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Taylor Bugbee

As seen in: Nature, eLife
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Articles by Taylor Bugbee

Dominant clones leverage developmental epigenomic states to drive ependymoma

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By Alisha Kardian, Hua Sun, Siri Ippagunta, Nicholas Laboe, Srinidhi Varadharajan, Kwanha Yu, Hsiao-Chi Chen, Tuyu Zheng, Jon P. Connelly, Yong-Dong Wang, Jiangshan Zhan, Hengxi Liu, Kimberley Lowe, Taylor Bugbee, Rakesh Pathak, Amanda Bland, Sanya Mehta, Amir Arabzade, Blake Holcomb, Tristen Wright, David S. Gee, Yi Xiao, Samuel K. McBrayer, Thomas E. Merchant, Jun Qi, Adam D. Durbin Verified, Lindsay A. Schwarz, Li Wang, Andrew M Donson, Nicholas Foreman, Sameer Agnihotri, Alfonso Lavado, Suzanne Baker, David Ellison, Hyun Lee, Shondra M. Pruett-Miller, Kelsey C. Bertrand, Benjamin Deneen, Stephen Mack, Erik Emanus, Riley M. Deneen, Sophie Cochiolo, Kaitlin M. Budd, Gabriele Kembuan, Emma Caesar, Amelia Hancock, Joel Murdoch
| Nature Verified
Abstract ZFTA–RELA is the most recurrent genetic alteration seen in paediatric supratentorial ependymoma (EPN) and is sufficient to initiate tumours in mice1. Despite its oncogenic potential, ZFTA–RELA (ZR) is observed nearly exclusively in childhood EPN, with tumours located distinctly in the supratentorial brain of the central nervous system1.
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Beta human papillomavirus 8E6 promotes alternative end-joining

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By Changkun Hu, Ibukun A. Akinyemi, Taylor Bugbee, Rachel Palinski
| eLife
Abstract Double strand breaks (DSBs) are one of the most lethal DNA lesions in cells. The E6 protein of beta-human papillomavirus (HPV8 E6) impairs two critical DSB repair pathways; homologous recombination (HR) and non-homologous end-joining (NHEJ). However, HPV8 E6 only delays DSB repair. How DSBs are repaired in cells with HPV8 E6 remains to be studied. We hypothesize that HPV8 E6 promotes a less commonly used DSB repair pathway, alternative end-joining (Alt-EJ).
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