Akt Suppresses Apoptosis by Stimulating the Transactivation Potential of the RelA/p65 Subunit of NF-κB

By L. Madrid, Cun-Yu Wang, D. Guttridge, A. Schottelius, A. Baldwin, Marty W. Mayo. Molecular and Cellular Biology, 2000

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Akt-Directed Glucose Metabolism Can Prevent Bax Conformation Change and Promote Growth Factor-Independent Survival (2003, background): “This could be because Akt may mediate its survival effects based on induction of new transcription and translation, such as that caused by Akt-mediated activation of the survival-promoting transcription factor NF- B (29, 33, 34, 39, 50).”
The p65 (RelA) Subunit of NF-κB Interacts with the Histone Deacetylase (HDAC) Corepressors HDAC1 and HDAC2 To Negatively Regulate Gene Expression (2001, methodology): “When the in vitro transcribed and translated p65 was incubated with GST-HDAC1, interactions were seen with full-length p65 as well as with all three C-terminal deletions [p65 wt, p65(1-521), p65(1-313), and p65(1-276)] (Fig.”
Modulation of NF-κB Activity by Exchange of Dimers (2003, background): “…affect the activ- Canonical and Noncanonical NF- B Activation Pathways in DCsity of Rel proteins in response to stimulation (Bonnard et al., 2000; Madrid et al., 2000; Zhong et al., 1997). moDCs are the in vitro counterpart of immature myeloid dendritic cells (imDCs) (Mellman and Steinman, 2001).”