Author

L. Sepaniac

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

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Cancer Biology· 1

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Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:chromatin & epigenetic regulation· 1 Approach:experimental assay· 1 Approach:genetic perturbation / CRISPR· 1 Organism:mouse· 1 Assay:proteomics· 1

Frequent Co-Authors

A. Langfald· 1 shared C. A. Day· 1 shared D. J. Daniels· 1 shared E. H. Hinchcliffe· 1 shared F. Grigore· 1 shared F. L. Hakkim· 1 shared J. P. Robinson· 1 shared J. Stumpff· 1 shared

Activity by Year

2022-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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1 shared paperCancer Biology

A. Langfald

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1 paper

Recent·Most cited

The histone H3.3 K27M mutation found in diffuse midline gliomas coordinately disrupts adjacent H3.3 Ser31 phosphorylation and the fidelity of chromosome segregation

C. A. Day, F. Grigore, F. L. Hakkim, A. Langfald, S. Fadness, P. Schwab, L. Sepaniac, J. Stumpff, D. J. Daniels, K. T. Vaughan, J. P. Robinson, E. H. Hinchcliffe

This paper shows that the H3.3 K27M mutation in gliomas reduces Ser31 phosphorylation, leading to chromosome missegregation and tumor formation.

bioRxiv · May 27, 2022 · PreprintCancer Biology