Abstract
The requirement for cytokines in hematopoiesis is partly attributable to the protection of cells from apoptosis. Since IL-7 is required for normal T cell development, we evaluated the role of Bax in vivo by generating mice deficient in both Bax and the IL-7 receptor alpha chain (IL-7R). Starting at birth, we observed complete recovery of all stages of alphabeta thymocyte development up to 4 weeks of age. However, by 12 weeks of age, thymic cellularity had reverted to that of mice deficient in IL-7R alone. The BH3 only proteins, Bad and Bim, were also part of the death pathway repressed by IL-7. Thus, in young mice, Bax emerges as an essential protein in the death pathway induced by IL-7 deficiency.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Aging / physiology
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Animals
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Apoptosis / physiology*
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Cell Differentiation / physiology
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Interleukin-7 / physiology*
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Mice
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Mice, Transgenic
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Proto-Oncogene Proteins / physiology*
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Proto-Oncogene Proteins c-bcl-2*
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Receptors, Antigen, T-Cell, alpha-beta / physiology
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Receptors, Interleukin-7 / deficiency
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Receptors, Interleukin-7 / physiology*
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T-Lymphocytes / cytology
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T-Lymphocytes / physiology*
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bcl-2-Associated X Protein
Substances
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Bax protein, mouse
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Interleukin-7
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Proto-Oncogene Proteins
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Proto-Oncogene Proteins c-bcl-2
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Receptors, Antigen, T-Cell, alpha-beta
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Receptors, Interleukin-7
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bcl-2-Associated X Protein
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interleukin-7 receptor, alpha chain