Molecules and Cells

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Fig. 1.

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Fig. 1. RANK stimulation by RANKL binding induces the recruitment and activation of a major adaptor protein, TRAF6. TRAF6 activates NF-κB either by interacting with p62 and aPKC or via TAK1 phosphorylation to regulate the IKK complex. Gab2 and PLCγ2 are other molecules that are required for NF-κB activation; they are recruited to RANK and activated. In addition, TRAF6 complexes with TAK1-TABs or TAK1-RACK1-MKK6 to facilitate the activation of MAPKs such as p38, JNK, and ERK. ROS produced by the RANK-TRAF6-Rac1-Nox1 cascades regulate MAPK activation. Activation of NF-κB and MAPKs leads to the induction of c-Fos at the initial stage of RANK signaling. RANK, receptor activator of nuclear factor-κB; RANKL, receptor activator of nuclear factor-κB ligand; TRAF6, TNF receptor-associated factors 6; NF-κB, nuclear factor-κB; aPCK, atypical protein kinase C; IKK, IκB kinase; TAK1, TGFβ-activated kinase 1; Gab2, growth factor receptor-bound protein 2 (Grb2)-associated binder-2; PLCγ2, phospholipase Cγ2; TAB, TAK1-binding protein; RACK1, receptor for activated C kinase 1; MAPKs, mitogen-activated protein kinases; JNK, c-Jun N-terminal kinase; ERK, extracellular signal-regulated kinase; ROS, reactive oxygen species; NOX1, NADPH oxidase 1; AP-1, activator protein-1; NFATc1, nuclear factor of activated T-cells cytoplasmic 1.
Mol. Cells 2017;40:706~713
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