Rb protein
/ AR-bee PROH-teen /
Picture a gatekeeper standing at a turnstile, blocking it shut. As long as the gatekeeper holds the gate, no one can pass through to the next room. Only when a proper ticket arrives does the gatekeeper step aside and let people through. In the cell, the Rb protein is that gatekeeper, standing at the gate between resting and dividing, holding it shut until the cell is truly cleared to divide.
More precisely, Rb (short for retinoblastoma protein) is a tumor suppressor protein that controls the most important checkpoint of the cell cycle — the 'restriction point' near the end of the G1 phase, just before a cell commits to copying its DNA. In its active state, Rb clamps onto a family of transcription factors (called E2F) and keeps the genes for DNA replication switched off. When the cell receives proper growth signals, enzymes called cyclin-dependent kinases attach phosphate tags to Rb, which makes it let go of E2F; the division genes switch on and the cell proceeds. So Rb is the brake that is released only on cue.
Rb matters because it was the very first tumor suppressor ever discovered, found through a rare childhood eye cancer called retinoblastoma, and it inspired Knudson's two-hit model. When both copies of the RB1 gene are lost, the gate hangs permanently open and cells slip into division uncontrolled. A common misconception is that Rb 'pushes' cells to divide; in truth it does the opposite — it holds them back, and losing it removes a key restraint.
In hereditary retinoblastoma, a child inherits one broken RB1 copy in every cell. It takes just one more 'hit' — losing the second copy in a single retinal cell — for that cell to lose its gatekeeper and grow into an eye tumor. This pattern is exactly what led Knudson to propose that two hits are needed.
Rb guards the G1 restriction point; losing both copies opens the gate.
Rb holds cells back from dividing; it does not push division. Losing it removes a brake rather than adding an accelerator.