The p53MH algorithm and its application in detecting p53-responsive genes

By J. Hoh, S. Jin, T. Parrado, Joanne Edington, Arnold J. Levine, Jurg Ott. Proceedings of the National Academy of Sciences of the United States of America, 2002

307 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/663b7b74f713abff0ecd9c9b92023ac970a9a463

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Citations in the corpus

Transcriptional control of human p53-regulated genes (2008, methodology): “This method could also be used to identify p53-like sites on retroviruses and LINE elements (repetitive elements in the genome), both of which are observed by p53 RE algorithms (see below”
Malignant astrocytic glioma: genetics, biology, and paths to treatment. (2007, background): “…through its function as a transcription factor: Upon being post-translationally modified by various genotoxic and cytotoxic stress-sensing agents, p53 is stabilized, then binds and transcriptionally regulates the promoters of >2500 potential effector genes (Hoh et al. 2002; Levine et al. 2006).”
The p53 pathway: positive and negative feedback loops (2005, methodology): “An algorithm that identifies p53-responsive genes in the human and mouse genome has been utilized to detect a number of new genes regulated by the p53 protein (Hoh et al., 2002).”
The regulation of AMPK beta1, TSC2, and PTEN expression by p53: stress, cell and tissue specificity, and the role of these gene products in modulating the IGF-1-AKT-mTOR pathways. (2007, background): “(29) developed a novel algorithm (p53MH) for genome-wide scanning for putative p53 consensus binding elements.”
Unbiased mapping of transcription factor binding sites along human chromosomes 21 and 22 points to widespread regulation of noncoding RNAs. (2004, methodology): “…to the exact consensus and with the idea that these noncoding RNAs merely represent tran- availability of a weight matrix from an independent study scriptional noise, but instead suggest that they may (Hoh et al., 2002), a search for inexact matches was have biological functions. implemented.”
MicroRNA-34b and MicroRNA-34c are targets of p53 and cooperate in control of cell proliferation and adhesion-independent growth. (2007, methodology): “Towards this aim, we took advantage of the p53MH algorithm (17), which has previously identified novel p53responsive genes (22), to search 5 kb upstream and downstream of each down-regulated miRNA.”
Blinded by the Light: The Growing Complexity of p53. (2009, methodology): “The original consensus site recognized by p53 consisting of two copies of the sequence—RRRCA/TT/AGYYY (R, purine; Y, pyrimidine)—has been refined by using bioinformatics analysis (Hoh et al., 2002; Miled et al., 2005; Riley et al., 2008; Sbisa et al., 2007) and experimental approaches using chromati”