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.
Our selection of compounds is from a large virtual library of over 60 billion molecules. The production and distribution of these compounds are managed by our partner Reaxense.
The library includes a list of the most promising modulators annotated with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Also, each compound is presented with its optimal docking poses, affinity scores, and activity scores, providing a comprehensive overview.
We utilise our cutting-edge, exclusive workflow to develop focused libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
It includes in-depth molecular simulations of both the catalytic and allosteric binding pockets, with ensemble virtual screening focusing on their conformational flexibility. For modulators, the process includes considering the structural shifts due to reaction intermediates to boost activity and selectivity.
Key features that set our library apart include:
partner
Reaxense
upacc
P15170
UPID:
ERF3A_HUMAN
Alternative names:
G1 to S phase transition protein 1 homolog
Alternative UPACC:
P15170; J3KQG6; Q96GF2
Background:
Eukaryotic peptide chain release factor GTP-binding subunit ERF3A, also known as GSPT1 or G1 to S phase transition protein 1 homolog, plays a crucial role in translation termination. It forms part of the eRF1-eRF3-GTP ternary complex, which mediates translation termination at stop codons UAA, UAG, and UGA. This protein is essential for delivering ETF1/ERF1 to stop codons, facilitating GTP hydrolysis, and inducing conformational changes for translation termination. Additionally, ERF3A is a component of the SURF complex, involved in nonsense-mediated decay (NMD) and is required for SHFL-mediated translation termination, which inhibits programmed ribosomal frameshifting.
Therapeutic significance:
Understanding the role of Eukaryotic peptide chain release factor GTP-binding subunit ERF3A could open doors to potential therapeutic strategies.