We found that Msx2-interacting nuclear target protein (MINT) competed with the intracellular region of Notch for binding to a DNA binding protein RBP-J and suppressed the transactivation activity of Notch signaling. Although MINT null mutant mice were embryonic lethal, MINT-deficient splenic B cells differentiated about three times more efficiently into marginal zone B cells with a concomitant reduction of follicular B cells. MINT is expressed in a cell-specific manner: high in follicular B cells and low in marginal zone B cells. Since Notch signaling directs differentiation of marginal zone B lymphocytes and suppresses that of follicular B lymphocytes in mouse spleen, the results indicate that high levels of MINT negatively regulate Notch signaling and block differentiation of precursor B cells into marginal zone B cells. MINT may serve as a functional homolog of Drosophila Hairless.
Pubmed ID: 12594956 RIS Download
Mesh terms: Animals | B-Lymphocyte Subsets | B-Lymphocytes | Cell Differentiation | DNA-Binding Proteins | Drosophila | Drosophila Proteins | Gene Targeting | Immunoglobulin J Recombination Signal Sequence-Binding Protein | Liver | Membrane Proteins | Mice | Mice, Knockout | Nuclear Proteins | Protein Binding | Receptors, Notch | Signal Transduction | Transcriptional Activation
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