Journal
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume 283, Issue 5, Pages 2654-2662Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M708218200
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Funding
- NCI NIH HHS [R01 CA124311-03, R01 CA124311, R01 CA130752-02, R01 CA 124311, R01 CA130752, R01 CA130752-01A1] Funding Source: Medline
- NCRR NIH HHS [P20 RR 020152, P20 RR020152] Funding Source: Medline
- NIDCR NIH HHS [DE 017008, R21 DE017008] Funding Source: Medline
- NIGMS NIH HHS [GM 48045, R01 GM048045] Funding Source: Medline
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microRNA-155 is an oncogenic microRNA that has been shown to be critical for B-cell maturation and immunoglobulin production in response to antigen. In line with its function in B-cell activation, miR-155, and its primary transcript, B-cell integration cluster (BIC), is induced by B-cell receptor (BCR) cross-linking. Using pharmacological inhibitors in the human B-cell line, Ramos, we show that activation of BIC and miR-155 expression by BCR signaling occurs through the extracellular signaling-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) pathways but not the p38 pathway. BCR activation results in the induction of c-Fos, FosB, and JunB, and expression of these are suppressed by ERK and JNK inhibitors. Reporter analysis established a key role for a conserved AP-1 site similar to 40 bp upstream from the site of initiation but not an upstream NF-kappa B site or a putative c-Ets located at the site of initiation. Lastly, chromatin immunoprecipitation analysis demonstrated the recruitment of FosB and JunB to the miR-155 promoter following BCR activation. These results identify key determinants of BCR-mediated induction of BIC/miR-155.
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