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. 2014 Dec 2;3(6):433–443. doi: 10.2217/cns.14.43

Figure 2.  . Schematic presentation of mutations in H3F3A gene leading to gliomagenesis.

Figure 2.  

(A) substitution of methionine at lysine 27 in the histone tail leads to a decrease in the repressive histone mark H3K27me3 via the inactivation of the histone methyltransferase EZH2 (part of the PRC2), leading to the transcriptional activation of oncogenes. (B) substitution of arginine or valine at glycine 34 leads to a decrease in K36me3 on the same or nearby nucleosomes and upregulation of the MYCN oncogene. (C) SETD2 (H3K36 methyltransferase), hypothesized to play a role in gliomagenesis via depletion of H3K36 and consequent upregulation of the MYCN oncogene. SETD2 mutations can cause temozolomide resistance and MSI, leading to defective MMR.

MMR: Mismatch repair; MSI: Microsatellite instability.