Negative Regulation of JAK2 by H3K9 Methyltransferase G9a in Leukemiaopen access
- Authors
- Son, Hye-Ju; Kim, Ji-Young; Hahn, Yoonsoo; Seo, Sang-Beom
- Issue Date
- Sep-2012
- Publisher
- AMER SOC MICROBIOLOGY
- Citation
- MOLECULAR AND CELLULAR BIOLOGY, v.32, no.18, pp 3681 - 3694
- Pages
- 14
- Journal Title
- MOLECULAR AND CELLULAR BIOLOGY
- Volume
- 32
- Number
- 18
- Start Page
- 3681
- End Page
- 3694
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/15163
- DOI
- 10.1128/MCB.00673-12
- ISSN
- 0270-7306
1098-5549
- Abstract
- Histone methylation at specific lysine residues is a crucial regulatory process in transcriptional regulation. Using chromatin immunoprecipitation with microarray technology (ChIP-chip) analysis, we found that the H3K9-me2 target gene JAK2 was an important factor during differentiation of the HL-60 promyelocytic leukemia cell line by all-trans-retinoic acid (ATRA) treatment. Here, we report that the H3K9 methyltransferase G9a negatively regulated JAK2 transcription in histone methyltransferase activity and in a YY1-dependent manner during ATRA-mediated leukemia cell differentiation. We found that G9a knockdown repressed ATRA-mediated HL-60 cell differentiation. We demonstrated that G9a interacts with YY1 and is recruited to the JAK2 promoter along with corepressors, including histone deacetylase, that induced H3K9-me2. Repression of JAK2 transcription by G9a decreased H3Y41 phosphorylation and promoted inhibition of the recently identified JAK2-H3Y41P-HP1 alpha pathway-mediated leukemogenesis.
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