{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nRTF2 functions as a critical regulator in the maintenance of genome integrity by ensuring the efficient restart of stalled replication forks. Under conditions of replication stress, RTF2 is actively removed from stalled forks—a process mediated by the proteasomal shuttle proteins DDI1 and DDI2—which is essential to prevent the accumulation of single‐stranded DNA, hyperactivation of DNA damage signaling, and ensuing chromosome instability. Without proper removal of RTF2, cells exhibit replication defects and heightened sensitivity to replication inhibitors, underscoring its pivotal role in promoting fork recovery."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its function in replication, RTF2 also serves as a novel host restriction factor during influenza A virus infection. Acting primarily within the nucleus, RTF2 impedes the early transcriptional events of the virus, thereby limiting viral gene expression and replication. Moreover, the absence of RTF2 not only fosters increased viral transcription but is also associated with a concomitant downregulation of interferon-induced antiviral effectors, highlighting its role in modulating antiviral immunity."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nCollectively, these findings reveal that RTF2 is a multifunctional protein integrating the cellular responses to both DNA replication stress and viral infection. By coordinating the removal from stalled forks to ensure genomic stability and restricting influenza virus transcription in the nucleus to enhance innate immune responses, RTF2 emerges as a key factor in safeguarding cellular homeostasis in diverse stress conditions."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Molly C Kottemann, Brooke A Conti, Francis P Lach, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Removal of RTF2 from Stalled Replisomes Promotes Maintenance of Genome Integrity."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Mol Cell (2018)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.molcel.2017.11.035"}], "href": "https://doi.org/10.1016/j.molcel.2017.11.035"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "29290612"}], "href": "https://pubmed.ncbi.nlm.nih.gov/29290612"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Bing Shao Chia, Bo Li, Ang Cui, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Loss of the Nuclear Protein RTF2 Enhances Influenza Virus Replication."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Virol (2020)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1128/JVI.00319-20"}], "href": "https://doi.org/10.1128/JVI.00319-20"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "32878895"}], "href": "https://pubmed.ncbi.nlm.nih.gov/32878895"}]}]}]}