The retinoblastoma (RB) gene encodes a phosphoprotein that negatively regulates the cell cycle. This activity is critical for the classic RB-mediated tumor suppression function. Mutations in the retinoblastoma susceptibility gene lead to childhood retinal cancer, and the RB pathway is altered in 70% of human cancer types. Upon mitogenic signaling, RB protein is inhibited by hyperphosphorylation, which disrupts RB transcriptional repression complexes to allow G1 to S phase transition. RB also induces S phase arrest, triggered by the intra-S phase checkpoint in the presence of DNA-damaging agents, such as cisplatin and VP-16. RB also participates in other cellular processes, such as terminal cell differentiation and maintenance of genetic stability. It has also been suggested that RB can exert an anti-apoptotic function and that RB is cleaved by caspases during apoptosis induced by VP-16 and tumor necrosis factor-α (TNF-α).
Anti-pRb [S807/S811] (J112-906)-166Er—50 Tests