Ccnd3 Blocking Peptide (N-Term) Blocking Peptide

CCND3: Regulatory component of the cyclin D3-CDK4 (DC) complex that phosphorylates and inhibits members of the retinoblastoma (RB) protein family including RB1 and regulates the cell-cycle during G(1)/S transition. Phosphorylation of RB1 allows dissociation of the transcription factor E2F from the RB/E2F complex and the subsequent transcription of E2F target genes which are responsible for the progression through the G(1) phase. Hypophosphorylates RB1 in early G(1) phase. Cyclin D-CDK4 complexes are major integrators of various mitogenenic and antimitogenic signals. Also substrate for SMAD3, phosphorylating SMAD3 in a cell-cycle-dependent manner and repressing its transcriptional activity. Component of the ternary complex, cyclin D3/CDK4/p27Kip1, required for nuclear translocation and activity of the cyclin D-CDK4 complex. Interacts with the CDK4 and CDK6 protein kinases to form a serine/threonine kinase holoenzyme complex. The cyclin subunit imparts substrate specificity to the complex. Interacts with ATF5. Interacts with EIF3K. Component of the ternary complex cyclin D/CDK4/p27Kip1 required for nuclear translocation and modulation of CDK4-mediated kinase activity. Can form similar complexes with either p21Cip1 or CDKN2A. Belongs to the cyclin family. Cyclin D subfamily. 2 isoforms of the human protein are produced by alternative splicing.

Protein type: Nuclear receptor co-regulator; Activator; Cell cycle regulation

Cellular Component: cyclin-dependent protein kinase holoenzyme complex; cytoplasm; focal adhesion; nucleus; plasma membrane

Molecular Function: cyclin-dependent protein kinase activity; protein kinase binding

Biological Process: G1/S transition of mitotic cell cycle; hyaluronan biosynthetic process; positive regulation of cell proliferation; positive regulation of cyclin-dependent protein kinase activity; positive regulation of protein amino acid phosphorylation; regulation of cell cycle; response to glucose stimulus; response to organic substance; response to peptide hormone stimulus; signal transduction; T cell proliferation