Enhancer of Zeste Homolog 2 Protein
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Subject Areas on Research
- Acute myeloid leukemia ontogeny is defined by distinct somatic mutations.
- Alternative Splicing of EZH2 pre-mRNA by SF3B3 Contributes to the Tumorigenic Potential of Renal Cancer.
- An oncogenic Ezh2 mutation induces tumors through global redistribution of histone 3 lysine 27 trimethylation.
- CDKN1C (p57) is a direct target of EZH2 and suppressed by multiple epigenetic mechanisms in breast cancer cells.
- EZH2 regulates the transcription of estrogen-responsive genes through association with REA, an estrogen receptor corepressor.
- Environmental estrogens differentially engage the histone methyltransferase EZH2 to increase risk of uterine tumorigenesis.
- Epigenetic silencing of tumor suppressor Par-4 promotes chemoresistance in recurrent breast cancer.
- Inhibition of PRC2 activity by a gain-of-function H3 mutation found in pediatric glioblastoma.
- Loss of tumor suppressor IGFBP4 drives epigenetic reprogramming in hepatic carcinogenesis.
- Loss of tumor suppressor KDM6A amplifies PRC2-regulated transcriptional repression in bladder cancer and can be targeted through inhibition of EZH2.
- TP53 genomic status regulates sensitivity of gastric cancer cells to the histone methylation inhibitor 3-deazaneplanocin A (DZNep).
- Targeting EZH2 histone methyltransferase activity alleviates experimental intestinal inflammation.
- The Genetic Basis of Hepatosplenic T-cell Lymphoma.