Correlation Engine 2.0
Clear Search sequence regions


Sizes of these terms reflect their relevance to your search.

Mammalian cells have evolved multiple pathways to repair DNA double strand breaks (DSBs) and ensure genome stability. In addition to non-homologous end-joining (NHEJ) and homologous recombination (HR), cells evolved an error-prone repair pathway termed microhomology-mediated end joining (MMEJ). The mutagenic outcome of MMEJ derives from the activity of DNA polymerase theta (Polθ) - a multidomain enzyme that is minimally expressed in normal tissue but overexpressed in tumors. Polθ expression is particularly crucial for the proliferation of HR deficient cancer cells. As a result, this mutagenic repair emerged as an attractive target for cancer therapy, and inhibitors are currently in pre-clinical development. Here, we review the multifunctionality of this enigmatic polymerase, focusing on its role during DSB repair in mammalian cells and its impact on cancer genomes. Copyright © 2020 Elsevier Ltd. All rights reserved.

Citation

Alessandra Brambati, Raymond Mario Barry, Agnel Sfeir. DNA polymerase theta (Polθ) - an error-prone polymerase necessary for genome stability. Current opinion in genetics & development. 2020 Feb;60:119-126

Expand section icon Mesh Tags

Expand section icon Substances


PMID: 32302896

View Full Text