H3K9me2: Perbedaan antara revisi

'''H3K9me2''' adalah sebuah modifikasi [[Epigenetika|epigenetik]] kepada protein [[histon H3]] dengan adanya [[Metilasi|dimetilasi]] pada residu [[lisina]] ke-9 di [[protein]] histon H3. H3K9me2 berhubungan kuat dengan aktivitas represi transkripsi,<ref name="Histome H3K9me2">{{cite web|title=H3K9me2|url=http://www.actrec.gov.in/histome/ptm_sp.php?ptm_sp=H3K9me2|publisher=HIstome: The Histone Infobase|access-date=8 June 2018}}</ref><ref name="Nestler1">{{cite journal|date=October 2011|title=Transcriptional and epigenetic mechanisms of addiction|journal=Nature Reviews. Neuroscience|volume=12|issue=11|pages=623–37|doi=10.1038/nrn3111|pmc=3272277|pmid=21989194|quote=<!--ΔFosB has been linked directly to several addiction-related behaviors&nbsp;... Importantly, genetic or viral overexpression of ΔJunD, a dominant negative mutant of JunD which antagonizes ΔFosB- and other AP-1-mediated transcriptional activity, in the NAc or OFC blocks these key effects of drug exposure^14,22–24. This indicates that ΔFosB is both necessary and sufficient for many of the changes wrought in the brain by chronic drug exposure. ΔFosB is also induced in D1-type NAc MSNs by chronic consumption of several natural rewards, including sucrose, high fat food, sex, wheel running, where it promotes that consumption^14,26–30. This implicates ΔFosB in the regulation of natural rewards under normal conditions and perhaps during pathological addictive-like states.

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