Hypoxic reprograming of H3K27me3 and H3K4me3 at the INK 4A locus
Activation of Raf reduces the repressive histone mark H3K27me3 at the INK 4a locus by inducing the H3K27me3 demethylase JMJD 3. During hypoxia, the catalyitc activity of JMJD 3 is reduced due to the limited availability of O 2 as a substrate. In our study, we found that hypoxia prevented Raf‐induced...
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| Veröffentlicht in: | FEBS letters 2016-10, Vol.590 (19), p.3407-3415 |
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| container_title | FEBS letters |
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| creator | Chang, Soojeong Park, Bongju Choi, Kang Moon, Yunwon Lee, Ho‐Youl Park, Hyunsung |
| description | Activation of Raf reduces the repressive histone mark H3K27me3 at the
INK
4a
locus by inducing the H3K27me3 demethylase
JMJD
3. During hypoxia, the catalyitc activity of
JMJD
3 is reduced due to the limited availability of O
2
as a substrate. In our study, we found that hypoxia prevented Raf‐induced
JMJD
3 from demethylating H3K27me3 at the
INK
4a
locus. Nonetheless, hypoxia did not prevent Raf signaling from inducing
INK
4a
mRNA
. Interestingly, we found that hypoxia strongly enhanced the active histone mark H3K4me3 at the
INK
4a
locus by inhibiting the H3K4me3 demethylases
JARID
1A and
JARID
1B. Therefore, this study demonstrates that the O
2
concentration in the microenvironment differentially affects the repressive methylation on K27 and the activating methylation on K4 at the
INK
4a
locus by inhibiting the H3K27me3 and H3K4me3 demethylases. |
| doi_str_mv | 10.1002/1873-3468.12375 |
| format | Article |
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INK
4a
locus by inducing the H3K27me3 demethylase
JMJD
3. During hypoxia, the catalyitc activity of
JMJD
3 is reduced due to the limited availability of O
2
as a substrate. In our study, we found that hypoxia prevented Raf‐induced
JMJD
3 from demethylating H3K27me3 at the
INK
4a
locus. Nonetheless, hypoxia did not prevent Raf signaling from inducing
INK
4a
mRNA
. Interestingly, we found that hypoxia strongly enhanced the active histone mark H3K4me3 at the
INK
4a
locus by inhibiting the H3K4me3 demethylases
JARID
1A and
JARID
1B. Therefore, this study demonstrates that the O
2
concentration in the microenvironment differentially affects the repressive methylation on K27 and the activating methylation on K4 at the
INK
4a
locus by inhibiting the H3K27me3 and H3K4me3 demethylases.</description><identifier>ISSN: 0014-5793</identifier><identifier>EISSN: 1873-3468</identifier><identifier>DOI: 10.1002/1873-3468.12375</identifier><language>eng</language><ispartof>FEBS letters, 2016-10, Vol.590 (19), p.3407-3415</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c865-fbeee5718b34b148c8b280bd118b715cc3409bfd582ea9c848a3dfa0fec68beb3</citedby><cites>FETCH-LOGICAL-c865-fbeee5718b34b148c8b280bd118b715cc3409bfd582ea9c848a3dfa0fec68beb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids></links><search><creatorcontrib>Chang, Soojeong</creatorcontrib><creatorcontrib>Park, Bongju</creatorcontrib><creatorcontrib>Choi, Kang</creatorcontrib><creatorcontrib>Moon, Yunwon</creatorcontrib><creatorcontrib>Lee, Ho‐Youl</creatorcontrib><creatorcontrib>Park, Hyunsung</creatorcontrib><title>Hypoxic reprograming of H3K27me3 and H3K4me3 at the INK 4A locus</title><title>FEBS letters</title><description>Activation of Raf reduces the repressive histone mark H3K27me3 at the
INK
4a
locus by inducing the H3K27me3 demethylase
JMJD
3. During hypoxia, the catalyitc activity of
JMJD
3 is reduced due to the limited availability of O
2
as a substrate. In our study, we found that hypoxia prevented Raf‐induced
JMJD
3 from demethylating H3K27me3 at the
INK
4a
locus. Nonetheless, hypoxia did not prevent Raf signaling from inducing
INK
4a
mRNA
. Interestingly, we found that hypoxia strongly enhanced the active histone mark H3K4me3 at the
INK
4a
locus by inhibiting the H3K4me3 demethylases
JARID
1A and
JARID
1B. Therefore, this study demonstrates that the O
2
concentration in the microenvironment differentially affects the repressive methylation on K27 and the activating methylation on K4 at the
INK
4a
locus by inhibiting the H3K27me3 and H3K4me3 demethylases.</description><issn>0014-5793</issn><issn>1873-3468</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><recordid>eNo9j0FPwjAYhhujiRM8e-0fGLT72vXbTULUEYhcuDdt1-IMY0uLifx7GRpP7_s-hzd5CHnibMYZK-YcFeQgSpzxApS8Idk_uSUZY1zkUlVwTx5S-mSXjbzKyHN9Hvrv1tHoh9jvo-na4572gdawLlTngZpjMw5x7Sd6-vB09b6mYkEPvftKU3IXzCH5x7-ckN3ry25Z55vt22q52OQOS5kH672XiqMFYblAh7ZAZht-IYpL50CwyoZGYuFN5VCggSYYFrwr0XoLEzL_vXWxTyn6oIfYdiaeNWd69NejrR5t9dUffgAHwUs7</recordid><startdate>201610</startdate><enddate>201610</enddate><creator>Chang, Soojeong</creator><creator>Park, Bongju</creator><creator>Choi, Kang</creator><creator>Moon, Yunwon</creator><creator>Lee, Ho‐Youl</creator><creator>Park, Hyunsung</creator><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>201610</creationdate><title>Hypoxic reprograming of H3K27me3 and H3K4me3 at the INK 4A locus</title><author>Chang, Soojeong ; Park, Bongju ; Choi, Kang ; Moon, Yunwon ; Lee, Ho‐Youl ; Park, Hyunsung</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c865-fbeee5718b34b148c8b280bd118b715cc3409bfd582ea9c848a3dfa0fec68beb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chang, Soojeong</creatorcontrib><creatorcontrib>Park, Bongju</creatorcontrib><creatorcontrib>Choi, Kang</creatorcontrib><creatorcontrib>Moon, Yunwon</creatorcontrib><creatorcontrib>Lee, Ho‐Youl</creatorcontrib><creatorcontrib>Park, Hyunsung</creatorcontrib><collection>CrossRef</collection><jtitle>FEBS letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chang, Soojeong</au><au>Park, Bongju</au><au>Choi, Kang</au><au>Moon, Yunwon</au><au>Lee, Ho‐Youl</au><au>Park, Hyunsung</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hypoxic reprograming of H3K27me3 and H3K4me3 at the INK 4A locus</atitle><jtitle>FEBS letters</jtitle><date>2016-10</date><risdate>2016</risdate><volume>590</volume><issue>19</issue><spage>3407</spage><epage>3415</epage><pages>3407-3415</pages><issn>0014-5793</issn><eissn>1873-3468</eissn><abstract>Activation of Raf reduces the repressive histone mark H3K27me3 at the
INK
4a
locus by inducing the H3K27me3 demethylase
JMJD
3. During hypoxia, the catalyitc activity of
JMJD
3 is reduced due to the limited availability of O
2
as a substrate. In our study, we found that hypoxia prevented Raf‐induced
JMJD
3 from demethylating H3K27me3 at the
INK
4a
locus. Nonetheless, hypoxia did not prevent Raf signaling from inducing
INK
4a
mRNA
. Interestingly, we found that hypoxia strongly enhanced the active histone mark H3K4me3 at the
INK
4a
locus by inhibiting the H3K4me3 demethylases
JARID
1A and
JARID
1B. Therefore, this study demonstrates that the O
2
concentration in the microenvironment differentially affects the repressive methylation on K27 and the activating methylation on K4 at the
INK
4a
locus by inhibiting the H3K27me3 and H3K4me3 demethylases.</abstract><doi>10.1002/1873-3468.12375</doi><tpages>9</tpages></addata></record> |
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| ispartof | FEBS letters, 2016-10, Vol.590 (19), p.3407-3415 |
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| language | eng |
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| source | Wiley Journals; Wiley Free Content; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| title | Hypoxic reprograming of H3K27me3 and H3K4me3 at the INK 4A locus |
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