Tumor Suppressor Protein Antibody Sampler Kit

Background

p130, Retinoblastoma-like protein 2 (Rb2), is a key regulator of entry into cell division. It is directly involved in heterochromatin formation by maintaining overall chromatin structure and, in particular, that of constitutive heterochromatin by stabilizing histone methylation. p130 recruits and targets histone methyltransferases KMT5B and KMT5C, leading to epigenetic transcriptional repression. It controls histone H4 'Lys-20' trimethylation and probably acts as a transcription repressor by recruiting chromatin-modifying enzymes to promoters. It is a potent inhibitor of E2F-mediated trans-activation, associates preferentially with E2F5. It binds to cyclins A and E as well as binds to and may be involved in the transforming capacity of the adenovirus E1A protein. p16, Cyclin Dependent Kinase Inhibitor 2A (CDK2NA), generates several transcripts/proteins which differ from each other in their first exons. In spite of the structural and some functional differences, all the proteins encoded by the CDKN2A gene are capable of inducing cell cycle arrest in G1 and G2 phases. Acts as a negative regulator of the proliferation of normal cells by interacting strongly with CDK4 and CDK6. This inhibits their ability to interact with cyclins D and to phosphorylate the retinoblastoma protein. p27, p27Kip is a cyclin-dependent kinase inhibitor that shares a limited similarity with CDK inhibitor CDKN1A/p21. p27 binds to and prevents the activation of cyclin E-CDK2 or cyclin D-CDK4 complexes, and thus controls the cell cycle progression at G1. The degradation of this protein, which is triggered by its CDK dependent phosphorylation and subsequent ubiquitination by SCF complexes, is required for the cellular transition from quiescence to the proliferative state.