School of Biology and Environmental Science & Conway Institute of Biomolecular and Biomedical Research, University College Dublin (UCD), D04 N2E5 Dublin, Ireland.
Int J Mol Sci. 2019 Aug 12;20(16):3916. doi: 10.3390/ijms20163916.
Autophagy (particularly macroautophagy) is a bulk degradation process used by eukaryotic cells in order to maintain adequate energy levels and cellular homeostasis through the delivery of long-lived proteins and organelles to the lysosome, resulting in their degradation. It is becoming increasingly clear that many of the molecular requirements to fulfil autophagy intersect with those of conventional and unconventional membrane trafficking pathways. Of particular interest is the dependence of these processes on multiple members of the Rab family of small GTP binding proteins. Rab33b is a protein that localises to the Golgi apparatus and has suggested functions in both membrane trafficking and autophagic processes. Interestingly, mutations in the gene have been reported to cause the severe skeletal disorder, Smith-McCort Dysplasia; however, the molecular basis for Rab33b in this disorder remains to be determined. In this review, we focus on the current knowledge of the participation of Rab33b and its interacting partners in membrane trafficking and macroautophagy, and speculate on how its function, and dysfunction, may contribute to human disease.
自噬（特别是巨自噬）是真核细胞用来维持适当能量水平和细胞内稳态的一种批量降解过程，通过将寿命长的蛋白质和细胞器递送到溶酶体，导致它们降解。越来越明显的是，满足自噬的许多分子要求与传统和非传统膜运输途径的要求相交。特别有趣的是，这些过程对 Rab 家族的多种小 GTP 结合蛋白的依赖性。Rab33b 是一种定位在高尔基体上的蛋白质，在膜运输和自噬过程中具有功能。有趣的是，已经报道了基因中的突变会导致严重的骨骼疾病 Smith-McCort 发育不良;然而，Rab33b 在这种疾病中的分子基础仍有待确定。在这篇综述中，我们重点介绍了 Rab33b 及其相互作用伙伴在膜运输和巨自噬中的参与的最新知识，并推测其功能和功能障碍如何导致人类疾病。
