Cyclins and cyclin-dependent kinases (cdks) are evolutionarily conserved proteins that are essential for cell-cycle control in eukaryotes. Cyclins (regulatory subunits) bind to cdks (catalytic subunits) to form complexes that regulate the progression of the cell cycle. The main cyclin-cdks complexes formed in vertebrae cells are cyclin-cdks complexes that regulate the progression of the cell cycle. The main cyclin-cdks complexes formed in vertebrae cells are cyclin D-cdk4 (G0/G1), cyclin E-cdk2 (G1/S), cyclin A-cdk2 (S) and cyclin B1-cdk1 (G2/M). These complexes are regulated by activating and inhibitory phosphorylation events, as well as by interactions with small regulatory proteins including p21 and p27[Kip1]. Specific substrates for cdk-cyclin complexes include nuclear lamins, histones, oncogenes (e.g., c-abl and SV40) large T-Ag), tumor suppressor genes (e.g., retinoblastoma protein, Rb) nucleolin and others. Cyclin B1 is a mitotic cyclin complex; expression is normally low in G0/G1, increases in S, and is maximal during G2/M. Cyclin B1 is rapidly degraded at the end of mitosis and is required for cells to exit from mitosis. Clone GNS-1 recognizes an epitope between amino acids 1-21 of human Cyclin B1. GNS-1 crossreacts with hamster and mouse cyclin B1 by western blot analysis; however, it has not been evaluated for crossreactivity by flow cytometry. Recombinant human cyclin B1 was used as immunogen.
