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Human DNA Cross-Link Repair 1A (DCLRE1A, SNM1A); A Target Enabling Package

Documentation:
A description of the materials and methods is included within the TEP datasheet. Cancer cells experience genomic instability, probably through a combination of excessive replicative activity and the loss of function of checkpoint and DNA repair pathways that may have contributed to the oncogenic transformation. Chemotherapy by DNA-damaging agents such as cisplatin and nitrogen mustards create DNA interstrand crosslinks (ICL), which can lead to double-strand breaks and cell death when the cells replicate their DNA. Genotoxic drugs are counteracted by the cell’s DNA damage response. Hence, it is expected that inhibiting DNA repair proteins would sensitise cells to chemotherapy. Here we address an enzyme that participates in the repair of ICLs, DCLRE1A. The TEP includes expression clones and methods for producing the catalytic domain and high-throughput activity assays. Furthermore, we provide a crystallization system that generates thousands of reproducible crystals that allow soaking of small-molecule ligands. We provide crystal structures of several small molecule fragments and inhibitors, opening the way to development of more potent and selective inhibitors.
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1

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Institution:
University of Oxford
Division:
MSD
Department:
NDM
Sub department:
Structural Genomics Consortium
Role:
Researcher, Creator

Contributors

Department:
Oncology
Role:
Researcher, Data collector
Role:
Principal Investigator (PI)
Institution:
University of Oxford
Division:
MSD
Department:
NDM
Sub department:
Structural Genomics Consortium
Role:
Researcher
Institution:
University of Oxford
Division:
MPLS
Department:
Chemistry
Sub department:
Organic Chemistry
Role:
Researcher
Institution:
University of Oxford
Division:
MPLS
Department:
Chemistry
Sub department:
Organic Chemistry
Role:
Researcher



Publisher:
University of Oxford
Publication date:
2018
Version number:
1
DOI:

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