◀ Back to AKT3
AKT3 — HDAC3
Text-mined interactions from Literome
De Sarno et al., Neuropharmacology 2002
:
Two other inhibitors of
histone deacetylase , a recently identified target of sodium valproate, also
caused gradual increases in the phosphorylation of
Akt and GSK3beta
Chen et al., J Biol Chem 2005
:
Histone acetylation independent
effect of
histone deacetylase inhibitors on
Akt through the reshuffling of protein phosphatase 1 complexes
Lefebvre et al., Mol Endocrinol 2006
:
Through direct phosphorylation of the corepressor silencing mediator for retinoic and thyroid hormone receptors ( SMRT ),
Akt stabilized
RAR/SMRT interaction, leading to an increased tethering of SMRT to the RARbeta2 promoter, decreased histone acetylation, down-regulation of the RARbeta2 expression, and impaired cellular differentiation in response to retinoid
Furuya et al., Mol Cell Biol 2007
(Thyroid Neoplasms) :
Conversely, lowering cellular
NCoR by siRNA knockdown in tumor cells
led to overactivated
p-AKT and increased cell proliferation and motility
Lee et al., Mol Pharmacol 2008
:
Finally, activation of
Akt and CaM kinase II may eventually
lead to the acetylation of histone residues and phosphorylation of
histone deacetylase
Furuya et al., Steroids 2009
(Thyroid Neoplasms) :
Over-expression of
NCoR in thyroid tumor cells of TRbeta ( PV/PV ) mice
reduces AKT-mTOR-p70 ( S6K ) signaling ... Conversely, lowering cellular
NCoR by siRNA knockdown in tumor cells
leads to over activated
PI3K-AKT signaling to increase cell proliferation and motility
Zampetaki et al., Circulation 2010
(Atherosclerosis) :
Enforced expression of
HDAC3 resulted in increased phosphorylation of
Akt and upregulation of its kinase activity
Moskowitz et al., Curr Oncol Rep 2012
(Hodgkin Disease) :
Additional agents that have demonstrated activity in HL include
histone deacetylase inhibitors, such as panobinostat, entinostat, and mocetinostat,
PI3-kinase/Akt/Mtor pathway
inhibitors , such as everolimus, as well as lenalidomide and bendamustine