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PMID:21297943

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Citation

Santi, SA and Lee, H (2011) Ablation of Akt2 induces autophagy through cell cycle arrest, the downregulation of p70S6K, and the deregulation of mitochondria in MDA-MB231 cells. PLoS ONE 6:e14614

Abstract

Akt/PKB is a promising anticancer therapeutic target, since abnormally elevated Akt activity is directly correlated to tumor development, progression, poor prognosis and resistance to cancer therapies. Currently, the unique role of each Akt isoform and their relevance to human breast cancer are poorly understood.

Links

PubMed PMC3031501 Online version:10.1371/journal.pone.0014614

Keywords

Autophagy/drug effects; Autophagy/genetics; Breast Neoplasms/pathology; Cell Cycle; Cell Cycle Proteins; Cell Line, Tumor; Cell Proliferation; Cell Survival; Down-Regulation; Drug Delivery Systems/methods; Female; Humans; Mitochondria/pathology; Protein Isoforms; Proto-Oncogene Proteins c-akt/deficiency; Proto-Oncogene Proteins c-akt/genetics; RNA, Small Interfering/pharmacology; Ribosomal Protein S6 Kinases, 70-kDa/genetics

Significance

Annotations

Gene product Qualifier GO Term Evidence Code with/from Aspect Extension Notes Status

HUMAN:AKT2

GO:2000144: positive regulation of DNA-dependent transcription, initiation

ECO:0000314:

P

Figure 2A shows that the use of AKT2 siRNA, causes a decrease in the transcriptional levels of Cdk2, while scrambled or uninhibited AKT2 allows for transcriptional up-regulation of Ckd2.

complete
CACAO 7774


See also

References

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