Abstract
Cancer A cell's telomeres progressively shorten with each mitotic division, which eventually halts proliferation. Robinson et al. uncovered a mechanism that supports a type of telomere maintenance called alternative lengthening of telomeres (ALT) (see the Focus by Churikov and Géli). In cancer cell lines that maintain telomere length through ALT, the telomere-binding protein RAP1 was modified, dissociated from telomeres, and localized to the cytoplasm, where it promoted ALT-associated gene expression. This work reveals potential therapeutic opportunities to halt the growth of some tumors. Sci. Signal. 14 , eabe9613, eabj1166 (2021)
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