Published in Mol Cell Biol on July 01, 1998
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Loss of PML cooperates with mutant p53 to drive more aggressive cancers in a gender-dependent manner. Cell Cycle (2013) 0.88
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Unbalanced replication as a major source of genetic instability in cancer cells. Am J Blood Res (2012) 0.77
Wild-type p53 binds to MYC promoter G-quadruplex. Biosci Rep (2016) 0.76
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Binding of basal transcription factor TFIIH to the acidic activation domains of VP16 and p53. Mol Cell Biol (1994) 3.46
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The p53 tumour suppressor protein is phosphorylated at serine 389 by casein kinase II. EMBO J (1990) 2.38
p53-catalyzed annealing of complementary single-stranded nucleic acids. EMBO J (1993) 2.16
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Inhibition of viral and cellular promoters by human wild-type p53. J Virol (1992) 1.83
p53 is covalently linked to 5.8S rRNA. Mol Cell Biol (1992) 1.65
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Cytoplasmic sequestration of wild-type p53 protein impairs the G1 checkpoint after DNA damage. Mol Cell Biol (1996) 1.61
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Two critical hydrophobic amino acids in the N-terminal domain of the p53 protein are required for the gain of function phenotypes of human p53 mutants. Oncogene (1995) 1.52
Modulation of cellular and viral promoters by mutant human p53 proteins found in tumor cells. J Virol (1992) 1.44
Alternatively spliced forms in the carboxy-terminal domain of the p53 protein regulate its ability to promote annealing of complementary single strands of nucleic acids. Mol Cell Biol (1995) 1.43
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Transcriptional activation of the human epidermal growth factor receptor promoter by human p53. Mol Cell Biol (1996) 1.37
Tight DNA binding and oligomerization are dispensable for the ability of p53 to transactivate target genes and suppress transformation. EMBO J (1993) 1.25
A mutant p53 protein is required for maintenance of the transformed phenotype in cells transformed with p53 plus ras cDNAs. Proc Natl Acad Sci U S A (1992) 1.16
The transforming and suppressor functions of p53 alleles: effects of mutations that disrupt phosphorylation, oligomerization and nuclear translocation. EMBO J (1993) 1.13
Progression toward tumor cell phenotype is enhanced by overexpression of a mutant p53 tumor-suppressor gene isolated from nasopharyngeal carcinoma. Proc Natl Acad Sci U S A (1993) 1.05
The single-stranded DNA end binding site of p53 coincides with the C-terminal regulatory region. Nucleic Acids Res (1996) 1.02
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