Shao Jieya, Welch William J, Diprospero Nicholas A, Diamond Marc I
Departments of Neurology and Cellular and Molecular Pharmacology, UCSF, San Francisco, California 94143, USA.
Mol Cell Biol. 2008 Sep;28(17):5196-208. doi: 10.1128/MCB.00079-08. Epub 2008 Jun 23.
Y-27632, an inhibitor of the Rho-associated kinase ROCK, is a therapeutic lead for Huntington disease (HD). The downstream targets that mediate its inhibitory effects on huntingtin (Htt) aggregation and toxicity are unknown. We have identified profilin, a small actin-binding factor that also interacts with Htt, as being a direct target of the ROCK1 isoform. The overexpression of profilin reduces the aggregation of polyglutamine-expanded Htt and androgen receptor (AR) peptides. This requires profilin's G-actin binding activity and its direct interaction with Htt, which are both inhibited by the ROCK1-mediated phosphorylation of profilin at Ser-137. Y-27632 blocks the phosphorylation of profilin in HEK293 cells and primary neurons, which maintains profilin in an active state. The knockdown of profilin blocks the inhibitory effect of Y-27632 on both AR and Htt aggregation. A signaling pathway from ROCK1 to profilin thus controls polyglutamine protein aggregation and is targeted by a promising therapeutic lead for HD.
Y-27632是一种Rho相关激酶ROCK的抑制剂,是亨廷顿舞蹈病(HD)的一种治疗先导药物。介导其对亨廷顿蛋白(Htt)聚集和毒性产生抑制作用的下游靶点尚不清楚。我们已确定原肌球蛋白(一种也与Htt相互作用的小肌动蛋白结合因子)是ROCK1亚型的直接靶点。原肌球蛋白的过表达减少了多聚谷氨酰胺扩展的Htt和雄激素受体(AR)肽的聚集。这需要原肌球蛋白的G-肌动蛋白结合活性及其与Htt的直接相互作用,而这两者都会被ROCK1介导的原肌球蛋白在Ser-137位点的磷酸化所抑制。Y-27632可阻断HEK293细胞和原代神经元中原肌球蛋白的磷酸化,从而使原肌球蛋白维持在活性状态。原肌球蛋白的敲低会阻断Y-27632对AR和Htt聚集的抑制作用。因此,从ROCK1到原肌球蛋白的信号通路控制着多聚谷氨酰胺蛋白的聚集,并且是一种有前景的HD治疗先导药物的作用靶点。