Author

F. M. Johnson

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Cancer Biology· 3

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Organism:human· 3 Research Focus:cancer & tumor microenvironment· 2 Research Focus:cell type annotation· 2 Assay:bulk RNA-seq· 1 Research Focus:differential expression· 1 Research Focus:drug response / drug discovery· 1 Research Focus:gene regulatory network inference· 1

Frequent Co-Authors

J. Wang· 3 shared L. Shen· 3 shared C. R. Pickering· 2 shared A. Hefner· 1 shared A. Poteete· 1 shared A. Sheth· 1 shared B. Beadle· 1 shared B. Zhang· 1 shared

Activity by Year

2020-2020 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 29 mutual co-author links

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3 shared papersCancer Biology

J. Wang

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3 papers

Recent·Most cited

Lung cancer models reveal SARS-CoV-2-induced EMT contributes to COVID-19 pathophysiology

C. A. Stewart, C. M. Gay, K. Ramkumar, K. R. Cargill, R. J. Cardnell, M. B. Nilsson, S. Heeke, E. M. Park, S. T. Kundu, L. Diao, Q. Wang, L. Shen, Y. Xi, B. Zhang, C. M. Della Corte, , L. A. Byers

The paper investigates how SARS-CoV-2 infection induces epithelial-mesenchymal transition (EMT) in lung cancer models, leading to changes in gene expression and potential therapeutic targets.

bioRxiv · May 28, 2020 · PreprintCancer Biology

Inhibition of histone acetyltranserase function radiosensitizes CREBBP/EP300 mutants via repression of homologous recombination, potentially targeting a novel gain of function.

M. Kumar, D. Molkentine, J. Molkentine, K. Bridges, T. Xie, L. Yang, A. Hefner, M. Gao, M. J. Frederick, S. Seth, M. Abdelhakiem, B. Beadle, F. M. Johnson, J. Wang, L. Shen, , H. D. Skinner

The paper identifies CREBBP/EP300 as radiosensitization targets in mutant tumors by inhibiting histone acetyltransferase, which represses homologous recombination and increases radiation sensitivity.

bioRxiv · Apr 10, 2020 · PreprintCancer Biology

Inhibition of nonsense-mediated decay rescues functional p53β/γ isoforms in MDM2-amplified cancers

J. P. Gudikote, T. Cascone, A. Poteete, P. Sitthideatphaiboon, Q. Wu, N. Morikawa, F. Zhang, S. Peng, P. Tong, L. Li, L. Shen, M. Nilsson, P. Jones, E. P. Sulman, J. Wang, , J. Heymach

The paper shows that inhibiting nonsense-mediated decay increases expression of p53β/γ isoforms, which are resistant to MDM2 degradation, thereby restoring p53 function in cancers with MDM2 amplification, HPV infection, or specific p53 mutations.

bioRxiv · Apr 6, 2020 · PreprintCancer Biology