Inactivation of the p53 gene expression by a splice donor site mutation in a human T-cell leukemia cell line.
An abnormally sized 3.5 kb p53 transcript was detected in the KE-37R human leukemic T-cell line in which no p53 protein could be detected by immunoprecipitation. S1 nuclease protection experiments and sequencing analysis indicated conservation of the entire intron 4 (755 bp) in the 3.5 kb transcript and the presence of a G to A substitution in the last exonic nucleotide of the splice donor site. These data support the notion that p53 gene inactivation by point mutations in splice junctions also exists in hemopoietic neoplasia.
Soudon
J
J
Unité 301 INSERM, Institut de Génétique Moléculaire, Paris, France.
Caron de Fromentel
C
C
Bernard
O
O
Larsen
C J
CJ
D000818:Animals; D001483:Base Sequence; D004247:DNA / Q000235:genetics; D004274:DNA, Recombinant / Q000235:genetics*; D015973:Gene Expression Regulation, Leukemic / Q000235:genetics*; D016158:Genes, p53 / Q000235:genetics*; D006801:Humans; D007438:Introns / Q000235:genetics; D015458:Leukemia, T-Cell / Q000235:genetics*; D051379:Mice; D008969:Molecular Sequence Data; D009154:Mutation; D012333:RNA, Messenger / Q000235:genetics; D014158:Transcription, Genetic / Q000502:physiology; D014407:Tumor Cells, Cultured
D004274:DNA, Recombinant; D012333:RNA, Messenger; D004247:DNA