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AKT1 — CDKN1B

Pathways - manually collected, often from reviews:

• KEGG Pathways in cancer: AKT1/AKT2/AKT3 → CDKN1B (protein-protein, inhibition)
• KEGG Prostate cancer: AKT1/AKT2/AKT3 → CDKN1B (protein-protein, inhibition)
• KEGG Chronic myeloid leukemia: AKT1/AKT2/AKT3 → CDKN1B (protein-protein, inhibition)
• KEGG ErbB signaling pathway: AKT1/AKT2/AKT3 → CDKN1B (protein-protein, inhibition)
• NCI Pathway Database Class I PI3K signaling events mediated by Akt: AKT1 (AKT1) → p27Kip1 (CDKN1B) (modification, activates) Shin et al., Nat Med 2002, Liang et al., Nat Med 2002, Viglietto et al., Nat Med 2002
  Evidence: mutant phenotype, assay, physical interaction
• NCI Pathway Database Integrins in angiogenesis: AKT1 (AKT1) → p27Kip1 (CDKN1B) (cell adhesion, collaborate) Persad et al., J Biol Chem 2001, Cruet-Hennequart et al., Oncogene 2003*
• Reactome Reaction: AKT1 → CDKN1B (reaction) Viglietto et al., Nat Med 2002, Malanga et al., Cell cycle (Georgetown, Tex.) 2008*
• WikiPathways PI3K-AKT-mTOR signaling pathway and therapeutic opportunities: AKT1 → FOXO3/FOXO1/BAD/CDKN1B/GSK3B/FOXO4 (activation)
  
• WikiPathways Apoptosis-related network due to altered Notch3 in ovarian cancer: AKT1 → CDKN1B (unknown)
• WikiPathways Signaling Pathways in Glioblastoma: AKT1/AKT2/AKT3 → CDKN1B (mim-inhibition)
• WikiPathways Association Between Physico-Chemical Features and Toxicity Associated Pathways: AKT1 → Complex of CDKN1A-CDKN1B (mim-inhibition)

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: AKT1 — CDKN1B (direct interaction, enzymatic study) Fujita et al., J Biol Chem 2002*
• IRef Biogrid Interaction: AKT1 — CDKN1B (physical association, affinity chromatography technology) Fujita et al., J Biol Chem 2002*
• IRef Hprd Interaction: AKT1 — CDKN1B (in vitro) Shin et al., Nat Med 2002
• IRef Hprd Interaction: AKT1 — CDKN1B (in vivo) Shin et al., Nat Med 2002
• IRef Innatedb Interaction: AKT1 — CDKN1B (unknown, -) Nacusi et al., Cell division 2006*
• IRef Innatedb Interaction: AKT1 — CDKN1B (unknown, -) Fujita et al., J Biol Chem 2002*
• IRef Innatedb Interaction: AKT1 — CDKN1B (unknown, -) Fujita et al., J Biol Chem 2003*
• IRef Intact Interaction: AKT1 — CDKN1B (phosphorylation reaction, coimmunoprecipitation) Fujita et al., J Biol Chem 2002*
• IRef Intact Interaction: AKT1 — CDKN1B (phosphorylation reaction, experimental interaction detection) Fujita et al., J Biol Chem 2002*

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
Hashimoto et al., Cancer Res 2004 : In addition, caffeine did not affect p16INK4 or p27Kip1 protein levels, but inhibited the phosphorylation of protein kinase B ( Akt ) and glycogen synthase kinase 3beta
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 ... 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
Yang et al., Leuk Res 2012 (Cell Transformation, Neoplastic...) : AKT1 induces caspase mediated cleavage of the CDK inhibitor p27Kip1 during cell cycle progression in leukemia cells transformed by FLT3-ITD ... Taken together, these findings indicate that AKT1 induces caspase mediated cleavage of p27Kip1 , required for G1-S progression in FLT3-ITD cells