MECHANISM; STRESS; TRANSACTIVATION;

APOPTOSIS; BASE SEQUENCE; CELL LINE, TUMOR; DNA DAMAGE; DOXORUBICIN; G1 PHASE; GENES, P53; HUMANS; INTRONS; MOLECULAR SEQUENCE DATA; PROMOTER REGIONS, GENETIC; PROTEIN ISOFORMS; TRANSCRIPTIONAL ACTIVATION; TUMOR SUPPRESSOR PROTEIN P53;

EID: 78651277059     PISSN: 13509047     EISSN: 14765403     Source Type: Journal    
DOI: 10.1038/cdd.2010.91     Document Type: Article

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