MUTATIONAL INACTIVATION OF THE P53 GENE IN THE HUMAN ERYTHROID LEUKEMIC K562 CELL-LINE

被引:130
作者
LAW, JC
RITKE, MK
YALOWICH, JC
LEDER, GH
FERRELL, RE
机构
[1] UNIV PITTSBURGH, GRAD SCH PUBL HLTH, DEPT HUMAN GENET, PITTSBURGH, PA 15261 USA
[2] UNIV PITTSBURGH, SCH MED, DEPT PHARMACOL, PITTSBURGH, PA 15261 USA
[3] UNIV PITTSBURGH, PITTSBURGH CANC INST, PITTSBURGH, PA 15261 USA
[4] UNIV PITTSBURGH, SCH MED, DEPT SURG, PITTSBURGH, PA 15261 USA
关键词
P53; K562; HUMAN ERYTHROID LEUKEMIA; MUTATION; CELL LINE;
D O I
10.1016/0145-2126(93)90161-D
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The K562 human chronic myelogenous leukemia (CML) cell line has attained widespread use as a model for studying hematologic malignancy and erythroid differentiation. Sequencing of the p53 gene in the K562 cell line demonstrated a mutation in exon 5 characterized by a single base insertion (cytosine) between codons 135 and 136. This frameshift mutation leads to an N-terminal truncated protein of 147 amino acids. Only the mutated sequence was present suggesting that the normal allele has been lost. Reverse transcription PCR (RT-PCR) detected a p53 transcript but Western blotting and immunohistochemical staining of cells failed to detect p53 protein. The identification of an inactivation mutation of p53 in the K562 cell line further supports the argument that p53 mutations play a role in myeloid blast transformation of CML.
引用
收藏
页码:1045 / 1050
页数:6
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