Transcriptional control of human p53-regulated genes

By Todd Riley, Eduardo Sontag, Patricia Chen, Arnold J. Levine. Nature reviews. Molecular cell biology, 2008

1,967 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/24d47a1a5e02f14390b6d66c6522f6407ffe1012

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Citations in the corpus

Roles, Functions, and Mechanisms of Long Non-coding RNAs in Cancer (2016, background): “For example, the transcription factor p53 regulates many genes [88], including lncRNAs such as lncRNA-p21, PANDA, H19, and loc285184, which serve as effectors of p53 by leading to p53-associated cellular functions such as cell cycle arrest and apoptosis [89].”
The DNA Damage Response: Making it safe to play with knives (2010, background): “…regulated by ATM and CHK2 in response to DSBs (Figure 1A) (Zhou and Elledge, 2000). p53 induces cell-cycle arrest, apoptosis, or senescence in response to DNA damage by transcriptionally regulating, among others, the CDK inhibitor p21 and the proapoptotic BAX and PUMA proteins (Riley et al., 2008).”
Autophagy in malignant transformation and cancer progression (2015, positive): “…bearing irreparable molecular defects (mainly DNA damage), via transcriptional as well as transcription-independent mechanisms (Moll et al , 2005; Riley et al , 2008), stress-stabilized TP53 can transactivate various genes involved in autophagic responses (Maiuri et al , 2010; Pietrocola et al ,…”
iRegulon: From a Gene List to a Gene Regulatory Network Using Large Motif and Track Collections (2014, background): “Identification of the TFs that operate a perturbed gene network, and detecting their target genes, are instrumental steps in uncovering key insights into oncogenic programs, including the discovery of therapeutic targets [9–12].”
A large intergenic non-coding RNA induced by p53 mediates global gene repression in the p53 response (2010, background): “…Systems Wewere intrigued by the p53 transcriptional target lincRNA-p21, which resides 15 Kb upstream of the gene encoding the critical cell-cycle regulator Cdkn1a (also known as p21), a canonical transcriptional target of p53 (Riley et al., 2008) (Figures 2A–2C, Figure S2A, and Table S1, parts C–”
Mutant p53: one name, many proteins. (2012, background): “Wild-type p53 functions as a homotetramer in cells, binding to p53 response elements composed of two decamers separated by a spacer of 0–14 nucleotides (59-RRRCWWGYYYn0–14RRRCWWGYYY-39) [(A) adenine; (T) thymine; (C) cytosine; (G) guanine; (R) purine; (Y) pyrimidine; (W) A/T; (n) any nucleotide] (el”
Long Non-Coding RNA in the Pathogenesis of Cancers (2019, background): “P21 is a canonical transcriptional target of p53 and plays a critical role in cell cycle and tumorigenensis [259].”
Tumour suppression by p53: a role for the DNA damage response? (2009, background): “However, given the many hundreds of genes that are thought to be regulated by p53 (Ref”
TP53 mutations in human cancers: origins, consequences, and clinical use. (2010, background): “p53 regulates transcription through specific binding to response elements in the promoters or introns of target genes (Riley et al. 2008). p53REs are variations of a consensus constituted by two decamers (PuPuPuC(A/T)(T/A) GPyPyPy) separated by a spacer of variable length (El-Deiry et al. 1992).”
p53 opens the mitochondrial permeability transition pore to trigger necrosis (2012, background): “…apoptosis involves transcriptional induction of components of the death receptor and mitochondrial pathways including CD95, Puma, Noxa, Bax, and others, which cooperatively 1536 Cell 149, 1536–1548, June 22, 2012 ª2012 Elsevier Inc. promote cell death (Brady et al., 2011; Riley et al., 2008).”