IndraLab

Statements

UCHL1 increases the amount of Ubiquitin. 13 / 15
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"UCHL1 increases free ubiquitin levels and accelerates the lysosomal degradation of APP by promoting its ubiquitination."
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"UCH-L1 can increase levels of monomeric ubiquitin in neurons by binding and stabilizing ubiquitin monomers and by deubiquitinating ubiquitin precursors [XREF_BIBR, XREF_BIBR]."
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"Pharmacological inhibition of UCH-L1 activity reduces monomeric ubiquitin levels and results in spine enlargement with a concomitant decrease in spine density and synapse number (XREF_FIG)."
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"Pharmacological suppression of UCH-L1 activity reduces monomeric ubiquitin levels and leads to dramatic alterations to synaptic structure."
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"In addition to the deubiquitinating or ubiquitination promoting activity, UCHL1 stabilizes monoubiquitin and increases the level of ubiquitin in neuron (Osaka et al., 2003), which is consistent with o[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Mutations in UCHL1 can cause a reduction in deubiquitinating activity and reduced ubiquitin levels that limit the supply of ubiquitin monomers necessary for the clearance of additional unwanted protei[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"UCH-L1 may also elevate free Ub levels by facilitating recycling of Ub (XREF_FIG)."
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"UCHL1 increases free ubiquitin level and accelerates the lysosomal degradation of APP by promoting its ubiquitination."
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"A20 overexpression or UCH-L1 inhibition increased expression of synaptoporin and nephrin but decreased desmin expression and ubiquitin accumulation level in podocytes."
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"Ubiquitin C-terminal hydrolase L1 (UCHL1) plays an important role in maintenance of nervous system integrity, and overexpression of UCHL1 has been shown to increase ubiquitin levels within neurons."
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"Ubiquitin C-terminal hydrolase L1 (UCHL1) plays an important role in maintenance of nervous system integrity, and in vitro, overexpression of UCHL1 has been shown to increase ubiquitin levels, ensuring ubiquitin stability within neurons [2]."
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"Consistent with podocyte culture data (Fig. 2b, c), the expression of I93M-UCH-L1 but not of WT-UCH-L1 increased glomerular ubiquitin levels in vivo (Fig. 4d)."
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"Conversely, pharmacological inhibition of UCH-L1 significantly reduces monomeric ubiquitin levels and causes dramatic alterations in synaptic protein distribution and spine morphology."
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