English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

Replication fork progression is blocked by a variety impediments including DNA damage, aberrant DNA structures, or nucleotide depletion [1-3]. The response to replication fork stalling varies according the type of replication inhibition, the number of stalled forks and the duration of the treatment [3-7]. Stalled replication forks are at increased risk for DNA damage, which can lead to mutation or cell death [7-13]. The cell relies on the Intra-S phase checkpoint and DNA damage response proteins to preserve fork structure to allow recovery and resumption of the cell cycle [5, 10, 14-19]. Thus, the mechanisms that maintain replica‐ tion fork structure are crucial for genome maintenance, and form a primary barrier to malig‐ nant transformation [20, 21].

Preserving the Replication Fork in Response to Nucleotide Starvation: Evading the Replication Fork Collapse Point