RETRACTED ARTICLE: MAVS protects cells from apoptosis by negatively regulating VDAC1

Abstract

The mitochondrial antiviral signaling, MAVS, plays important roles in many aspects of cellular function, especially in the innate immunity. Previous reports showed that MAVS is involved in apoptosis. However, the functions of MAVS in apoptosis are still unknown. In this article, we demonstrate that the voltage-dependent anion channel 1 (VDAC1) protein can be physically associated with MAVS in vitro. MAVS interacted with VDAC1 through its Pro domain, and VDAC1 interacted with MAVS through its N terminal (1-26 amino acids). Expression of MAVS results in a potent inhibition of apoptosis and VDAC1-mediated cytochrome c release. Furthermore, a striking reduction in the abundance of endogenous VDAC1 with overexpressed MAVS was found. These findings indicate that MAVS negatively regulates the stability of VDAC1 and thereby inhibits apoptosis in the response to release of cytochrome c.