p(HGNC:UCHL1)
However, mice homozygous for both UCH-L1 and UCH-L3 deletions die early due to dysphagia and display degeneration of the nucleus tractus solitarius and area postrema in addition to the degeneration of the gracile tract that is observed in GAD mice that only have a UCH-L1 deletion PubMed:14556719
However, mice homozygous for both UCH-L1 and UCH-L3 deletions die early due to dysphagia and display degeneration of the nucleus tractus solitarius and area postrema in addition to the degeneration of the gracile tract that is observed in GAD mice that only have a UCH-L1 deletion PubMed:14556719
Activated PKA induces transcription of ApUCH (UCH-L1 in mammals), a deubiquitinating enzyzme, which has been found to be critical for the induction of long-term facilitation (Hegde et al. 1997). PubMed:22908190
Although UCH-L1 is genetically associated with Parkinson’s disease (i.e., it is the PARK5 gene; Belin and Westerlund 2008), it has also been implicated in the pathogenesis of AD PubMed:22908190
Although UCH-L1 is genetically associated with Parkinson’s disease (i.e., it is the PARK5 gene; Belin and Westerlund 2008), it has also been implicated in the pathogenesis of AD PubMed:22908190
The decrease in Uch-L1 depends on NF-κB pathway since NF-κB p65 can interact with the −300 bp and −109 bp NF-κB binding sequences of the Uch-L1 gene promoter [55]. PubMed:27288790
It has been reported recently that while the monomeric form of UCH-L1 catalyzes deubiquitination, the dimers display a ubiquitin ligase activity that generates ubiquitin-K63 bonds (Liu et al., 2002). PubMed:14556719
Mono- and diubiquitinated alphaSYN were polyubiquitinated by the enzyme, suggesting that it acts as an E4 (Koegl et al., 1999) PubMed:14556719
However, mice homozygous for both UCH-L1 and UCH-L3 deletions die early due to dysphagia and display degeneration of the nucleus tractus solitarius and area postrema in addition to the degeneration of the gracile tract that is observed in GAD mice that only have a UCH-L1 deletion PubMed:14556719
However, mice homozygous for both UCH-L1 and UCH-L3 deletions die early due to dysphagia and display degeneration of the nucleus tractus solitarius and area postrema in addition to the degeneration of the gracile tract that is observed in GAD mice that only have a UCH-L1 deletion PubMed:14556719
However, mice homozygous for both UCH-L1 and UCH-L3 deletions die early due to dysphagia and display degeneration of the nucleus tractus solitarius and area postrema in addition to the degeneration of the gracile tract that is observed in GAD mice that only have a UCH-L1 deletion PubMed:14556719
Although UCH-L1 is genetically associated with Parkinson’s disease (i.e., it is the PARK5 gene; Belin and Westerlund 2008), it has also been implicated in the pathogenesis of AD PubMed:22908190
Although UCH-L1 is genetically associated with Parkinson’s disease (i.e., it is the PARK5 gene; Belin and Westerlund 2008), it has also been implicated in the pathogenesis of AD PubMed:22908190
Moreover, administration of UCH-L1 can reverse the amyloid b-protein–induced synaptic dysfunction and memory loss in transgenic mice overexpressing APP and PS1 (Gong et al. 2006). PubMed:22908190
Moreover, administration of UCH-L1 can reverse the amyloid b-protein–induced synaptic dysfunction and memory loss in transgenic mice overexpressing APP and PS1 (Gong et al. 2006). PubMed:22908190
Aβ 42 mediated increase in BACE1 expression is accompanied by a decrease in Uch-L1 expression and activity in dif- ferent cellular models and in sporadic AD brains, which interferes with the lysosomal degradation of BACE1 [52,56]. PubMed:27288790
Aβ 42 mediated increase in BACE1 expression is accompanied by a decrease in Uch-L1 expression and activity in dif- ferent cellular models and in sporadic AD brains, which interferes with the lysosomal degradation of BACE1 [52,56]. PubMed:27288790
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