Author

D. J. Daniels

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· 2

Signature Assays, Organisms & Methods

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Research Focus:cancer & tumor microenvironment· 2 Research Focus:chromatin & epigenetic regulation· 2 Approach:experimental assay· 2 Research Focus:cell signaling & trafficking· 1 Assay:ChIP-seq· 1 Approach:genetic perturbation / CRISPR· 1 Organism:human· 1 Organism:mouse· 1

Frequent Co-Authors

A. Langfald· 1 shared C. A. Day· 1 shared D. Fang· 1 shared E. H. Hinchcliffe· 1 shared F. Grigore· 1 shared F. L. Hakkim· 1 shared H. Gan· 1 shared H. Zhou· 1 shared

Activity by Year

2017-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 21 mutual co-author links

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1 shared paperCancer Biology

A. Langfald

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2 papers

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

H3K27me3-mediated silencing of Wilms Tumor 1 supports the proliferation of brain tumor cells harboring the H3.3K27M mutation

D. Fang, H. Gan, L. Cheng, J.-H. Lee, H. Zhou, J. N. Sarkaria, D. J. Daniels, Z. Zhang

This study shows that H3K27me3 silencing of WT1 supports DIPG cell proliferation, despite global H3K27me3 loss due to H3.3K27M mutation.

bioRxiv · Mar 6, 2017Cancer Biology