Abstract
The retinoblastoma protein is an inhibitor of cell cycle progression from the G1 to the S phase of the cell cycle. It acts through its ability to interact with cellular target molecules such as E2F transcription factors. The function of pRB is negatively regulated by a cell-cycle dependent phosphorylation catalyzed by cyclin-dependent kinases in the late G1 cell cycle phase. Recent evidence indicates that this pRB inactivation is a key molecular event leading to the S-phase commitment at the G1 restriction point in the cell cycle. Deregulated inactivation of pRB in G1 phase may be a universal mechanism underlying cellular transformation.
MeSH Terms
Animals
Apoptosis/physiology
Cell Cycle/physiology
Cell Cycle Proteins
Cell Transformation, Neoplastic
Cyclin D
Cyclin E/metabolism
Cyclin-Dependent Kinase Inhibitor p21
Cyclin-Dependent Kinase Inhibitor p27
Cyclins/metabolism,physiology
Discoidin Domain Receptor 1
Fungal Proteins/metabolism
G1 Phase/physiology
Gene Expression Regulation
Mammals/physiology
Mice
Mice, Knockout
Microtubule-Associated Proteins/physiology
Models, Biological
Phosphorylation
Protein Processing, Post-Translational
Protein-Tyrosine Kinases/metabolism
Receptor Protein-Tyrosine Kinases/physiology
Retinoblastoma Protein/physiology
S Phase/physiology
Saccharomyces cerevisiae/cytology,metabolism
Signal Transduction
Tumor Suppressor Proteins
Chemicals
Cdkn1a protein, mouse
Cdkn1b protein, mouse
Cell Cycle Proteins
Cyclin D
Cyclin E
Cyclin-Dependent Kinase Inhibitor p21
Cyclins
Fungal Proteins
Microtubule-Associated Proteins
Retinoblastoma Protein
Tumor Suppressor Proteins
Cyclin-Dependent Kinase Inhibitor p27
DDR1 protein, human
Discoidin Domain Receptor 1
Protein-Tyrosine Kinases
Receptor Protein-Tyrosine Kinases
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Hatakeyama M
Whitehead Institute for Biomedical Research, Massachusetts Institute of Technology, Cambridge 02142, USA.
Weinberg R A