DNA Repair Mechanisms
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Human PIF1 primarily functions as a DNA translocase that clears secondary DNA structures by coupling unwinding with rapid rewinding, with only modest net unwinding observed.
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Cohesin's dual functions in genome maintenance include sister chromatid cohesion and chromatin loop extrusion, crucial for DNA repair and genome stability.
Programmable DNA protonuclei reveal that environmental factors like confinement and viscoelasticity critically influence FUS protein phase separation, with a significant impact on disease-related transitions.
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RO7589831, a WRN inhibitor, shows manageable safety and a 74.2% disease control rate in MSI solid tumors at doses of 150 mg and 600 mg BID.
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Cooperative action of two conserved Glu/Asp residues is essential for early ATP hydrolysis in GHKL ATPases, with mutations impairing activity in human disease variants.
- Open access
Kilobase-sized indels and point mutations drive centromere evolution in Arabidopsis thaliana, with point mutations occurring nearly ten times faster than elsewhere in the genome.
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Inhibition of microhomology-mediated end joining reduces ecDNA levels and impairs cancer cell fitness by targeting TA-rich breakage sites.
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Single-cell mapping reveals that 42% of chromosome breaks in human cells occur at common fragile sites, with 58% occurring at rare, replication-timing-dependent regions.
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SNI1/NSE5 acts as a temperature-sensitive brake on class II crossovers, increasing crossover bias toward subtelomeric regions in Arabidopsis at low temperatures.
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Replication stress drives tumor evolution and creates therapeutic vulnerabilities, with over 100 clinical trials exploring ATR, CHK1, and WEE1 inhibitors.
DNA double-strand break repair pathway choice is governed by complex mechanisms involving chromatin modifications and key repair factors, with BRCA1-BARD1 and 53BP1 playing antagonistic roles.
Disruption of the BRCA1 coiled-coil domain does not impair suppression of tandem duplications in mouse cells and tumor models, indicating a non-essential role in this process.
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Yeast Rad55-Rad57-SHU complex enhances Rad51 filament formation through dynamic structural and nucleotide-regulated mechanisms.
Loss of rice ZEP1 disrupts homologous recombination, causing asynapsis and chromosome fragmentation, highlighting its crucial role in meiotic genome integrity.
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Cohesin-mediated loop extrusion reorganizes replication fork contacts to promote fork slowing and reversal during replication stress, enhancing genome stability.
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PARG stabilizes RAD51AP1 through a PARylation-ubiquitination switch, promoting homologous recombination repair and contributing to chemoresistance in gastric cancer.
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Loss of LDHA in breast cancer cells disrupts R-loop homeostasis, causing increased R-loop accumulation and DNA damage, with 199 peaks rising and 81 decreasing.
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Base editing at PCSK9 in human embryos achieves high efficiency with normal development, supporting the derivation of homozygous edited stem cell lines.
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