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c-Jun NH2-terminal kinase (JNK)1 and JNK2 have similar and stage-dependent roles in regulating T cell apoptosis and proliferation.

Apoptotic and mitogenic stimuli activate c-Jun NH2-terminal kinases (JNKs) in T cells. Although T cells express both JNK1 and JNK2 isozymes, the absence of JNK2 alone can result in resistance to anti-CD3-induced thymocyte apoptosis and defective mature T cell proliferation. Similar defects in thymocyte apoptosis and mature T cell proliferation, the latter due to reduced interleukin 2 production, are also caused by JNK1 deficiency. Importantly, T cell function was compromised in Jnk1(+/-)Jnk2(+/-) double heterozygous mice, indicating that JNK1 and JNK2 play similar roles in regulating T cell function. The reduced JNK dose results in defective c-Jun NH2-terminal phosphorylation in thymocytes but not in peripheral T cells, in which nuclear factors of activated T cells (NK-ATs)-DNA binding activity is affected. Thus, JNK1 and JNK2 control similar functions during T cell maturation through differential targeting of distinct substrates.

Pubmed ID: 11157052

Authors

  • Sabapathy K
  • Kallunki T
  • David JP
  • Graef I
  • Karin M
  • Wagner EF

Journal

The Journal of experimental medicine

Publication Data

February 5, 2001

Associated Grants

None

Mesh Terms

  • Animals
  • Antigens, CD3
  • Apoptosis
  • B-Lymphocytes
  • Cell Differentiation
  • Cell Division
  • Cell Survival
  • DNA-Binding Proteins
  • Lymphocyte Activation
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Mitogen-Activated Protein Kinase 8
  • Mitogen-Activated Protein Kinase 9
  • Mitogen-Activated Protein Kinases
  • NFATC Transcription Factors
  • Nuclear Proteins
  • Phosphorylation
  • T-Lymphocytes
  • Transcription Factors