Division of Biology, California Institute of Technology, Pasadena, CA, USA.
Autophagy. 2011 Sep;7(9):1091-2. doi: 10.4161/auto.7.9.16489. Epub 2011 Sep 1.
Specific p97 inhibitors are valuable research tools to carry out mechanistic and cellular investigations of p97 biology. p97 is an abundant, ubiquitin-selective chaperone that has multiple functions and is essential for life. Therefore, genetic methods that require long incubations like siRNA or expression of dominant-negative p97 mutants are likely to generate complicated outcomes due to secondary consequences that arise upon slow depletion of p97 activity. We recently identified a small molecule p97 inhibitor, N ( 2) ,N ( 4) -dibenzylquinazoline-2,4-diamine (DBeQ), and documented its effects on blocking autophagic degradation of LC3-II and proteasomal degradation of a p97-dependent ubiquitin-proteasome system (UPS) substrate. What distinguishes DBeQ from conventional proteasome inhibitors is that DBeQ affects both the UPS and autophagic protein degradation pathways and rapidly activates cell death. Whether DBeQ activates autophagic and/or apoptotic cell death will require further work to evaluate its detailed mechanism of action. An exciting goal for the future will be to generate p97 inhibitors that affect one or the other pathway. We propose that generation of 'separation of function' inhibitors will be a challenging adventure for chemical biologists but will yield extremely powerful tools to study p97 and enable evaluation of the therapeutic potential of targeting distinct p97 complexes.
特定的 p97 抑制剂是进行 p97 生物学机制和细胞研究的有价值的研究工具。p97 是一种丰富的、泛素选择性伴侣,具有多种功能,对生命至关重要。因此,需要长时间孵育的遗传方法,如 siRNA 或表达显性负性 p97 突变体,由于 p97 活性缓慢耗尽而产生的次级后果,可能产生复杂的结果。我们最近鉴定了一种小分子 p97 抑制剂,N(2),N(4)-二苄基喹唑啉-2,4-二胺(DBeQ),并记录了其对阻断 LC3-II 自噬降解和 p97 依赖性泛素-蛋白酶体系统(UPS)底物的蛋白酶体降解的影响。DBeQ 与传统蛋白酶体抑制剂的区别在于,DBeQ 同时影响 UPS 和自噬蛋白降解途径,并迅速激活细胞死亡。DBeQ 是否激活自噬和/或凋亡细胞死亡需要进一步工作来评估其详细的作用机制。未来的一个令人兴奋的目标将是生成影响一种或另一种途径的 p97 抑制剂。我们提出,生成“功能分离”抑制剂将是化学生物学家的一项具有挑战性的冒险,但将产生极其强大的工具来研究 p97,并能够评估靶向不同 p97 复合物的治疗潜力。