Description
Protocol
Available protocols: ELISA+
Specificity / Sensitivity
PathScan
Species Reactivity: Human, Monkey
Background
The retinoblastoma tumor suppressor protein Rb regulates cell proliferation by controlling progression through the restriction point within the G1-phase of the cell cycle (1). Rb has three functionally distinct binding domains and interacts with critical regulatory proteins including the E2F family of transcription factors, c-Abl tyrosine kinase, and proteins with a conserved LXCXE motif (2-4). Cell cycle-dependent phosphorylation by a CDK inhibits Rb target binding and allows cell cycle progression (5). Rb inactivation and subsequent cell cycle progression likely requires an initial phosphorylation by cyclin D-CDK4/6 followed by cyclin E-CDK2 phosphorylation (6). Specificity of different CDK/cyclin complexes has been observed (6-8) and cyclin D1 is required for Ser780 phosphorylation (9).
Alternate Names
exon 17 tumor GOS561 substitution mutation causes premature stop; GOS563 exon 17 substitution mutation causes premature stop; OSRC; p105-Rb; p110-RB1; pp110; PPP1R130; pRb; prepro-retinoblastoma-associated protein; protein phosphatase 1, regulatory subunit 130; Rb; RB transcriptional corepressor 1; RB1; retinoblastoma 1; retinoblastoma suspectibility protein; Retinoblastoma-associated protein
