Cytoplasmic localization of p21Cip1/WAF1 by Akt-induced phosphorylation in HER-2/neu-overexpressing cells

By Binhua P. Zhou, Y. Liao, W. Xia, B. Spohn, Mong-Hong Lee, M. Hung. Nature Cell Biology, 2001

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Molecular mechanisms of cisplatin resistance (2012, background): “Mitsuuchi et al., 2000; Zhou et al., 2001; Ikeguchi and Kaibara, 2001; Citri and Yarden, 2006; Fijolek et al., 2006 HSPs Chaperones that exert prosurvival functions in response to a variety of stress conditions.”
Systems biology of cisplatin resistance: past, present and future (2014, background): “arrest that is required for the repair of CDDP-induced DNA lesions.(191,192) Along similar lines, dual-specificity Y-phosphorylation-regulated kinase 1B (DYRK1B, also known as MIRK) appears to sustain CDDP resistance as it favors the expression of various antioxidant enzymes.”
PHLPP and a second isoform, PHLPP2, differentially attenuate the amplitude of Akt signaling by regulating distinct Akt isoforms. (2007, background): “Akt directly phosphorylates p27, resulting in cytosolic sequestration of p27, promoting progression through the cell cycle (Viglietto et al., 2002; Zhou et al., 2001).”
Malignant astrocytic glioma: genetics, biology, and paths to treatment. (2007, background): “…which binds the miz-1 transcriptional repressor to block p21 gene induction (Herold et al. 2002; Seoane et al. 2002), while Akt impacts on p53 function by phosphorylation of Mdm2 (Zhou et al. 2001; Shin et al. 2002; Feng et al. 2004) in addition to the direct inhibition of p21 discussed earlier.”