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Publication : Defective T cell differentiation in the absence of Jnk1.

First Author  Dong C Year  1998
Journal  Science Volume  282
Issue  5396 Pages  2092-5
PubMed ID  9851932 Mgi Jnum  J:51510
Mgi Id  MGI:1316842 Doi  10.1126/science.282.5396.2092
Citation  Dong C, et al. (1998) Defective T cell differentiation in the absence of Jnk1. Science 282(5396):2092-5
abstractText  The c-Jun NH2-terminal kinase (JNK) signaling pathway has been implicated in the immune response that is mediated by the activation and differentiation of CD4 helper T (TH) cells into TH1 and TH2 effector cells. JNK activity observed in wild-type activated TH cells was severely reduced in TH cells from Jnk1-/- mice. The Jnk1-/- T cells hyperproliferated, exhibited decreased activation-induced cell death, and preferentially differentiated to TH2 cells. The enhanced production of TH2 cytokines by Jnk1-/- cells was associated with increased nuclear accumulation of the transcription factor NFATc. Thus, the JNK1 signaling pathway plays a key role in T cell receptor-initiated TH cell proliferation, apoptosis, and differentiation.
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