a member of the highly conserved cyclin family, whose members are characterized by a dramatic periodicity in protein abundance through the cell cycle. Cyclins function as regulators of CDK kinases. Forms a complex with and functions as a regulatory subunit of CDK4 or CDK6, whose activity is required for cell cycle G1/S transition. This protein has been shown to interact with tumor suppressor protein Rb and the expression of this gene is regulated positively by Rb. Note: This description may include information from UniProtKB.
Protein type: Nuclear receptor co-regulator; Cell cycle regulation; Oncoprotein; Activator
Molecular Function: protein binding; enzyme binding; histone deacetylase binding; protein complex binding; kinase activity; cyclin-dependent protein kinase regulator activity; transcription corepressor activity; protein kinase binding; transcription factor binding; protein kinase activity
Biological Process: fat cell differentiation; lactation; G1 DNA damage checkpoint; re-entry into mitotic cell cycle; positive regulation of cyclin-dependent protein kinase activity; negative regulation of Wnt receptor signaling pathway; regulation of cell cycle; positive regulation of mammary gland epithelial cell proliferation; negative regulation of epithelial cell differentiation; negative regulation of transcription from RNA polymerase II promoter; Wnt receptor signaling pathway through beta-catenin; protein amino acid phosphorylation; Leydig cell differentiation; regulation of transcription, DNA-dependent; positive regulation of cell proliferation; Wnt receptor signaling pathway; transcription, DNA-dependent; unfolded protein response; mammary gland epithelial cell proliferation; response to organic nitrogen; cell cycle; cell division; positive regulation of protein amino acid phosphorylation; regulation of cyclin-dependent protein kinase activity; regulation of protein kinase activity; response to DNA damage stimulus; G1/S transition of mitotic cell cycle
LTP: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.