Anti-Rb (Human) mAb

Mutation of the retinoblastoma tumor suppressor gene alone is sufficient to cause retinoblastoma in humans, suggesting that it might play a role in the normal coordination of cell proliferation and cell death. Deletion or mutational inactivation of the retinoblastoma tumor suppressor protein (Rb) is correlated with the genesis of a variety of human cancers including retinoblastoma, osteosarcoma, and carcinomas of the breast, bladder, and lung. Rb protein is phosphorylated by cyclinD-Cdk4/Cdk6 and cyclinA/cyclinE-Cdk2 during the G1/S transition. This phosphorylation causes the inactivation of the growth inhibitory functions of Rb. Rb undergoes phosphorylation and functional inactivation, permitting the cell to proceed into late G1.