More Like this

1. The DNA repair helicase RECQ1 has a checkpoint-dependent role in mediating DNA damage responses induced by gemcitabine

   https://doi.org/10.1074/jbc.RA119.008420  

   Parvathaneni, Swetha ; Sharma, Sudha ( October 2019 , Journal of Biological Chemistry)
2. Gene Co-Expression Analysis of Human RNASEH2A Reveals Functional Networks Associated with DNA Replication, DNA Damage Response, and Cell Cycle Regulation

   https://doi.org/10.3390/biology10030221  

   Marsili, Stefania ; Tichon, Ailone ; Kundnani, Deepali ; Storici, Francesca ( March 2021 , Biology)

   null (Ed.)

   Ribonuclease (RNase) H2 is a key enzyme for the removal of RNA found in DNA-RNA hybrids, playing a fundamental role in biological processes such as DNA replication, telomere maintenance, and DNA damage repair. RNase H2 is a trimer composed of three subunits, RNASEH2A being the catalytic subunit. RNASEH2A expression levels have been shown to be upregulated in transformed and cancer cells. In this study, we used a bioinformatics approach to identify RNASEH2A co-expressed genes in different human tissues to underscore biological processes associated with RNASEH2A expression. Our analysis shows functional networks for RNASEH2A involvement such as DNA replication and DNA damage response and a novel putative functional network of cell cycle regulation. Further bioinformatics investigation showed increased gene expression in different types of actively cycling cells and tissues, particularly in several cancers, supporting a biological role for RNASEH2A but not for the other two subunits of RNase H2 in cell proliferation. Mass spectrometry analysis of RNASEH2A-bound proteins identified players functioning in cell cycle regulation. Additional bioinformatic analysis showed that RNASEH2A correlates with cancer progression and cell cycle related genes in Cancer Cell Line Encyclopedia (CCLE) and The Cancer Genome Atlas (TCGA) Pan Cancer datasets and supported our mass spectrometry findings. 

   more » « less
3. Structure, function and evolution of the Helix-hairpin-Helix DNA glycosylase superfamily: Piecing together the evolutionary puzzle of DNA base damage repair mechanisms

   https://doi.org/10.1016/j.dnarep.2021.103231  

   Trasviña-Arenas, C.H. ; Demir, Merve ; Lin, Wen-Jen ; David, Sheila S. ( December 2021 , DNA Repair)

   null (Ed.)
4. An electrochemical biosensor based on Hairpin-DNA modified gold electrode for detection of DNA damage by a hybrid cancer drug intercalation

   https://doi.org/10.1016/j.bios.2019.02.071  

   Lozano Untiveros, Katherine ; da Silva, Emanuella Gomes ; de Abreu, Fabiane Caxico ; da Silva-Júnior, Edeildo Ferreira ; de Araújo-Junior, João Xavier ; Mendoça de Aquino, Thiago ; Armas, Stephanie M. ; de Moura, Ricardo Olímpio ; Mendonça-Junior, Francisco J.B. ; Serafim, Vanessa Lima ; et al ( May 2019 , Biosensors and Bioelectronics)
5. Persistent DNA damage signaling and DNA polymerase theta promote broken chromosome segregation

   https://doi.org/10.1083/jcb.202106116  

   Clay, Delisa E. ; Bretscher, Heidi S. ; Jezuit, Erin A. ; Bush, Korie B. ; Fox, Donald T. ( October 2021 , Journal of Cell Biology)

   Cycling cells must respond to DNA double-strand breaks (DSBs) to avoid genome instability. Missegregation of chromosomes with DSBs during mitosis results in micronuclei, aberrant structures linked to disease. How cells respond to DSBs during mitosis is incompletely understood. We previously showed that Drosophilamelanogaster papillar cells lack DSB checkpoints (as observed in many cancer cells). Here, we show that papillar cells still recruit early acting repair machinery (Mre11 and RPA3) and the Fanconi anemia (FA) protein Fancd2 to DSBs. These proteins persist as foci on DSBs as cells enter mitosis. Repair foci are resolved in a stepwise manner during mitosis. DSB repair kinetics depends on both monoubiquitination of Fancd2 and the alternative end-joining protein DNA polymerase θ. Disruption of either or both of these factors causes micronuclei after DNA damage, which disrupts intestinal organogenesis. This study reveals a mechanism for how cells with inactive DSB checkpoints can respond to DNA damage that persists into mitosis.

    

   more » « less