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Immunity. 2008 May;28(5):630-8. doi: 10.1016/j.immuni.2008.04.002. Epub 2008 May 1.

MicroRNA-155 suppresses activation-induced cytidine deaminase-mediated Myc-Igh translocation.

Author information

1
Laboratory of Molecular Immunology, The Rockefeller University, New York, NY 10065, USA.

Abstract

MicroRNAs (miRNAs) are small noncoding RNAs that regulate vast networks of genes that share miRNA target sequences. To examine the physiologic effects of an individual miRNA-mRNA interaction in vivo, we generated mice that carry a mutation in the putative microRNA-155 (miR-155) binding site in the 3'-untranslated region of activation-induced cytidine deaminase (AID), designated Aicda(155) mice. AID is required for immunoglobulin gene diversification in B lymphocytes, but it also promotes chromosomal translocations. Aicda(155) caused an increase in steady-state Aicda mRNA and protein amounts by increasing the half-life of the mRNA, resulting in a high degree of Myc-Igh translocations. A similar but more pronounced translocation phenotype was also found in miR-155-deficient mice. Our experiments indicate that miR-155 can act as a tumor suppressor by reducing potentially oncogenic translocations generated by AID.

PMID:
18455451
PMCID:
PMC2713656
DOI:
10.1016/j.immuni.2008.04.002
[Indexed for MEDLINE]
Free PMC Article

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