A large-scale RNAi screen in human cells identifies new components of the p53 pathway

By K. Berns, E. M. Hijmans, J. Mullenders, T. Brummelkamp, A. Velds, Mike Heimerikx, R. Kerkhoven, Mandy Madiredjo, Wouter Nijkamp, B. Weigelt and 8 more. Nature, 2004

1,125 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/30a8dd867a0fba0f69ea5151647062754f0ecbf7

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In Molecular Biology

1. David M. Sabatini
2. J. Blenis
3. Brent R. Stockwell
4. Anne E Carpenter
5. Jesús Gil
6. R. Anjum
7. W. Gu
8. Weimin He

Citations in the corpus

• RNA silencing: Methods and protocols (2006, methodology): “elegans is that it is systemic in that the silencing can spread between tissues throughout the adult as well as its progeny (1,3,4).”
• The KLF4 tumour suppressor is a transcriptional repressor of p53 that acts as a context-dependent oncogene (2005, methodology): “For RNA interference experiments, we used pSUPER–p21 CIP1 (ref”
• Activation and Function of the MAPKs and Their Substrates, the MAPK-Activated Protein Kinases (2011, background): “cell growth arrest (23) and in oncogene-induced cellular se-”
• Second-generation shRNA libraries covering the mouse and human genomes (2005, background): “Several groups, including our own, previously described the design and construction of arrayed shRNA libraries that covered a fraction (approximately one-third) of human gene”
• Plasminogen activator inhibitor-1 is a critical downstream target of p53 in the induction of replicative senescence (2006, neutral): “As p21 CIP1 is an essential p53 target in the senescence response of human fibroblast”
• Chemokine signaling via the CXCR2 receptor reinforces senescence. (2008, methodology): “Genetic Screening IMR-90 cells (passage 20; see Figure S1A), were infected with the appropriate controls or pools of constructs of the NKI RNAi library (Berns et al., 2004).”
• Oncogene-induced senescence relayed by an interleukin-dependent inflammatory network. (2008, background): “For example, function-based genomewide screens have unraveled unanticipated tumorigenic mechanisms (Peeper et al., 2002; Berns et al., 2004; Rowland et al., 2005).”
• The molecular biology of head and neck cancer (2011, background): “There is the unlikely possibility that mutations have been missed, but it is more plausible that other genes encoding proteins in the p53 pathway are targeted in selected case”
• The RSK family of kinases: emerging roles in cellular signalling (2008, background): “, and RSK4 participates in p53-dependent cell-growth arres”
• Acetylation is indispensable for p53 activation. (2008, background): “…protein induces p53 acetylation at lysine 120 (K120) within the DNA-binding domain , and that Tip60/hMOF, which shares no homology with the CBP/p300 or PCAF acetyltransferases, is required for p53- mediated transcriptional activation (Tang et al., 2006; Sykes et al., 2006; Berns et al., 2004).”