Signaling crosstalk between NF-κB and JNK
Signaling crosstalk between NF-κB and JNK
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DOI：
10.1016/j.it.2004.05.007
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发表时间：
2004-08-01
影响因子：
16.8
通讯作者：
Nakano, H
中科院分区：
文献类型：
--
作者：
Nakano, H
c-Jun N-末端激酶（JNK）的激活以特定的方式促进细胞凋亡。NF-κ B的抗凋亡功能部分通过其下调JNK活化的能力介导。候选分子，包括GADD 45 β（生长停滞和DNA损伤诱导蛋白β），XIAP（X染色体连锁的凋亡抑制剂），和活性氧物种最近被报道参与NF-κ B和JNK之间的串扰。在这里，我讨论了Papa等人最近的工作，其提出GADD 45 β通过结合并抑制JNK激酶，丝裂原活化蛋白激酶激酶7（MKK 7）来调节JNK活化。
Activation of c-Jun N-terminal kinase (JNK) promotes apoptosis in a context-specific fashion. The anti-apoptotic function of NF-kappaB is mediated in part through its ability to downregulate JNK activation. Candidate molecules, including GADD45beta (growth arrest and DNA damage-inducing protein beta), XIAP (X-chromosome-linked inhibitor of apoptosis), and reactive oxygen species have recently been reported to be involved in crosstalk between NF-kappaB and JNK. Here, I discuss recent work from Papa et al., which proposes that GADD45beta modulates JNK activation by binding to, and inhibiting, the JNK kinase, mitogen-activated protein kinase kinase 7 (MKK7).