Abstract :
Activation of c-Jun N-terminal kinase (JNK) promotes apoptosis in a context-specific fashion. The anti-apoptotic function of NF-κB is mediated in part through its ability to downregulate JNK activation. Candidate molecules, including GADD45β (growth arrest and DNA damage-inducing protein β), XIAP (X-chromosome-linked inhibitor of apoptosis), and reactive oxygen species have recently been reported to be involved in crosstalk between NF-κB and JNK. Here, I discuss recent work from Papa et al., which proposes that GADD45β modulates JNK activation by binding to, and inhibiting, the JNK kinase, mitogen-activated protein kinase kinase 7 (MKK7).