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The H3K36me2 writer-reader dependency in H3K27M-DIPG
MAT2A and methionine dependency are indispensible for H3K27M mutant gliomas.
Histone H3 lysine27-to-methionine (H3K27M) gain-of-function mutations occur in highly aggressive pediatric gliomas. Here, we establish a Drosophila animal model for the pathogenic histone H3K27M mutation and show that its overexpression resembles Polycomb repressive complex 2 (PRC2) loss-of-function...
ORGANISM(S): Drosophila melanogaster 
Multiple modes of PRC2 inhibition elicit global chromatin alterations in H3K27M pediatric glioma
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