Anti-CCND3: Mouse Cyclin D3 Antibody

D-type Cyclins couple extracellular signals to the biochemical machinery that governs progression through G1 phase of the mammalian cell division cycle. Induced by growth factor stimulation, D-type Cyclins assemble with Cyclin-dependent kinases CDK4 and CDK6 to form holoenzymes that facilitate exit from G1 by phosphorylating key substrates, including the retinoblastoma protein. Activation of the holoenzymes is antagonized by polypeptide inhibitors of CDK activity, which are induced by antiproliferative signals. Once cells pass a late G1 restriction point, Cyclin-D-dependent kinases are unnecessary for completion of the cell cycle, implying that their primary role is to sense the cell’s readiness to replicate DNA and to enforce the commitment to enter S phase.³ Of the three D-type Cyclins, each of which binds Cyclin-dependent kinase (CDK), it is Cyclin D1 overexpression that is predominantly associated with human tumorigenesis and cellular metastases. In recent years accumulating evidence suggests that in addition to its original description as a CDK-dependent regulator of the cell cycle, Cyclin D1 also conveys cell cycle or CDK-independent functions. Cyclin D1 associates with, and regulates activity of, transcription factors, coactivators and corepressors that govern histone acetylation and chromatin remodeling proteins. The recent findings that Cyclin D1 regulates cellular metabolism, fat cell differentiation and cellular migration have refocused attention on novel functions of Cyclin D1 and their possible role in tumorigenesis.⁴