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AKT2 — CDKN1B
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Mirza et al., Cell Growth Differ 2000
(Cell Transformation, Neoplastic) :
In accord with this is the observation that activation of M+
Akt : ER*
led to decreased expression of the
cyclin dependent kinase inhibitor p27Kip1 with a concomitant increase in cyclin dependent kinase-2 activity
Potente et al., J Biol Chem 2003
:
These results indicate that EET induced endothelial cell proliferation is associated with the phosphatidylinositol
3-kinase/Akt dependent phosphorylation and inactivation of FOXO factors and the subsequent decrease in expression of the
cyclin dependent kinase inhibitor p27Kip1
Zhang et al., Neuroreport 2004
(Stroke) :
Collectively, our data suggest that stroke induced neural progenitor proliferation is mediated by down-regulation of
p27Kip1 and
activation of
Akt
Zhang et al., Oncogene 2004
:
We found that ARF antagonized protein kinase B
(PKB)/Akt mediated
p27Kip1 phosphorylation and increased p27 stability in HER2/neu overexpressing cells
Yang et al., Oncogene 2005
(Cell Transformation, Neoplastic) :
Constitutively active FOXO4 inhibits
Akt activity,
regulates p27 Kip1 stability, and suppresses HER2 mediated tumorigenicity
Rosner et al., Amino Acids 2007
(Tuberous Sclerosis) :
Akt also
regulates the cytoplasmic/nuclear localization of the
cyclin dependent kinase inhibitor p27
Hennenlotter et al., Oncol Rep 2008
(Carcinoma, Renal Cell...) :
Furthermore,
Akt activation may not
result in a decreased
p27Kip1 , the latter being retained and overexpressed in the majority of renal cell cancers when compared with the corresponding benign renal parenchyma
Heo et al., Growth Factors 2008
:
Moreover, TGF-alpha increased cyclin D/CDK 4 and cyclin E/CDK 2 levels, while decreasing p21cip1/waf1 and
p27kip1 , which were
blocked by the inhibition of
Akt , mTOR and Notch