1. Combinatorial interactions of cyclins and cyclin-dependent kinases (cdks) during the cell cycle. Progression from G0 through the restriction point in G1 requires the continued presence of growth factors. This requirement is overcome by oncogenes, such as Myc, Ras, or Raf, or tyrosine kinases. Progression through G1 can be blocked by antimitogens, TGFβ, or the p53 or Rb tumor-suppressor genes. Cyclins D and E in complexes with cdks are required for progression through G1 and entry into S phase. Cyclins A and B form complexes with cdk2 later in the cell cycle and are involved in progression from G2 to M. The activity of cyclin-D complexes can be inhibited by p15 and p16, thus preventing the advance of the cell from G1 to S. Other inhibitors of cyclin-dependent kinases, p21 and p27, can act throughout the cell cycle. Cyclins and inhibitors found altered in human cancers are shown in grey.
Source: Oncogenes, The Online Metabolic and Molecular Bases of Inherited Disease
Citation: Valle D, Beaudet AL, Vogelstein B, Kinzler KW, Antonarakis SE, Ballabio A, Gibson K, Mitchell G. The Online Metabolic and Molecular Bases of Inherited Disease; 2014 Available at: Accessed: October 09, 2017
Copyright © 2017 McGraw-Hill Education. All rights reserved