This study identifies a novel protein, Beclin, which interacts with the antiapoptotic protein Bcl-2. Beclin is a 60-kDa coiled-coil protein expressed in neurons and other tissues. In yeast two-hybrid assays, Beclin interacts with Bcl-2 and other Bcl-2-like proteins, such as Bcl-xL, but not with Bax, a pro-apoptotic protein. Beclin overexpression in virally infected neurons in mice significantly reduces Sindbis virus-induced mortality, viral replication, and apoptotic cell death.病毒感染的小鼠存活率显著提高，病毒复制显著降低，凋亡细胞数量显著减少。此外，Beclin的Bcl-2结合域对于其抗病毒、抗凋亡和促存活作用至关重要。这些发现表明，Beclin通过与Bcl-2样分子的相互作用，在中枢神经系统中发挥抗病毒宿主防御作用。Beclin可能通过保护Bcl-2（或Bcl-2样分子）免受caspases的切割，或通过阻断由Sindbis病毒包膜糖蛋白触发的内质网应激信号，来抑制病毒复制和神经元死亡。此外，Beclin在保护机制中可能与Bel-2或Bel-xL等Bcl-2样分子相互作用，而Bel-2可能是生物上重要的Beclin结合伴侣。This study identifies a novel protein, Beclin, which interacts with the antiapoptotic protein Bcl-2. Beclin is a 60-kDa coiled-coil protein expressed in neurons and other tissues. In yeast two-hybrid assays, Beclin interacts with Bcl-2 and other Bcl-2-like proteins, such as Bcl-xL, but not with Bax, a pro-apoptotic protein. Beclin overexpression in virally infected neurons in mice significantly reduces Sindbis virus-induced mortality, viral replication, and apoptotic cell death.病毒感染的小鼠存活率显著提高，病毒复制显著降低，凋亡细胞数量显著减少。此外，Beclin的Bcl-2结合域对于其抗病毒、抗凋亡和促存活作用至关重要。这些发现表明，Beclin通过与Bcl-2样分子的相互作用，在中枢神经系统中发挥抗病毒宿主防御作用。Beclin可能通过保护Bcl-2（或Bcl-2样分子）免受caspases的切割，或通过阻断由Sindbis病毒包膜糖蛋白触发的内质网应激信号，来抑制病毒复制和神经元死亡。此外，Beclin在保护机制中可能与Bel-2或Bel-xL等Bcl-2样分子相互作用，而Bel-2可能是生物上重要的Beclin结合伴侣。