Yamashita Shun-Ichi, Fujiki Yukio
Department of Cellular Physiology, Graduate School of Medical and Dental Sciences, Niigata University, Niigata, 951-8510, Japan.
Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.
Methods Mol Biol. 2017;1595:243-248. doi: 10.1007/978-1-4939-6937-1_23.
In mammalian cells several hundred peroxisomes are maintained by a balance between the biogenesis and turnover by peroxisome homeostasis. Pexophagy, a form of autophagy specific for peroxisomes, is the main pathway for peroxisome degradation, but molecular mechanisms of mammalian pexophagy are largely unknown. This is due to the lack of well-established pexophagy-inducing conditions in mammalian cells. Recently, several conditions that induce pexophagy were described for mammalian cells, involving ubiquitin and adaptor proteins of autophagy. In this chapter, we describe the protocol for Pex3-induced pexophagy, the more readable and highly inducible pexophagy condition in mammalian cells.
在哺乳动物细胞中,几百个过氧化物酶体通过过氧化物酶体稳态下的生物发生和周转之间的平衡得以维持。过氧化物酶体自噬是一种对过氧化物酶体具有特异性的自噬形式,是过氧化物酶体降解的主要途径,但哺乳动物过氧化物酶体自噬的分子机制在很大程度上尚不清楚。这是由于在哺乳动物细胞中缺乏成熟的诱导过氧化物酶体自噬的条件。最近,已经描述了几种诱导哺乳动物细胞过氧化物酶体自噬的条件,涉及泛素和自噬衔接蛋白。在本章中,我们描述了由Pex3诱导的过氧化物酶体自噬的实验方案,这是在哺乳动物细胞中更具可读性且诱导性很强的过氧化物酶体自噬条件。