Akt-Mediated Regulation of Autophagy and Tumorigenesis Through Beclin 1 Phosphorylation
By Richard C. Wang, Yongjie Wei, Zhenyi An, Z. Zou, Guanghua Xiao, G. Bhagat, M. White, J. Reichelt, Beth Levine. Science, 2012
723 citations recorded by the source corpus.
Subfields: Epidemiology, Molecular Biology, Organic Chemistry
View Paper: https://www.semanticscholar.org/paper/a123e19ea0ea345782334b9616c571dc5c6a4603
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Epidemiology
- Guido Kroemer
- Beth Levine
- L. Galluzzi
- Douglas R. Green
- Alec C. Kimmelman
- P. Codogno
- D. Rubinsztein
- Eric H. Baehrecke
In Molecular Biology
- Guido Kroemer
- Beth Levine
- L. Galluzzi
- Douglas R. Green
- Seamus J. Martin
- F. Llambi
- D. Rubinsztein
- Eric H. Baehrecke
Citations in the corpus
- Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition) (2012, neutral): “be a useful technique to monitor the functional activity of this complex during autophagy modulation.(522,523,579)”
- Autophagy-Independent Functions of the Autophagy Machinery (2019, background): “Thus, it has become clear that autophagy occupies a central position in the biology of most eukaryotes, interfacing with the regulation of core metabolism (He et al., 2012; Sousa et al., 2016) , damage control (Ferná ndez et al., 2018; Khaminets et al., 2015; Mathew et al., 2007) , and cell death Wa”
- Autophagy in malignant transformation and cancer progression (2015, positive): “…the inactivating phosphorylation of the MTOR-repressing tumor sclerosis (TSC) complex, but also by phosphorylating and hence inhibiting BECN1 (Wang et al , 2012a), and perhaps by promoting the ability of TP53 to block autophagy in baseline or near-to-baseline conditions via a X-linked…”
- Cell Death Signaling. (2015, background): “Akt directly phosphorylates beclin 1, thus allowing it to bind to 14-3-3 (Wang et al. 2012).”
- Oxidative stress and autophagy: the clash between damage and metabolic needs (2014, background): “In support of this hypothesis, it has been reported that the two protein kinases positively regulating HKII activity, Akt and myotonic dystrophy protein kinase (DMPK), are negative modulators of autophagy.(58,59)”