The KLF4 tumour suppressor is a transcriptional repressor of p53 that acts as a context-dependent oncogene

By B. Rowland, René Bernards, D. Peeper. Nature Cell Biology, 2005

625 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/212ab5724d649d0ede1ef3c33e8d48deaa19cea6

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Citations in the corpus

Integrative genomic approaches identify IKBKE as a breast cancer oncogene. (2007, background): “These models have facilitated the identification of candidate oncogenes and tumor suppressor genes (Rowland et al., 2005; Westbrook et al., 2005).”
p21 in cancer: intricate networks and multiple activities (2009, background): “Intriguingly, KLF4 directly suppresses the TP53 promoter and exhibits paradoxical oncogenic activities through its ability to suppress senescence in response to oncogenic HRAS activatio”
Krüppel-like factor 4 regulates macrophage polarization. (2011, background): “This study and others suggest that the cellular context likely affects KLF4 action (48, 49).”
Strategies and new developments in the generation of patient-specific pluripotent stem cells. (2007, background): “Recently, the molecular mechanisms underlying the dual functions of KLF4 were partially elucidated (Rowland et al., 2005).”
Mammalian Krüppel-Like Factors in Health and Diseases (2010, background): “Inactivation of p21-induced cell cycle arrest by the upregulated cyclin D1 overcomes the suppressive effects of KLF4 and contributes to cell transformation (351).”
Chemokine signaling via the CXCR2 receptor reinforces senescence. (2008, background): “Downregulation of CXCR2 Expression Extends Cellular Life Span Identifying genes that regulate senescence can reveal novel tumorigenic mechanisms, and several notable examples have been uncovered in different contexts (Gil et al., 2004; Narita et al., 2006; Rowland et al., 2005).”
A human functional protein interaction network and its application to cancer data analysis (2010, background): “TP53 KLF4 [115] KLF4 is a direct suppressor of expression of TP53”
Oncogene-induced senescence relayed by an interleukin-dependent inflammatory network. (2008, methodology): “For example, function-based genomewide screens have unraveled unanticipated tumorigenic mechanisms (Peeper et al., 2002; Berns et al., 2004; Rowland et al., 2005).”
Senescence impairs successful reprogramming to pluripotent stem cells. (2009, background): “For example Klf4 is a context-dependent oncogene, able to induce a growth arrest in normal cells or conversely to bypass senescence induced by RAS (Rowland et al., 2005).”
Induction of pluripotent stem cells from mouse embryonic and adult fibroblast cultures by defined factors. (2006, background): “Klf4 has been shown to repress p53 directly (Rowland et al., 2005), and p53 protein has been shown to suppress Nanog during ES cell differentiation (Lin et al., 2004).”