![]() ![]() ![]() A role of VPS13C in the endolysosomal system is not at odds with the established genetic links to PD, given that many PD genes function in the endolysosomal system ( Abeliovich and Gitler, 2016). ![]() The localization of VPS13C at endolysosomes, but not mitochondria, was also supported by proximity labeling experiments ( Go et al., 2021 Liu et al., 2018), although genetic evidence for an impact of VPS13C on lysosome properties is still missing. However, subsequent studies showed that while VPS13A ( Kumar et al., 2018 Yeshaw et al., 2019) and VPS13D ( Guillen-Samander et al., 2021) localize to contact sites between the ER and mitochondria, VPS13C localizes instead to contact sites between the ER and late endosomes/lysosomes ( Kumar et al., 2018). This seemed to be consistent with evidence for a major role of defects in mitochondrial clearance in some familial forms of PD ( Pickrell and Youle, 2015). Such studies reported the presence of VPS13C in mitochondria-associated membrane fractions and showed that VPS13C knockdown causes mitochondrial dysfunction ( Lesage et al., 2016). Initial studies of VPS13C focused on a potential role in mitochondrial physiology ( Lesage et al., 2016), as at the time studies of the single yeast Vps13 protein had suggested a role of this protein in the transport of lipids to these organelles ( Lang et al., 2015). ![]()
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