Cytoplasmic relocalization and inhibition of the cyclin-dependent kinase inhibitor p27Kip1 by PKB/Akt-mediated phosphorylation in breast cancer
By G. Viglietto, M. L. Motti, P. Bruni, R. Melillo, A. D’alessio, D. Califano, F. Vinci, G. Chiappetta, P. Tsichlis, A. Bellacosa and 2 more. Nature Medicine, 2002
772 citations recorded by the source corpus.
Subfields: Cell Biology, Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/af3bbfc6a3deed1a566f67ec8972e30612fd31a2
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Citations in the corpus
- Living with or without cyclins and cyclin-dependent kinases. (2004, background): “The AKT kinase controls the subcellular localization of Cip/Kip proteins as well (Liang et al. 2002; Shin et al. 2002; Viglietto et al. 2002), providing yet another avenue for cyclin E–Cdk2 regulation in response to extracellular cues.”
- The oncogene HER2: its signaling and transforming functions and its role in human cancer pathogenesis (2007, background): “Akt is activated in HER2-amplified breast cancers (reviewed above) and activated Akt phosphorylates p27 inhibiting its function by excluding it from the nucleus (Liang et al., 2002; Shin et al., 2002; Viglietto et al., 2002).”
- AKT/PKB signaling: navigating downstream. (2007, positive): “Several groups have independently found that Akt phosphorylates the p27Kip1 cyclin-dependent kinase inhibitor on T157 (Liang et al., 2002; Shin et al., 2002; Viglietto et al., 2002), and this leads to cytosolic sequestration via 14-3-3 binding (Sekimoto et al.”
- Pten Dose Dictates Cancer Progression in the Prostate (2003, background): “It also remains to be resolved whether the reduction in p27Kip1 expression is also associated with its cytoplasmic relocalization, as previously reported in human breast cancer cells suffering AKT hyperactivation (Liang et al. 2002; Shin et al. 2002; Viglietto et al. 2002).”
- 14‐3‐3 suppresses the nuclear localization of threonine 157‐phosphorylated p27Kip1 (2004, background): “Phosphorylation of Thr157 of p27 by Akt also induces cytoplasmic localization of p27 in breast cancer (Liang et al, 2002; Shin et al, 2002; Viglietto et al, 2002), although the mechanism for this is currently unclear.”