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Claudia Wiese, Ph.D.

Assistant Professor,
Radiation Cancer Biology and Oncology

Office: 485 Molecular and Radiological Biosciences (MRB)
Office Phone: 970-491-7618


Dr. Wiese's Pubmed Publications




Ph.D.: Cell Biology and Genetics, Christian-Albrechts-University, Kiel, Germany: 1995

M.S.: Biochemistry and Radiation Biology, Technical University Darmstadt, Germany: 1990

B.S.: Biology, Technical University Darmstadt, Germany: 1986

Research Interests

Ionizing radiation is highly efficient in introducing DNA double-strand breaks (DSBs).  DSBs also arise from the attack of reactive oxygen species (produced by the cellular metabolism itself) or from the encounter of unrepaired single-strand breaks by DNA replication forks and are created during normal development of the immune system.  DSBs elicit a profound cellular response that involves the activation of cell cycle checkpoints to facilitate DSB repair.  Defects in the cellular response to DSBs underpin many human diseases, including disorders associated with cancer predisposition, immune system dysfunction, radiosensitivity, neurodegeneration and premature aging.  In human cells, many of the genes involved in DSB repair have been identified based on sequence homology to their respective orthologs in lower eukaryotes. However, it has become apparent that DSB repair pathways are much more complex in humans than in lower eukaryotes, and that lower eukaryotes frequently do not encode all of the proteins involved in human DSB repair. Since defects in DSB repair result in life-threatening syndromes in humans, it is important to identify all factors involved.

Studies in the Wiese lab have the following emphasis: (1) to gain detailed information on the molecular mechanisms of DNA DSB repair processes that maintain genome integrity, and (2) to establish the links between new factors in DSB repair and their roles in cancer avoidance. We are using biochemical, structural and cell biological methods, in combination with mouse genetics, to tackle different aspects of DSB repair and genome maintenance mechanisms from molecules to mice.

Selected Publications

Yue Y., Leung S.G., Liu Y., Huang Y., Grundt K., Østvold A.C., Jen K.Y., Schild D., Mao J.H., Wiese C. Nucks1 synergizes with Trp53 to promote radiation lymphomagenesis in mice. Oncotarget, 2016; 7(38): 61874-89.

Parplys A.C., Zhao W., Sharma N., Groesser T., Liang F., Maranon D.G., Leung S.G., Grundt K., Dray E., Idate R., Østvold A.C., Schild D., Sung P., Wiese C. NUCKS1 is a novel RAD51AP1 paralog important for homologous recombination and genome stability. Nucleic Acids Res. 2015; 43(20): 9817-34.


Zhao W., Vaithiyalingam S., San Filippo J., Maranon D. G., Jimenez-Sainz J., Fontenay G. V., Kwon Y., Leung S. G., Lu L., Jensen R. B., Chazin W. J., Wiese C., Sung P. Promotion of BRCA2-dependent homologous recombination by DSS1 via RPA targeting and DNA mimicry. Mol Cell 2015; 59(2): 176-87.


Snijders A. M., Mannion B. J., Leung S. G., Moon S. C., Kronenberg A., Wiese C. Micronucleus formation in human keratinocytes is dependent on radiation quality and tissue architecture. Environ Mol Mutagen 2015; 56: 22-31.

Parplys A. C., Kratz K., Speed M. C., Leung S. G., Schild D., Wiese C. RAD51AP1-deficiency in vertebrate cells impairs DNA replication. DNA Repair 2014; 24: 87-97.

Wiese C., Rudolph J. H., Jakob B., Fink D., Tobias F., Blattner C., Taucher-Scholz G. PCNA-dependent accumulation of CDKN1A into nuclear foci after ionizing radiation. DNA Repair 2012; 11:511-21.

Dunlop M. H., Dray E., Zhao W., San Fillipo J., Tsai M.-S., Leung S. G., Schild D., Wiese C., Sung P. Mechanistic insights into RAD51AP1 action in homologous DNA repair. J Biol Chem 2012; 287: 12343-7.

Dunlop M. H., Dray E., Zhao W., Tsai M.-S., Wiese C., Schild D., Sung P. RAD51-associated Protein 1 (RAD51AP1) interacts with the meiotic recombinase DMC1 through a conserved motif. J Biol Chem 2011; 286: 37328-34.

Dray E., Dunlop M. H., Kauppi L., San Filippo J., Wiese C., Tsai M.-S., Begovic S., Schild D., Jasin M., Keeney S., Sung P. Molecular Basis for Enhancement of the Meiotic DMC1 Recombinase by RAD51AP1.  Proc Natl Acad Sci USA 2011; 2011; 108: 3560-65.

Dray E., Etchin J., Wiese C., Saro D., Williams G. J., Hammel M., Yu X., Galkin V. E., Liu D., Tsai M.-S., Sy S. M., Schild D., Egelman E., Chen J., Sung P. Enhancement of the RAD51 Recombinase by the Tumor Suppressor PALB2. Nat Struct Mol Biol 2010; 17: 1255-1259.

Schild D., Wiese C. Overexpression of RAD51 suppresses recombination defects: a possible mechanism to reverse genomic instability. Nucleic Acids Res 2010; 38: 1061-70.

Zafar F., Seidler S. B., Kronenberg A., Schild D., Wiese C. Homologous recombination contributes to the repair of DNA double-strand breaks induced by high-energy iron ions. Radiat Res 2010; 173: 27-39.


Wiese C., Dray E., Groesser T., San Filippo J., Shi I., Collins D. W., Tsai M.-S., Williams G., Rydberg B., Sung P., Schild D. Promotion of homologous recombination and genomic stability by RAD51AP1 via RAD51 recombinase enhancement. Mol Cell 2007; 28: 482-90.




Kovalenko O. V., Wiese C., Schild D. RAD51AP2, a novel vertebrate- and meiotic-specific protein, shares a conserved RAD51-interacting C-terminal domain with RAD51AP1/PIR51. Nucleic Acids Res 2006; 34: 5081-92.

Wiese C, Hinz J. M., Tebbs R. S., Nham P. B., Urbin S. S., Collins D. W., Thompson L. H., Schild D. Disparate requirements for the Walker A and B ATPase motifs of human RAD51D in homologous recombination. Nucleic Acids Res 2006; 34: 2833-43.

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