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2. Why is pRB function compromised in human tumors through mutations of its encoding gene while...

2. Why is pRB function compromised in human tumors through mutations of its encoding gene while the genes encoding its two cousins, p170 and p130, have virtually never been found to suffer mutations in the genomes of cancer cells?

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  • pRb controls passage through the R point. If cells make it through the R-point they continue through growth and division.
  • If not, they are sent into the quiescent state. Other pocket proteins, p107 and p130, help determine growth vs. quiescence as well.
  • Hypophosphorylation of pRb blocks passage through the R-point. Hyperphosporylation of pRb permits passage.
  • p107 and p130 are only active in the G0, late G1 and S phases where the cell does not respond to mitogens.
  • But because pRb is active during early G1 and at the R point, and these are the locations where the cell responds to mitogens, compromised function of pRb is caused by mutations in the genomes of cancer cells.

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