Figure 8. Crosstalk between β-arrestin-2 and ER-stress-induced apoptosis. LPS induces β-arrestin-2 expression. β-arrestin-2 binds to BiP (an effect enhanced by salmeterol) and inhibits its activity by promoting its ubiquitination. By suppressing BiP, β-arrestin-2 overexpression impairs the binding between BiP and BIK, thus promoting BIK release and caspase cleavage. When β-arrestin-2 expression is normal or silenced, LPS does not alter BIK expression, so other BCL-2-family proteins may promote apoptosis under such conditions.