Regulation of PTEN transcription by p53.
By V. Stambolic, D. MacPherson, D. Sas, Yunping Lin, B. Snow, Y. Jang, S. Benchimol, T. Mak. Molecules and Cells, 2001
997 citations recorded by the source corpus.
Subfields: Molecular Biology, Oncology, Pathology and Forensic Medicine
View Paper: https://www.semanticscholar.org/paper/660d5176cf636f17c558531e46e7711170cd88d3
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In Molecular Biology
- David M. Sabatini
- M. Laplante
- Arnold J. Levine
- P. Pandolfi
- T. Franke
- Arkaitz Carracedo
- Moshe Oren
- Scott W. Lowe
In Oncology
- Arnold J. Levine
- David M. Sabatini
- Moshe Oren
- M. Soengas
- Arkaitz Carracedo
- M. Laplante
- William C. Hahn
- Scott W. Lowe
In Pathology and Forensic Medicine
Citations in the corpus
- Anoikis molecular pathways and its role in cancer progression. (2013, background): “Induction of autophagy is driven by the activation of proteins that sense cellular metabolic stress, such as AMP activated protein kinase (AMPK) [121,146].”
- Hydrogen peroxide sensing, signaling and regulation of transcription factors (2014, background): “On the other hand the phosphorylation of MDM2 through the PI3K/AKT pathway promotes MDM2 nuclear import, resulting in TP53 nuclear export [278][279][280].”
- Decision making by p53: life, death and cancer (2003, background): “Of particular note, p53 positively regulates the expression of the PTEN tumor-suppressor gene.(110)”
- The phosphatidylinositol 3-Kinase–AKT pathway in human cancer (2002, background): “Further interaction between the PI3K pathway and p53 is indicated by the finding that p53 can positively regulate the PTEN promote”
- mTOR signaling at a glance (2009, background): “Additionally, p53 negatively controls mTORC1 signaling by increasing the transcription of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) and TSC2, two negative regulators of the pathway (Feng et al., 2005; Stambolic et al., 2001).”
- Regulation of cancer cell metabolism (2011, methodology): “Wild-type p53 also supports the expression of PTEN, which inhibits the PI3K pathway, thereby suppressing glycolysis (as discussed above”
- PI3K/Akt: getting it right matters (2008, background): “Conversely, on the basis of the finding of a p53 binding site within the PTEN promoter, Stambolic et al. (2001) have presented evidence for the regulation of PTEN transcription by p53. mTOR and Akt: increasing cell size matters Although Akt promotes cell proliferation by regulating specific targets…”
- Malignant astrocytic glioma: genetics, biology, and paths to treatment. (2007, background): “For example, because p53 enhances PTEN transcription and represses the expression of p110 (cid:1) (Stambolic et al. 2001; Singh et al. 2002), the loss of p53 in cells with constitutively active RTK signaling can further potentiate PI3K pathway activation.”
- Tenets of PTEN tumor suppression. (2008, background): “Additionally, Stambolic et al. (2001) identified a putative p53binding element in the promoter sequence of PTEN and characterized a p53-mediated cellular survival mechanism that functions through the activation of PTEN transcription.”
- mTOR signaling in growth control and disease (2012, positive): “…the expression of Tsc2 and phosphatase and tensin homolog deleted on chromosome 10 (Pten), causing downregulation of the entire PI3K-mTORC1 axis (Feng et al., 2005; Stambolic et al., 2001), and activates AMPK through a mechanism that depends on the induction of Sestrin1/2 (Budanov and Karin, 2008).”