Carboxyl terminus of HSC70-interacting protein (CHIP) down-regulates NF-κB-inducing kinase (NIK) and suppresses NIK-induced liver injury

Abstract

Background: Abnormal NIK expression and activation trigger liver injury. Results: CHIP bound to NIK and promoted NIK ubiquitination/degradation; liver-specific overexpression of NIK triggered fatal liver injury; and coexpression of CHIP reversed NIK detrimental effects. Conclusion: CHIP negatively regulates NIK and protects against NIK-induced liver injury. Significance: This study sheds light on a novel regulation of the NIK pathways by CHIP.