Explore the Potential with AI-Driven Innovation
This extensive focused library is tailor-made using the latest virtual screening and parameter assessment technology, operated by the Receptor.AI drug discovery platform. This technique is more effective than traditional methods, offering compounds with improved activity, selectivity, and safety.
From a virtual chemical space containing more than 60 billion molecules, we precisely choose certain compounds. Our collaborator, Reaxense, aids in their synthesis and provision.
The library includes a list of the most effective modulators, each annotated with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Furthermore, each compound is shown with its optimal docking poses, affinity scores, and activity scores, offering a detailed summary.
Our top-notch dedicated system is used to design specialised libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
The procedure entails thorough molecular simulations of the catalytic and allosteric binding pockets, accompanied by ensemble virtual screening that factors in their conformational flexibility. When developing modulators, the structural modifications brought about by reaction intermediates are factored in to optimize activity and selectivity.
Key features that set our library apart include:
partner
Reaxense
upacc
Q9BQP7
UPID:
MGME1_HUMAN
Alternative names:
-
Alternative UPACC:
Q9BQP7; B2RDG5; D3DW29; Q96SW3
Background:
Mitochondrial genome maintenance exonuclease 1, encoded by the gene with accession number Q9BQP7, plays a crucial role in mitochondrial DNA (mtDNA) maintenance. It exhibits metal-dependent single-stranded DNA exonuclease activity, favoring 5'-3' exonuclease activity, and is also capable of endonuclease activity on linear substrates. This protein is essential for maintaining proper 7S DNA levels and is likely involved in mtDNA repair processes, including the processing of Okazaki fragments and DNA flaps.
Therapeutic significance:
Mitochondrial DNA depletion syndrome 11, a disorder characterized by progressive external ophthalmoplegia, muscle weakness, and respiratory insufficiency, is associated with variants affecting this gene. Understanding the role of Mitochondrial genome maintenance exonuclease 1 could open doors to potential therapeutic strategies for this syndrome, highlighting its importance in mitochondrial disorders.