Phone (Lab): 704.687.8529
Office: Woodward 490A
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All eukaryotes have evolved an elaborate network, DNA damage response (DDR), to detect aberrant DNA structures or stalled replication forks, and to coordinate DNA repair, checkpoint activation, cell cycle arrest, and senescence/apoptosis. From a broader perspective, the DDR machinery plays important roles in fundamental biomedical fields, such as DNA replication, DNA damage repair, cell cycle regulation, transcription, apoptosis, senescence, and autophogy. Defective DDR pathways compromise genomic integrity, leading to human diseases.
The research projects in the Yan lab focus on several essential questions linking DDR and human diseases, such as cancer, sepsis, aging, and neurodegenerative disorders. Using biochemical, molecular and cell biology approaches, our laboratory is interested in crucial issues in maintaining genomic stability, including checkpoint activation, DNA damage repair, and translesion synthesis (TLS) in response to DNA replication stress and oxidative stress as well as other stressful conditions. Ultimately, our research program will help to better understand how cells maintain genome stability and to provide novel clues for detection and treatment of human diseases. Xenopus egg extracts and mammalian cell lines will be used as model systems to investigate fundamental biomedical questions with cutting-edge technologies. One aim of this lab is to establish a motivated and productive research team. You are welcome to visit and/or join us!
(1) TopBP1-mediated checkpoint signaling in DNA replication stress response
(2) Molecular mechanisms of DNA damage response pathway in oxidative stress
(3) Single-strand break repair and signaling
(4) Translesion DNA synthesis and DNA damage response
(5) DNA repair and DNA damage response pathways in human diseases (cancer, sepsis, aging, and neurodegenerative diseases)
(1) Wallace BD§, Berman Z§, ¶,, Mueller GA, Lin Y#, Chang T, Andres SN, Wojtaszek JL, DeRose EF, Appel CD, London RE, Yan S,*, Williams RS*. 2017. APE2 Zf-GRF facilitates 3′-5′ resection of DNA damage following oxidative stress. Proceedings of the National Academy of Sciences of the United States of America. 114 (2):304-309. (PMCID: PMC5240719; PMID: 28028224)
(2) Li Z, Li J, Kong Y, Yan S, Ahmad N, Liu X*. 2017. Plk1 phosphorylation of Mre11 antagonizes DNA damage response. Cancer Research. 77(12): 3169-3180. (PMCID: PMC5504882; PMID: 28512243)
(3) Bai L, Michael WM, Yan S,*. 2014. Importin β-dependent nuclear import of TopBP1 in ATR-Chk1 checkpoint in Xenopus egg extracts. Cellular Signalling. 26 (5): 857-867. (PMCID: PMC3951582; PMID: 24440306)
(4) Willis J§,¶, Patel Y§,‡, Lentz B ‡, Yan S*. 2013. APE2 is required for ATR-Chk1 checkpoint activation in response to oxidative stress. Proceedings of the National Academy of Sciences of the United States of America. 110 (26): 10592-10597. (PMCID: PMC3696815; PMID: 23754435).
(5) Yan S,, Michael WM. 2009. TopBP1 and DNA polymerase-alpha directly recruit the 9-1-1 complex to stalled DNA replication forks. Journal of Cell Biology. 184(6): 793-804. PMCID: PMC2699152
Click the link for the video (~10 minutes): JoVE-Video
Willis J#, DeStephanis D#, Patel Y, Gowda V, and Yan S*. 2012. Study of the DNA damage checkpoint using Xenopus egg extracts. Journal of Visualized Experiments. (69): e4449 10.3791/4449. DOI: http://dx.doi.org/10.3791/4449 PMCID: PMC3514051.
Publications from the Yan Lab: http://www.researchgate.net/profile/Shan_Yan/
Department of Biology website: http://biology.uncc.edu/