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PMID:16027169
| Citation |
Manning, BD, Logsdon, MN, Lipovsky, AI, Abbott, D, Kwiatkowski, DJ and Cantley, LC (2005) Feedback inhibition of Akt signaling limits the growth of tumors lacking Tsc2. Genes Dev. 19:1773-8 |
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| Abstract |
The PTEN and TSC2 tumor suppressors inhibit mammalian target of rapamycin (mTOR) signaling and are defective in distinct hamartoma syndromes. Using mouse genetics, we find that Pten and Tsc2 act synergistically to suppress the severity of a subset of tumors specific to loss of each of these genes. Interestingly, we find that the slow-growing tumors specific to Tsc2+/- mice exhibit defects in signaling downstream of Akt. However, Pten haploinsufficiency restores Akt signaling in these tumors and dramatically enhances their severity. This study demonstrates that attenuation of the PI3K-Akt pathway in tumors lacking TSC2 contributes to their benign nature. |
| Links |
PubMed PMC1182339 Online version:10.1101/gad.1314605 |
| Keywords |
Animals; Cell Division; Cell Line, Tumor; Feedback; Humans; Mice; Mice, Inbred C57BL; Mice, Knockout; PTEN Phosphohydrolase; Phosphoric Monoester Hydrolases/genetics; Phosphoric Monoester Hydrolases/physiology; Polymerase Chain Reaction; Protein-Serine-Threonine Kinases/metabolism; Proto-Oncogene Proteins/metabolism; Proto-Oncogene Proteins c-akt; Repressor Proteins/genetics; Repressor Proteins/physiology; Signal Transduction; Tumor Suppressor Proteins/genetics; Tumor Suppressor Proteins/physiology |
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Significance
Annotations
| Gene product | Qualifier | GO ID | GO term name | Evidence Code | with/from | Aspect | Notes | Status |
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See also
References
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