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| Home > Publications Database > PSM04-06: Mitochondrial degeneration in PINK1 loss-of-function isrescued by TRAP1 |
| Home > Publications Database > PSM04-06: Mitochondrial degeneration in PINK1 loss-of-function isrescued by TRAP1 |
| Abstract/Journal Article | DZNE-2020-00839 |
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2013
Abstract: Mutations in PTEN-induced Kinase 1 (PINK1) cause early-onsetParkinson’s disease (PD). PINK1 is critical to maintain mitochon-drial function and protects cells from oxidative stress by suppressingCytochrome C release and thereby prevents cell death. Alterations inmitochondrial integrity and function is implicated in the etiology ofPD. It is known that application of mitochondrial toxins can causePD. Moreover, not only PINK1-linked but also sporadic PD patientsdisplay impaired function of mitochondrial complex I in post-mortem brains. Recent cell culture analysis implied that the protective effects of PINK1 are dependent on the downstream factorTNF receptor-associated protein 1 (TRAP1). We have recentlyshown that TRAP1 mitigates a-Synuclein induced toxicity in fliesand SH-SY5Y cells, highlighting the importance of this protein inPD pathology. So far, no in vivo studies on the interaction of PINK1and TRAP1 have been reported. Here we show that human TRAP1is able to mitigate PINK1 loss-of-function phenotypes in flies,including morphological abnormalities, impaired locomotion,decreased dopamine content and mitochondrial dysfunction. Inaddition, we show that TRAP1 is able to restore mitochondrialintegrity and function found to be impaired in PINK1 silenced SH-SY5Y cells. Thus, our data suggest a functional role of TRAP1 inmaintaining mitochondrial integrity of PINK1 deficient cells.Additionally, we provide evidence for TRAP1’s function withinthe PINK1/Parkin pathway
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