Jun N-terminal kinase 2 modulates thymocyte apoptosis and T cell activation through c-Jun and nuclear factor of activated T cell (NF-AT)

Axel Behrens; Kanaga Sabapathy; Isabella Graeft

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Jun N-terminal kinase 2 modulates thymocyte apoptosis and T cell activation through c-Jun and nuclear factor of activated T cell (NF-AT)

机译：Jun N末端激酶2通过c-Jun和活化T细胞的核因子（NF-AT）调节胸腺细胞凋亡和T细胞活化

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The Jun N-terminal kinases (JNKs) recently have been shown to be required for thymocyte apoptosis and T cell differentiation and/or proliferation. To investigate the molecular targets of JNK signaling in lymphoid cells. we used mice in which the serines phosphory- lated by JNK in c-Jun were replaced by homologous recombination with alanines (junAA mice). Lymphocytes from these mice showed no phosphorylation of c-Jun in response to activation stimuli, whereas c-Jun was rapidly phosphorylated in wild-type cells. Despite the fact that c-jun is essential for early development, junAA mice develop normaIly: however. c-Jun N-terminal phos- phorylation was required for efficient T cell receptor-induced and tumor necrosis factor-α-induced thymocyte apoptosis. In contrast, c-Jun phosphorylation by JNK is not required for T cell proliferation or differentiation. Because jnk2-/- T cells display a proliferation defect, we concluded that JNK2 must have other Substrates re- quired for lymphocyte function. Surprisingly, jnk2-/- T cells showed reduced NF-AT DNA-binding activity after activation. Fur- thermore, overexpression of JNK2 in Jurkat T cells strongly en- hanced NF-AT-dependent transcription. These results demonstrate that JNK signaling differentially uses c-Jun and NF-AT as molecular effectors during thymocyte apoptosis and T cell proliferation.

机译：最近已显示，Jun N末端激酶（JNKs）是胸腺细胞凋亡和T细胞分化和/或增殖所必需的。调查JNK信号在淋巴细胞中的分子靶标。我们使用的小鼠中，c-Jun中被JNK磷酸化的丝氨酸被丙氨酸的同源重组所取代（junAA小鼠）。这些小鼠的淋巴细胞对激活刺激没有显示c-Jun的磷酸化，而c-Jun在野生型细胞中迅速被磷酸化。尽管c-jun对早期发育至关重要，但是junAA小鼠正常发育。有效的T细胞受体诱导的和肿瘤坏死因子α诱导的胸腺细胞凋亡需要c-Jun N末端磷酸化。相反，T细胞增殖或分化不需要JNK的c-Jun磷酸化。因为jnk2-/-T细胞显示出增殖缺陷，所以我们得出结论，JNK2必须具有淋巴细胞功能所需的其他底物。令人惊讶地，jnk2-/-T细胞在活化后显示出降低的NF-AT DNA结合活性。此外，在Jurkat T细胞中JNK2的过表达大大增强了NF-AT依赖性转录。这些结果表明，在胸腺细胞凋亡和T细胞增殖过程中，JNK信号通路差异地使用c-Jun和NF-AT作为分子效应子。

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《Proceedings of the National Academy of Sciences of the United States of America》 |2001年第4期|p.1769-1774|共6页
作者
Axel Behrens; Kanaga Sabapathy; Isabella Graeft;
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收录信息美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
原文格式 PDF
正文语种 eng
中图分类自然科学总论;
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6. Jun N-terminal kinase 2 modulates thymocyte apoptosis and T cell activation through c-Jun and nuclear factor of activated T cell (NF-AT) [O] . Axel Behrens, Kanaga Sabapathy, Isabella Graef, 2001

机译：Jun N末端激酶2调节胸腺细胞凋亡并通过c-Jun激活T细胞和激活T的核因子电池（NF-AT）
7. Jun N-terminal kinase 2 modulates thymocyte apoptosis and T cell activation through c-Jun and nuclear factor of activated T cell (NF-AT) [O] . Behrens, Axel, Sabapathy, Kanaga, Graef, Isabella, 2001

机译：Jun N末端激酶2调节胸腺细胞凋亡并通过c-Jun激活T细胞和激活T的核因子电池（NF-AT）

Jun N-terminal kinase 2 modulates thymocyte apoptosis and T cell activation through c-Jun and nuclear factor of activated T cell (NF-AT)

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