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UCHL1 activates UCHL1. 15 / 15
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"Finally, as the authors reported both UCHL1 promoter hypomethylation and the epigenetic upregulation of UCHL1, they theorized that mutant p53 could be responsible for the transcriptional induction of UCHL1 in HGSOC (Tangri et al., 2021)."
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"Previous studies have shown that UCHL1 is specifically expressed in decidual cells within uterus during early pregnancy [24], and consistently, our findings indicate that the expression of UCHL1 was progressively increased during decidualization in both mice and humans, indicating a positive regulatory role of UCHL1 in this process."
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"Furthermore, it has very recently been shown that an aberrant UCH-L1 expression leads to a increase in Akt signaling in UCH-L1 transgenic mice [26] ."
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"LDN-57444 has been widely used to downregulate expression of UCH-L1 in certain tumors, such as in NSCLC (19), oral squamous cell carcinoma (103) and neuroblastoma (37), therefore showing that it inhibits activity of metastatic tumor cells by reducing the deubiquitination activity of UCH-L1 (103)."
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"In contrast , when CSMN are retrogradely transduced with AAV2-UCHL1-IRES-eGFP , which leads to the expression of both GFP and UCHL1 proteins , high level of UCHL1 expression is detected only in GFP + transduced CSMN ( Fig. 5d , g ) , confirming effective transduction and directed gene delivery only to CSMN ."
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"Bentz et al. demonstrated that KSHV infection induces UCH-L1 expression through the ability of the LANA protein to activate the uch-l1 promoter."
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"In this study, we demonstrate global DNA hypomethylation as one mechanism which causes UCHL1 promoter hypomethylation, and consequently, UCHL1 upregulation."
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"Moreover, overexpression of UCHL1 delays AD progression in mouse models, and UCHL1 gene therapy, to overexpress UCHL1, in the brain potentially could be a promising disease modifying strategy for AD therapeutics."
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"Interestingly, UCHL1 expression triggered the accumulation of free monoubiquitin similarly to UCHL1 (Fig. 8e, compare lane 4 with lane 2)."
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"A rare inherited form of PD, PARK5, is caused by a missense mutation in UCHL1."
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"The loss of Cav-1 and compact myelin proteins following hyperglycemia and NRG treatment was not due to neuronal loss, since the axons remained intact and there was no loss of PGP 9.5, an axonal marker protein."
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"This observation is consistent with a recent report that the over-expression of UCH-L1 induces testicular germ cell apoptosis in UCH-L1 transgenic mice."
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"Furthermore, there is frequent overexpression of PGP9.5 in NSCLC with higher expression correlating with advanced stage malignancy, which suggests involvement of the protein in lung carcinogenesis."
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"This is due to very high levels of UCH-L1 which lead to an increase in the UCH-L1 substrate and also more damaged UCH-L1."
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"Exogenous UCHL1 overexpression from cDNA plasmid resulted in dramatic upregulation of UCHL1 in H1299 and BEAS-2B cells (95 to 279-fold and 217 to 675-fold, respectively, Supplemental Figure 7, A‒D)."
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