| Autor: |
Morgan NE; School of Biology and Environmental Science & Conway Institute of Biomolecular and Biomedical Research, University College Dublin (UCD), D04 N2E5 Dublin, Ireland., Cutrona MB; School of Biology and Environmental Science & Conway Institute of Biomolecular and Biomedical Research, University College Dublin (UCD), D04 N2E5 Dublin, Ireland., Simpson JC; School of Biology and Environmental Science & Conway Institute of Biomolecular and Biomedical Research, University College Dublin (UCD), D04 N2E5 Dublin, Ireland. jeremy.simpson@ucd.ie. |
| Jazyk: |
angličtina |
| Zdroj: |
International journal of molecular sciences [Int J Mol Sci] 2019 Aug 12; Vol. 20 (16). Date of Electronic Publication: 2019 Aug 12. |
| DOI: |
10.3390/ijms20163916 |
| Abstrakt: |
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 RAB33B 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. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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