Analysis of p53-regulated gene expression patterns using oligonucleotide arrays.

By Renbin Zhao, K. Gish, M. Murphy, Yuxin Yin, D. Notterman, William H. Hoffman, E. Tom, D. Mack, Arnold J. Levine. Genes & Development, 2000

643 citations recorded by the source corpus.

Oligonucleotide microarrays were employed to quantitate mRNA levels from a large number of genes regulated by the p53 transcription factor. Responses to DNA damage and to zinc-inducible p53 were compared for their transcription patterns in cell culture. A cluster analysis of these data demonstrates that genes induced by gamma radiation, UV radiation, and the zinc-induced p53 form distinct sets and subsets with a few genes in common to all these treatments. Cell type- or cell line-specific p53 responses were detected. When p53 proteins were induced with zinc, the kinetics of induction or repression of mRNAs from p53-responsive genes fell into eight distinct classes, five different kinetics of induction, and three different kinetics of repression. In addition, low levels of p53 in a cell induced or repressed only a subset of genes observed at higher p53 levels. The results of this study demonstrate that the nature of the p53 response in diverse mRNA species depends on the levels of p53 protein in a cell, the type of inducing agent or event, and the cell type employed. Of 6000 genes examined for p53 regulatory responses, 107 induced and 54 repressed genes fell into categories of apoptosis and growth arrest, cytoskeletal functions, growth factors and their inhibitors, extracellular matrix, and adhesion genes.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/fe9fdf9611e26a1c04a6a919a0a50a0852acc357

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Citations in the corpus

Gene expression patterns in human liver cancers. (2002, methodology): “Interestingly, one of these genes, MST, also called hepatocyte growth factor-like protein, has been reported to be induced by p53 expression (Zhao et al., 2000), raising the possibility of a role for this putative growth factor in p53-dependent regulation of hepatocyte differentiation.”
Intrinsically disordered proteins in human diseases: introducing the D2 concept. (2008, background): “Cancers showing mutations in p53 are found in colon, lung, esophagus, breast, liver, brain, reticuloendothelial tissues, and hemopoietic tissues (68). p53 induces or inhibits over 150 genes, including p21, GADD45, MDM2, IGFBP3, and BAX (164).”
Oxidative Stress in Aging Human Skin (2015, background): “The main candidate for the cell cycle arrest is p21 that is a very potent cyclin-dependent kinase inhibitor acting on CDK2 and CDK4 [343,349,352–355].”
Flexible nets: disorder and induced fit in the associations of p53 and 14-3-3 with their partners (2008, background): “The p53 Page 2 of 20 (page number not for citation purposes) protein induces or inhibits over 150 genes, including p21, GADD45, MDM2, IGFBP3, and BAX[54].”
microRNAs join the p53 network — another piece in the tumour-suppression puzzle (2007, background): “For example, several studies indicated that p53 could also repress the expression of target genes through a mechanism that had not been fully elucidate”
Defying death after DNA damage (2000, background): “The advent of microarray and other genome-wide technologies has drawn attention to scores of newly transcribed molecules that might transmit the p53 signal to the apoptotic machiner”
Regulation of p53 activity by its interaction with homeodomain-interacting protein kinase-2 (2002, methodology): “c, GST–p53(1-80) or a point mutant of this fusion protein containing a Ser 46 to alanine exchange were employed as substrate proteins, typical autoradiograms are displayed.”
The first 30 years of p53: growing ever more complex (2009, positive): “It is also noteworthy that the first expression microarrays that were used to examine the genes regulated by a specific and inducible (by DNA damage) transcription factor were obtained using p53 for the initiating even”
A global map of p53 transcription-factor binding sites in the human genome. (2006, background): “In the past decade, numerous efforts have been made to identify p53-targeted genes through various gene-expression techniques, including microarray and SAGE combined with bioinformatics tools (Yu et al., 1999; Zhao et al., 2000; Kannan et al., 2001; Kho et al., 2004).”