Fig. 6: Integrating relative mutational difficulty to assess the functional status of PTEN and INK4A mutations.
From: Defining relative mutational difficulty to understand cancer formation
a Original and revised counts of indicated PTEN mutants. Expression of wild-type PTEN suppresses AKT signaling in 786-O cells, which do not express PTEN. PTEN Mutants with low revised counts (in blue) behave like wild-type PTEN and suppress downstream AKT signaling. PTEN mutants with high revised counts (in black) lose gene function and cannot suppress AKT signaling. The original and revised counts are listed below each mutant. b Expression wild-type INK4A suppress growth of U251 cells, in which the INK4A locus is deleted. b’ INK4A mutants with low revised counts retain wild-type gene function and suppressed U251 growth. b” CDKN2A mutants with high revised counts are defective in gene function and are well tolerated by U251 cells. The original and revised counts are listed below each mutant. c INK4A mutants with high revised counts (in black) cannot induce cell cycle arrest in U251 cells. CDKN2A mutants with low revised counts (in blue) behave like wild-type CDKN2A and induce G1/early S phase arrest in U251 cells.
