Klein Matthew E, Lioy Daniel T, Ma Lin, Impey Soren, Mandel Gail, Goodman Richard H
Vollum Institute, Oregon Health & Science University, Portland, Oregon 97239, USA.
Nat Neurosci. 2007 Dec;10(12):1513-4. doi: 10.1038/nn2010. Epub 2007 Nov 11.
Both increases and decreases in methyl CpG-binding protein 2 (MeCP2) levels cause neurodevelopmental defects. We found that MeCP2 translation is regulated by microRNA 132 (miR132). Block of miR132-mediated repression increased MeCP2 and brain-derived neurotrophic factor (BDNF) levels in cultured rat neurons and the loss of MeCP2 reduced BDNF and miR132 levels in vivo. This feedback loop may provide a mechanism for homeostatic control of MeCP2 expression.
甲基CpG结合蛋白2（MeCP2）水平的升高和降低都会导致神经发育缺陷。我们发现MeCP2的翻译受微小RNA 132（miR132）调控。在培养的大鼠神经元中，阻断miR132介导的抑制作用可提高MeCP2和脑源性神经营养因子（BDNF）的水平，而体内MeCP2的缺失则会降低BDNF和miR132的水平。这种反馈回路可能为MeCP2表达的稳态控制提供一种机制。
