HER-2/neu induces p53 ubiquitination via Akt-mediated MDM2 phosphorylation

By Binhua P. Zhou, Y. Liao, W. Xia, Y. Zou, B. Spohn, M. Hung. Nature Cell Biology, 2001

1,005 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/a3361ff0cb5818dfa62bc29a8dd54d8ee566c98d

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In Molecular Biology

1. David M. Sabatini
2. T. Franke
3. Siraj M. Ali
4. Dos D. Sarbassov
5. D. Fruman
6. U. Moll
7. O. Petrenko
8. Gautam Sethi

In Oncology

1. T. Franke
2. U. Moll
3. O. Petrenko
4. David M. Sabatini
5. Carlos L. Arteaga
6. Y. Xiong

Citations in the corpus

• FKBP51 Affects Cancer Cell Response to Chemotherapy by Negatively Regulating Akt (2009, positive): “Third, Akt phosphorylates MDM2, resulting in its translocation to the nucleus, and facilitating MDM2’s inhibition of p53 (Mayo and Donner, 2001; Zhou et al., 2001).”
• Insulin receptor signaling in normal and insulin-resistant states. (2014, background): “Akt phosphorylates cell cycle inhibitors p21Cip1/WAF1 and p27Kip1, resulting in cytoplasmic localization, cell growth, and inhibition of apoptosis (Zhou et al. 2001; Motti et al. 2004).”
• PI3K/Akt and apoptosis: size matters (2003, background): “Two alternative mechanisms of Aktdependent regulation of Mdm2/HDM2 have been described, and they include the induction of Mdm2 nuclear import (Mayo and Donner, 2001) or the regulation of Mdm2/HDM2-ubiquitin ligase enzymatic activity (Zhou et al., 2001b; Ashcroft et al., 2002; Ogawara et al., 2002).”
• Herceptin-induced inhibition of phosphatidylinositol-3 kinase and Akt Is required for antibody-mediated effects on p27, cyclin D1, and antitumor action. (2002, background): “62–65), and, more recently, p53 via MDM2-mediated phosphorylation and ubiquitination (66, 67).”
• Mutant PIK3CA promotes cell growth and invasion of human cancer cells. (2005, neutral): “, 1997), MDM2 (Mayo and Donner, 2001; Zhou et al., 2001), p21 (WAF1/CIP1) (Lawlor and Rotwein, 2000; Rossig et al.”
• Ribosomal Protein L11 Negatively Regulates Oncoprotein MDM2 and Mediates a p53-Dependent Ribosomal-Stress Checkpoint Pathway (2003, background): “The 491 residues of HDM2 can be divided into three functional domains: an N-terminal region which binds p53, a Cterminal RING finger domain that promotes p53 ubiquitination, and a central region of approximately 300 residues that contains multiple sites for binding and regulation by different protei”
• Growing roles for the mTOR pathway. (2005, background): “Akt/PKB is a key component of the insulin/PI3K signaling pathway and modulates cell survival and proliferation through downstream substrates such as the FOXO class of transcription factors (reviewed in [42]) and the p53-regulator mdm2 [43,44].”
• The MDM2-p53 interaction. (2003, background): “induces p53 ubiquitination via AKT-mediated MDM2 phosphorylation (83).”
• c-Myc can induce DNA damage, increase reactive oxygen species, and mitigate p53 function: a mechanism for oncogene-induced genetic instability. (2002, background): “Recent 2000), and other studies show that AKT activation leads 1%BSA/PBS-TX: pAb anti-hMre11, 1:200 (John Petrini, Madison,to MDM2-dependent p53 degradation (Mayo and DonWI); pAb anti-p95, 1:200 (JP); pAb gX l-9 antiphosphorylated H2AX,ner, 2001; Zhou et al., 2001).”