p21(WAF1) is associated with CDK2 and CDK4 protein during HL-60 cell differentiation by TPA treatment

TPA-treated HL-60 cells are mainly arrested in G1 by p21(WAF1) accumulation. We investigate the downstream changes following such accumulation. Increased p21(WAF1) is associated with CDK2 and CDK4. pRb is dephosphorylated in the presence of p21-CDK2/4 complexes, and the Rb-E2F1 complex increases aft...

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Bibliographic Details
Published in:Cell proliferation 2001-10, Vol.34 (5), p.267
Main Authors: Cho, J W, Jeong, Y W, Kim, K S, Oh, J Y, Park, J C, Lee, J C, Baek, W K, Suh, S I, Suh, M H
Format: Article
Language:English
Subjects:
CDC2-CDC28 Kinases
Cell Adhesion - drug effects
Cell Adhesion - physiology
Cell Cycle - drug effects
Cell Cycle - physiology
Cell Differentiation - drug effects
Cell Differentiation - physiology
Cyclin-Dependent Kinase 2
Cyclin-Dependent Kinase 4
Cyclin-Dependent Kinase Inhibitor p21
Cyclin-Dependent Kinases - metabolism
Cyclins - metabolism
DNA Fragmentation
Enzyme Inhibitors - metabolism
G1 Phase
HL-60 Cells
Humans
Phosphorylation
Protein-Serine-Threonine Kinases - metabolism
Proto-Oncogene Proteins
Retinoblastoma Protein - metabolism
Tetradecanoylphorbol Acetate - pharmacology
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Summary:TPA-treated HL-60 cells are mainly arrested in G1 by p21(WAF1) accumulation. We investigate the downstream changes following such accumulation. Increased p21(WAF1) is associated with CDK2 and CDK4. pRb is dephosphorylated in the presence of p21-CDK2/4 complexes, and the Rb-E2F1 complex increases after TPA treatment, whereas the Rb-HDAC1 complex decreases slightly. Our results suggest that increased p21(WAF1) is associated with CDK2/4, and that these complexes induce pRb dephosphorylation. In turn, hypophosphorylated pRb are mainly complexed with E2F1, but HDAC1 appears not to be a key component in this process.
ISSN:0960-7722
DOI:10.1046/j.0960-7722.2001.00208.x