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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.

http://www.ncbi.nlm.nih.gov/pubmed/11157052

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 RIS Download

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

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Mouse Genome Informatics (Data, Gene Annotation)

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