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Immunity
Article
License: Elsevier Non-Commercial
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Immunity
Article . 2003
License: Elsevier Non-Commercial
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Immunity
Article . 2003 . Peer-reviewed
License: Elsevier Non-Commercial
Data sources: Crossref
Immunity
Article . 2003
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Regulation of Marginal Zone B Cell Development by MINT, a Suppressor of Notch/RBP-J Signaling Pathway

Authors: Kuroda, Kazuki; Han, Hua; Tani, Shoichi; Tanigaki, Kenji; Tun, Tin; Furukawa, Takahisa; Taniguchi, Yoshihito; +4 Authors

Regulation of Marginal Zone B Cell Development by MINT, a Suppressor of Notch/RBP-J Signaling Pathway

Abstract

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.

Keywords

Transcriptional Activation, Immunology, B-Lymphocyte Subsets, Mice, Immunology and Allergy, Animals, Drosophila Proteins, Mice, Knockout, B-Lymphocytes, Receptors, Notch, Membrane Proteins, Nuclear Proteins, RNA-Binding Proteins, Cell Differentiation, DNA-Binding Proteins, Infectious Diseases, Liver, Immunoglobulin J Recombination Signal Sequence-Binding Protein, Gene Targeting, Drosophila, Cell Adhesion Molecules, Protein Binding, Signal Transduction

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    citations
    This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    243
    popularity
    This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
    Top 1%
    influence
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    Top 1%
    impulse
    This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
    Top 1%
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citations
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
243
Top 1%
Top 1%
Top 1%
hybrid