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Cancertype
Diploid human fibroblasts in which hPOT1 expression has been suppressed harbor telomeres that are longer than control cells.
unknown
PML depletion suppressed POT1 poly-ubiquitination, suggesting an interplay between USP7 and PML to trigger POT1 degradation in TSPYL5-depleted ALT(+) cells. We demonstrate that ALT telomeres need to be protected from POT1 degradation in ALT-associated PML bodies and identify TSPYL5 as an ALT(+) cancer-specific therapeutic target.
unknown