Description
Protocol
Available protocols: ELISA+
Specificity / Sensitivity
PathScan
Species Reactivity: Human, Mouse, Rat, Monkey
Background
Activity of the cyclin-dependent kinases CDK4 and CDK6 is regulated by T-loop phosphorylation, by the abundance of their cyclin partners (the D-type cyclins), and by association with CDK inhibitors of the Cip/Kip or INK family of proteins (1). The inactive ternary complex of cyclin D/CDK4 and p27 Kip1 requires extracellular mitogenic stimuli for the release and degradation of p27 concomitant with a rise in cyclin D levels to affect progression through the restriction point and Rb-dependent entry into S-phase (2). The active complex of cyclin D/CDK4 targets the retinoblastoma protein for phosphorylation, allowing the release of E2F transcription factors that activate G1/S-phase gene expression (3). Levels of cyclin D protein drop upon withdrawal of growth factors through downregulation of protein expression and phosphorylation-dependent degradation (4).
Alternate Names
B-cell CLL/lymphoma 1; B-cell lymphoma 1 protein; BCL-1; BCL-1 oncogene; BCL1; CCND1; CycD1; cyclin D1; D11S287E; G1/S-specific cyclin D1; G1/S-specific cyclin-D1; PRAD1; PRAD1 oncogene; U21B31
