Retinoblastoma-like protein 1 (RBL1)

Retinoblastoma-like protein 1 (RBL1, commonly referred to as p107) is a member of the retinoblastoma (RB) family of tumor suppressors, structurally related to RB1 and RBL2/p130. It functions primarily as a cell cycle regulator, influencing the G1-to-S phase transition by binding and inhibiting E2F transcription factors, thereby repressing the transcription of genes required for cell cycle progression. RBL1/p107 is further involved in the establishment and maintenance of heterochromatin, epigenetic gene silencing, and stabilization of histone methylation marks, all of which contribute to genomic integrity. RBL1/p107 function and stability are tightly controlled by phosphorylation via cyclin-dependent kinases (CDK4/CDK6), as well as proteasome- and calpain-mediated degradation. Dysregulation or loss of RBL1/p107 contributes to tumor initiation and progression, though it is generally considered a weaker tumor suppressor than RB1, and its role is highly context-dependent. RBL1/p107 also plays roles in apoptosis, DNA damage response, and immune cell regulation within tumors.

Other names

p107cp107PRB1107 kDa retinoblastoma-associated proteinretinoblastoma-like 1retinoblastoma-like protein 1RBL1pRb1CP107

CDK4/CDK6 inhibitors prevent RBL1/p107 phosphorylation, thereby maintaining it in an active, cell cycle-suppressive state. Indirect restoration of tumor-suppressive function via modulation of upstream signaling pathways.