IndraLab

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UCHL1 inhibits APP. 18 / 20
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"In APP and PS1 mice, injection of UCH-L1 improves the retention of contextual learning through the PKA-CREB pathway [XREF_BIBR] and reduces Abeta production, increased free ubiquitin and accelerates proteosomal degradation of APP [XREF_BIBR]."
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"In APP and PS1 mice, injection of UCH-L1 improves the retention of contextual learning through the PKA-CREB pathway [XREF_BIBR] and reduces Abeta production, increased free ubiquitin and accelerates proteosomal degradation of APP [XREF_BIBR]."
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"Over-expression of UCHL1 decreased APP C-terminal fragment C99 and Abeta levels in HUCH cells."
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"UCHL1 also accelerates beta-secretase degradation, impairs APP processing and decreases Abeta 109."
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"The Uchl1 overexpression, induced by intracranial injection of Uchl1 expressing virus, decreases the Abeta production and protects AD model mice against memory impairment."
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"This may be mechanistically attributed to the fact that loss of UCHL1 and UCHL3 accelerates the degradation of APP, thus accounting for the overproduction of Aβ (Zhang, Cai, Zhang, Zhang, & Song, 2014) (Table 2).2.5 Therapeutic implications."
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"The expression of ciRS-7, UCHL1, and p65 was significantly upregulated after breviscapine or BMSCs treatment, and there was increased APP and BAEC1 degradation."
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"Other work proposes that UCHL1 has specific substrates and may increase UPP dependent degradation of the beta-site amyloid precursor protein (APP) cleaving enzyme 1 (BACE1)."
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"UCH-L1 null mice have higher levels of brain Abeta, while overexpression of UCH-L1 slows the deposition of Abeta and attenuates cognitive decline in a mouse model of AD (Zhang et al., 2012)."
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"Zhang et al. reported that the overexpression of UCHL1 decreased Abeta in the uchl1-null AD mice (Zhang et al., 2012)."
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"In the latter scenario all of the symptoms of AD that are caused by oligomeric Aβ, not just memory loss, could be targeted by enhancing the relevant activity of UCH-L1.Gong et al. propose that UCH-L1 [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"For example, the expression of circRNA ciRS-7, which originates from cerebellar degeneration-related protein 1 antisense transcript (CDR1AS), leads to the activation of Ubiquitin C-Terminal Hydrolase L1 (UCHL1), which then promotes APP and BACE1 degradation, consequently leading to impeded amyloid plaque growth [128]."
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"The mechanism by which Uch-L1 reduces Abeta accumulation and toxicity is unclear."
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"Facilitation of APP degradation by UCHL1 could be through the lysosomal or proteasomal pathway."
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"Our results indicated that UCHL1 promoted the degradation of APP via the lysosomal pathway."
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"In SH-SY5Y cells , overexpression of ciRS-7 reduced Abeta deposition by upregulating UCHL1 to degrade APP and BAEC1 , but these effects were reversed with inhibition of NF-kB signaling ."
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"Our data also suggest that ciRS-7 modulates APP and BACE1 levels in a nuclear factor-kappaB (NF-kappaB)-dependent manner : ciRS-7 expression inhibits translation of NF-kappaB and induces its cytoplasmic localization, thus derepressing expression of UCHL1, which promotes APP and BACE1 degradation."
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"Disruption of UCHL1 gene expression significantly increased APP CTFs in the hippocampi of APP23 and gad mice compared to APP23 mice (XREF_FIG)."
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