ArticleNature communications2020
SDE2 integrates into the TIMELESS-TIPIN complex to protect stalled replication forks.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Germline variants and breast cancer survival in patients with distant metastases at primary breast cancer diagnosis.Scientific reports · 2021Pooled it
- USP5 acts as a proteolytic switch to control SDE2 function via UBL-directed cleavage.Nature communications · 2026Article
- Two fork protection complexes at the replication fork play distinct roles in fork progression and stress response.Research square · 2026Article
- Inhibition of SDE2 promotes autophagy-dependent ferroptosis in multiple myeloma.Redox biology · 2026Article
- Identification of key miRNAs and target genes in psoriasis vulgaris and obesity co-morbidity.European journal of medical research · 2026Article
- Transcriptome and weighted gene co-enrichment analysis revealed modules and candidate genes associated with barley response to low potassium stress.Frontiers in plant science · 2026Article
- A new model for coordinating the functions of TIMELESS at the replication fork.bioRxiv : the preprint server for biology · 2025Article
- TIPIN coordinates ATM-dependent checkpoint and NF-κB signaling to counteract DNA replication damage from topoisomerase inhibition.Communications biology · 2025Article
- Loss of DNA replication fork protection by TIMELESS degradation supports oncogene-induced senescence.Biochemical and biophysical research communications · 2025Article
- The DNA-PKcs/JNK/p53 pathway underlies changes in cell fate decision toward death during DNA replication catastrophe.Nucleic acids research · 2025Article
- The fork protection complex generates DNA topological stress-induced DNA damage while ensuring full and faithful genome duplication.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Intrinsic PARG inhibitor sensitivity is mimicked byNAR cancer · 2024Article
- The TIMELESS and PARP1 interaction suppresses replication-associated DNA gap accumulation.Nucleic acids research · 2024Article
- Poly(ADP-ribosyl)ation of TIMELESS limits DNA replication stress and promotes stalled fork protection.Cell reports · 2024Article
- Timeless-Tipin interactions with MCM and RPA mediate DNA replication stress response.Frontiers in cell and developmental biology · 2024Article
- SP3-induced Timeless transcription contributes to cell growth of lung adenocarcinoma cells.PloS one · 2024Article
- Review
- Replisome dysfunction upon inducible TIMELESS degradation synergizes with ATR inhibition to trigger replication catastrophe.Nucleic acids research · 2023Article
- The Adaptive Mechanisms and Checkpoint Responses to a Stressed DNA Replication Fork.International journal of molecular sciences · 2023Review
- Zinc Finger MYND-Type Containing 8 (ZMYND8) Is Epigenetically Regulated in Mutant Isocitrate Dehydrogenase 1 (IDH1) Glioma to Promote Radioresistance.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Protecting replication fork integrity during DNA replication is essential for maintaining genome stability. Here, we report that SDE2, a PCNA-associated protein, plays a key role in maintaining active replication and counteracting replication stress by regulating the replication fork protection complex (FPC). SDE2 directly interacts with the FPC component TIMELESS (TIM) and enhances its stability, thereby aiding TIM localization to replication forks and the coordination of replisome progression. Like TIM deficiency, knockdown of SDE2 leads to impaired fork progression and stalled fork recovery, along with a failure to activate CHK1 phosphorylation. Moreover, loss of SDE2 or TIM results in an excessive MRE11-dependent degradation of reversed forks. Together, our study uncovers an essential role for SDE2 in maintaining genomic integrity by stabilizing the FPC and describes a new role for TIM in protecting stalled replication forks. We propose that TIM-mediated fork protection may represent a way to cooperate with BRCA-dependent fork stabilization.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.