<i>miR-146a</i> is a significant brake on autoimmunity, myeloproliferation, and cancer in mice

Mark Boldin(Regulus Therapeutics (United States)), Konstantin D. Taganov(Regulus Therapeutics (United States)), Dinesh S. Rao(California Institute of Technology), Lili Yang(California Institute of Technology), Jimmy L. Zhao(California Institute of Technology), Manorama Kalwani(California Institute of Technology), Yvette Garcia-Flores(California Institute of Technology), Mui Luong(California Institute of Technology), Asli Devrekanli(California Institute of Technology), Jessica Xu(Regulus Therapeutics (United States)), Guizhen Sun(Regulus Therapeutics (United States)), Jia Tay(Regulus Therapeutics (United States)), Peter S. Linsley(Regulus Therapeutics (United States)), David Baltimore(California Institute of Technology)
The Journal of Experimental Medicine
May 9, 2011
Cited by 866Open Access
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Abstract

Excessive or inappropriate activation of the immune system can be deleterious to the organism, warranting multiple molecular mechanisms to control and properly terminate immune responses. MicroRNAs (miRNAs), ∼22-nt-long noncoding RNAs, have recently emerged as key posttranscriptional regulators, controlling diverse biological processes, including responses to non-self. In this study, we examine the biological role of miR-146a using genetically engineered mice and show that targeted deletion of this gene, whose expression is strongly up-regulated after immune cell maturation and/or activation, results in several immune defects. Collectively, our findings suggest that miR-146a plays a key role as a molecular brake on inflammation, myeloid cell proliferation, and oncogenic transformation.


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