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UCHL1 decreases the amount of APP. 9 / 12
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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)."
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"Inhibition of UCHL1 by the compound LDN57444 has been shown to elevate APP levels ."
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"Mature APP level was reduced by UCHL1 as expected (p < 0.05) (XREF_FIG), and was further reduced by ubiquitin expression (p < 0.01) (XREF_FIG)."
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"Overexpression of either UCHL1 or ubiquitin depleted APP levels while increasing its ubiquitination (Fig. 3f; Supplementary Fig. 4j)."
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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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"Overexpressing Uch-L1 reduces BACE1 activity and Abeta levels, whereas Uch-L1 null mice exhibit increased number of Abeta plaques and neurofibrillary tangles, thus displaying an inverse relationship with Uch-L1 levels."
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"Inhibition of UCHL1 activity significantly increased concentrations of amyloid β, whereas overexpression of UCHL1 decreased amyloid β levels and delayed AD progression [51]."
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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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"To investigate whether UCHL1 reduced APP protein level by the lysosomal degradation, Haw cells were transfected with UCHL1 and then treated with 100muM chloroquine (XREF_FIG)."
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