Development of UCHL1-Based Stroke Therapy

Ubiquitin carboxy-terminal hydrolase L1 (UCHL1) is a neuron-specific protein. At the same time, it is an essential component of the ubiquitin proteasome pathway (UPP) in neurons. The ability of UPP to remove misfolded or damaged proteins in neurons helps ensure normal neuronal function and prevents the accumulation of abnormal proteins. Therefore, maintaining the normal function of UCHL1 during brain disease episodes is critical for disease recovery. Many studies have shown that maintaining or restoring UCHL1 activity is a potential therapeutic strategy for stroke. Therefore, Ace Therapeutics provides comprehensive services to facilitate the development of stroke drugs targeting UCHL1.

Development of Stroke Therapies to Restore UCHL1 Activity

Given that studies have shown that maintaining or restoring the activity of UCHL1 is a potential treatment for stroke. Therefore, Ace Therapeutics offers comprehensive services to explore the development of methods to maintain or restore UCHL1 activity for stroke relief.

• We enhance the ability of UCHL1 to enter and function in the brain through chemical modifications.
• We enhance the ability of UCHL1 to enter and function in the brain through biological modifications.
• We offer comprehensive modification services and evaluation technology for the TAT-UCHL1 therapeutic pathway.

Development of Stroke Therapies Targeting the C152 of UCHL1

White matter damage is an important cause of disability after stroke, but there are few stroke treatment options that target white matter damage. Studies have shown that the mutation of the cysteine residue 152 (C152)-reactive lipid-binding site of UCHL1 may reduce stroke damage to gray and white matter and thereby restore motor function after stroke. In view of this, Ace Therapeutics offers comprehensive services to explore the development of stroke therapies based on mutations in C152 of UCHL1.

• We offer different in vitro and in vivo stroke models for stroke therapy development.
• We study the effect of C152 mutation on stroke pathology by mutating C152 of UCHL1 and combining gene microarray and protein microarray technologies.
• Different stroke therapies are screened for the different effects of C152 mutation in UCHL1.
• We obtain inhibitors that effectively inhibit the binding of substrates of C152 to C152 by high-throughput screening.
• We obtain enhancers of UCHL1 after stroke by high-throughput screening.
• For drug candidates, we provide comprehensive evaluation and testing services.

To explore the impact of mutations in other sites of UCHL1 on stroke, we also provide adequate research services to facilitate the development of stroke therapies regarding UCHL1. If you would like to learn more about our services, please feel free to contact us.

1. Graham, S. H. Liu, H., Life and death in the trash heap: The ubiquitin proteasome pathway and uchl1 in brain aging, neurodegenerative disease and cerebral ischemia. Ageing Res Rev, 2017. 34: p. 30-38.