Dai R M, Li C C
Intramural Research Support Program, SAIC Frederick, National Cancer Institute at Frederick, Frederick, Maryland 21702, USA.
Nat Cell Biol. 2001 Aug;3(8):740-4. doi: 10.1038/35087056.
The ubiquitin-proteasome (Ub-Pr) degradation pathway regulates many cellular activities, but how ubiquitinated substrates are targeted to the proteasome is not understood. We have shown previously that valosin-containing protein (VCP) physically and functionally targets the ubiquitinated nuclear factor kappaB inhibitor, IkappaBalpha to the proteasome for degradation. VCP is an abundant and a highly conserved member of the AAA (ATPases associated with a variety of cellular activities) family. Besides acting as a chaperone in membrane fusions, VCP has been shown to have a role in a number of seemingly unrelated cellular activities. Here we report that loss of VCP function results in an inhibition of Ub-Pr-mediated degradation and an accumulation of ubiquitinated proteins. VCP associates with ubiquitinated proteins through the direct binding of its amino-terminal domain to the multi-ubiquitin chains of substrates. Furthermore, its N-terminal domain is required in Ub-Pr-mediated degradation. We conclude that VCP is a multi-ubiquitin chain-targeting factor that is required in the degradation of many Ub-Pr pathway substrates, and provide a common mechanism that underlies many of the functions of VCP.
泛素 - 蛋白酶体(Ub-Pr)降解途径调节许多细胞活动,但泛素化底物如何靶向蛋白酶体尚不清楚。我们之前已经表明,含缬酪肽蛋白(VCP)在物理和功能上可将泛素化的核因子κB抑制剂IκBα靶向蛋白酶体进行降解。VCP是AAA(与多种细胞活动相关的ATP酶)家族中丰富且高度保守的成员。除了在膜融合中作为伴侣蛋白发挥作用外,VCP还在许多看似不相关的细胞活动中发挥作用。在此我们报告,VCP功能丧失会导致Ub-Pr介导的降解受到抑制以及泛素化蛋白积累。VCP通过其氨基末端结构域与底物的多聚泛素链直接结合而与泛素化蛋白相关联。此外,其N末端结构域在Ub-Pr介导的降解中是必需的。我们得出结论,VCP是一种多聚泛素链靶向因子,是许多Ub-Pr途径底物降解所必需的,并提供了一种作为VCP许多功能基础的共同机制。