Literature summary for 3.4.19.12 extracted from

Lansbury, P.T.
Improving synaptic function in a mouse model of AD (2006), Cell, 126, 655-657.

Search for more literature for 3.4.19.12

Application

Application	Comment	Organism
medicine	activation of UCH-L1 may be a useful therapeutic approach for treating Alzheimers disease. Administration of a UCH-L1 fused to the transduction domain of the HIV-transactivator protein to supplement endogenous UCH-L1 has a protective effect on memory loss in a mouse model of Alzheimers disease. It restores long term potentiation and contextual memory to normal levels, whereas levels of the regulatory subunit of protein kinase A decrease, which, in turn, leads to increased levels of phosopho-cAMP response element binding protein	Mus musculus
medicine	expression of UCH-L1 is increased during long-term facilitation, which is related to synaptic plasticity and learning	Aplysia sp.
medicine	UCH-L1 has a putative but still undefined role in the ubiquitin-dependent protein degradation pathway. Postmortem analysis of human brains shows this pathway to be compromised in Alzheimers disease. A polymorphism in the UCH-L1 gene increases the risk of Alzheimers disease in females and also effects the risk of Parkinsons disease in Asian populations	Homo sapiens

Protein Variants

Protein Variants	Comment	Organism
C90S	inhibits the protective action of endogenous UCH-L1. C90S-fusion protein does not rescue the deficit in long term potentiation induced by Abeta, acts as a dominant negative mutant, causes a deficit in long term potentiation in the absence of oligomeric Abeta	Mus musculus

Inhibitors

Inhibitors	Comment	Organism	Structure
additional information	treatment of hippocampal slices with a small-molecule inhibitor of UCH-L1 enzymatic activity produces a deficit in long term potentiation	Mus musculus
oligomeric Abeta	treatment of hippocampal slices produces a deficit in long term potentiation. Effect can be reversed by coadministering a recombinant UCH-L1 protein	Mus musculus

Organism

Organism	UniProt	Comment	Textmining
Aplysia sp.	-	-	-
Homo sapiens	-	-	-
Mus musculus	-	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
brain	-	Mus musculus	-
brain	-	Homo sapiens	-
hippocampus	-	Mus musculus	-
additional information	absence of UCHL1 in the gracile axonal dystrophy mouse, which results in neurodegeneration	Mus musculus	-

Synonyms

Synonyms	Comment	Organism
UCH-L1	-	Mus musculus
UCH-L1	-	Homo sapiens
UCH-L1	-	Aplysia sp.

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Release 2023.1 (January 2023)