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CDK4 — CDK5
Pathways - manually collected, often from reviews:
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Balajee et al., Nucleic Acids Res 2001
:
The efficiency and the time course of
PCNA complex induced by
BLM were identical in both normal and AT cells
González et al., J Biol Chem 2003
:
We show in this work that the inhibition of
Cdk4 ( 6 ) in Rb(-/-) 3T3 cells
enhances the accumulation of the p27 ( kip1 )
cyclin dependent kinase inhibitor when these cells are induced into quiescence
Lu et al., J Pharm Pharmacol 2007
:
AOA-GMe induced cell cycle arrest in G0/G1 and blocked G1-S transition, which correlated well with marked decreases in levels of cyclin D, cyclin dependent kinase
CDK4 and phosphorylated retinoblastoma protein, and
increases in the
cyclin dependent kinase inhibitor p15
McNally et al., BMC structural biology 2010
:
Fluorescence anisotropy binding experiments show that the inability of the mutant clamp proteins to stimulate RFC
ATPase activity is likely
caused by reduction in the affinity of the
RFC-PCNA complex for DNA
Kang et al., Apoptosis 2012
:
Cell cycle analysis indicated thioridazine induced the down-regulation of cyclin D1, cyclin A and
CDK4 , and the induction of p21 and p27, a
cyclin dependent kinase inhibitor
Stivala et al., Carcinogenesis 1993
:
X-rays, u.v.-C and
BLM induced a significant increase in
PCNA complex as compared to the control samples