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AKT3 — BCL6

Text-mined interactions from Literome

Oh et al., Cell Death Differ 2006 : DEX treatment upregulated cellular FLICE inhibitory protein ( cFLIP ) expression, but did not alter the protein levels of Bcl-2, Bcl-xL , Mcl-1, and cIAP as well as Akt activation
Bae et al., Cancer Res 2006 (Adenocarcinoma...) : Bcl-w overexpression also activated phosphoinositide 3-kinase (PI3K), Akt , and Sp1, and the blocking effects of each of these components using pharmacologic inhibitors, dominant negative mutants, or small interfering RNA abolished the ability of Bcl-w to induce MMP-2 and cell invasion
Kozuma et al., Journal of thrombosis and haemostasis : JTH 2007 : Continuous expression of Bcl-xL protein during megakaryopoiesis is post-translationally regulated by thrombopoietin mediated Akt activation, which prevents the cleavage of Bcl-xL
Longo et al., Blood 2008 (Leukemia, Lymphocytic, Chronic, B-Cell...) : Sustained activation of Akt resulted in increased leukemic cell viability and increased expression of the antiapoptotic proteins Mcl-1, Bcl-xL , and X-linked inhibitor of apoptosis protein ( XIAP ), thus largely recapitulating the effects of sustained BCR stimulation
Flacke et al., Apoptosis 2009 : Acidic preconditioning protects endothelial cells against apoptosis through p38- and Akt dependent Bcl-xL overexpression
Garofalo et al., PloS one 2008 : Our data provide evidence that Bcl-w is a new member of the Akt pathway and that Akt may induce anti-apoptotic signals at least in part through the regulation of the amount and activity of Bcl-w
Wang et al., Cancer Lett 2010 (Ovarian Neoplasms) : Meanwhile, the further study demonstrates that the chemoresistance caused by IL-6 is associated with increased expression of both multidrug resistance related genes ( MDR1 and GSTpi ) and apoptosis inhibitory proteins ( Bcl-2, Bcl-xL and XIAP ), as well as activation of Ras/MEK/ERK and PI3K/Akt signaling
Deeb et al., Carcinogenesis 2011 (Adenocarcinoma...) : Further, Akt , NF-?B and NF-?B regulated Bcl-2, Bcl-xL , survivin and cIAP1 appear to be the molecular targets of CDDO for inhibiting the progression of prostate cancer in TRAMP mice
Zhao et al., J Lipid Res 2012 : Further studies showed that TNF-a decreased expression of the antiapoptotic proteins Bcl-2 and Bcl-xL , decreased I?Ba and PPAR?, and also inhibited PI3K dependent Akt and EGFR signaling
Jacquin et al., Cell Death Differ 2013 : Active Akt prevents FoxO nuclear localization, which precludes Bcl-6 expression and leads to Bcl-xL overexpression