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Cell and Developmental Biology Commons

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Molecular Biosciences Faculty Publications

DNA Damage

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Full-Text Articles in Cell and Developmental Biology

A Novel Rrm3 Function In Restricting Dna Replication Via An Orc5-Binding Domain Is Genetically Separable From Rrm3 Function As An Atpase/Helicase In Facilitating Fork Progression, Salahuddin Syed, Claus Desler, Lene J Rasmussen, Kristina H Schmidt Dec 2016

A Novel Rrm3 Function In Restricting Dna Replication Via An Orc5-Binding Domain Is Genetically Separable From Rrm3 Function As An Atpase/Helicase In Facilitating Fork Progression, Salahuddin Syed, Claus Desler, Lene J Rasmussen, Kristina H Schmidt

Molecular Biosciences Faculty Publications

In response to replication stress cells activate the intra-S checkpoint, induce DNA repair pathways, increase nucleotide levels, and inhibit origin firing. Here, we report that Rrm3 associates with a subset of replication origins and controls DNA synthesis during replication stress. The N-terminal domain required for control of DNA synthesis maps to residues 186-212 that are also critical for binding Orc5 of the origin recognition complex. Deletion of this domain is lethal to cells lacking the replication checkpoint mediator Mrc1 and leads to mutations upon exposure to the replication stressor hydroxyurea. This novel Rrm3 function is independent of its established role …


Role Of Deubiquitinating Enzymes In Dna Repair, Younghoon Kee, Tony T. Huang Feb 2016

Role Of Deubiquitinating Enzymes In Dna Repair, Younghoon Kee, Tony T. Huang

Molecular Biosciences Faculty Publications

Both proteolytic and nonproteolytic functions of ubiquitination are essential regulatory mechanisms for promoting DNA repair and the DNA damage response in mammalian cells. Deubiquitinating enzymes (DUBs) have emerged as key players in the maintenance of genome stability. In this minireview, we discuss the recent findings on human DUBs that participate in genome maintenance, with a focus on the role of DUBs in the modulation of DNA repair and DNA damage signaling.