Abstract
T cells encounter two main checkpoints during development in the thymus. These checkpoints are critically dependent on signals derived from the thymic microenvironment as well as from the pre-T cell receptor (pre-TCR) and the alphabeta TCR. Here we show that T cell-specific deletion of beta-catenin impaired T cell development at the beta-selection checkpoint, leading to a substantial decrease in splenic T cells. In addition, beta-catenin also seemed to be a target of TCR-CD3 signals in thymocytes and mature T cells. These data indicate that beta-catenin-mediated signals are required for normal T cell development.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Cell Differentiation / immunology*
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Cytoskeletal Proteins / deficiency*
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Cytoskeletal Proteins / genetics
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Flow Cytometry
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Gene Deletion
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Immune System / growth & development
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Immunity, Cellular / genetics*
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Immunity, Cellular / physiology
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Mice
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Mice, Transgenic
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Polymerase Chain Reaction
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Receptors, Antigen, T-Cell / immunology
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Spleen / cytology
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T-Lymphocytes / physiology*
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Trans-Activators / deficiency*
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Trans-Activators / genetics
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beta Catenin
Substances
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CTNNB1 protein, mouse
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Cytoskeletal Proteins
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Receptors, Antigen, T-Cell
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Trans-Activators
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beta Catenin