Publications by authors named "Anika Tella"
Article Synopsis
- * Mutations preventing K164 ubiquitination disrupt normal DNA replication and lead to increased replication stress, especially when paired with the DNA polymerase inhibitor aphidicolin.
- * The study highlights that impaired FANCD2 activity in response to K164 mutations reduces its ability to associate with chromatin, thereby hindering the mitotic DNA synthesis process, which is essential to prevent under-replicated DNA.
Faithful genome duplication is a challenging task for dividing mammalian cells, particularly under replication stress where timely resolution of late replication intermediates (LRIs) becomes crucial prior to cell division. In human cancer cells, mitotic DNA repair synthesis (MiDAS) is described as a final mechanism for the resolution of LRIs to avoid lethal chromosome mis-segregation. RAD52-driven MiDAS achieves this mission in part by generating gaps/breaks on metaphase chromosomes, which preferentially occur at common fragile sites (CFS).
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