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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Bax deficiency partially corrects interleukin-7 receptor alpha deficiency.

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.[1]

References

  1. Bax deficiency partially corrects interleukin-7 receptor alpha deficiency. Khaled, A.R., Li, W.Q., Huang, J., Fry, T.J., Khaled, A.S., Mackall, C.L., Muegge, K., Young, H.A., Durum, S.K. Immunity (2002) [Pubmed]
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