IndraLab

Statements


UCHL1 decreases the amount of BACE1. 7 / 8
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"We found that inhibition of UCHL1 significantly increased BACE1 protein level in a time dependent manner."

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"Concordant with this fact, a research using different cellular models such as neuroblastoma SH-SY5Y and NT (2) neuronal cells shows that Abeta42 treatment downregulates UCHL-1 and this down-regulation is dependent on NF-kappaB activation and on impaired BACE1 lysosomal degradation.39 Ubiquitin C-terminal hydrolase-1 accelerates BACE1 degradation and affects APP processing and Abeta production.40 In conclusion, potentiation of UCHL-1 might be able to reduce the levels of BACE1 and Abeta in brain, and UCHL-1 may be a novel target for AD drug development."

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"This study suggests that potentiation of UCHL1 might be able to reduce the level of BACE1 and Abeta in brain, which makes it a novel target for AD drug development."

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"For example, inhibition of UCH-L1 increased levels of BACE1 leading to reduction of Aβ levels and it also affects the SNCA expression ( Liu et al., 2009 ; Pulliam et al., 2019 ; Zhang et al., 2012 )."

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"Thus, the restoration of Uch-L1 was able to completely prevent both the increase in BACE1 protein levels and the amount of cell death."

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"The restoration of Uch-L1 was able to completely prevent the increase of BACE1 protein levels both in control and Tg mice at 6 h post injury, as reported by the representative blot and by the densitometric analysis."

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"Inhibition of UCHL1 activity significantly increased BACE1 protein expression and increased concentrations of amyloid β, whereas overexpression of UCHL1 decreased amyloid β levels and delayed AD progression (Zhang et al., 2014; Zhang et al., 2012)."