Explore the Potential with AI-Driven Innovation
Our detailed focused library is generated on demand with advanced virtual screening and parameter assessment technology powered by the Receptor.AI drug discovery platform. This method surpasses traditional approaches, delivering compounds of better quality with enhanced 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 features a range of promising modulators, each detailed with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Plus, each compound is presented with its ideal docking poses, affinity scores, and activity scores, ensuring a thorough insight.
We utilise our cutting-edge, exclusive workflow to develop focused libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
The method includes detailed molecular simulations of the catalytic and allosteric binding pockets, along with ensemble virtual screening that considers their conformational flexibility. In the design of modulators, structural changes induced by reaction intermediates are taken into account to enhance activity and selectivity.
Our library distinguishes itself through several key aspects:
partner
Reaxense
upacc
O00635
UPID:
TRI38_HUMAN
Alternative names:
RING finger protein 15; Tripartite motif-containing protein 38; Zinc finger protein RoRet
Alternative UPACC:
O00635; B2R862
Background:
E3 ubiquitin-protein ligase TRIM38, also known as RING finger protein 15, Tripartite motif-containing protein 38, and Zinc finger protein RoRet, plays a pivotal role in innate immunity. It regulates type I interferon IFN-beta production through 'Lys-48'-linked polyubiquitination of AZI2/NAP1, leading to its degradation. Additionally, it inhibits TLR3-mediated type I interferon signaling by targeting TICAM1 for degradation. TRIM38 enhances the cGAS-STING pathway by sumoylating CGAS and STING, and independently suppresses NF-kappa-B signaling by promoting the degradation of TAB2 and TAB3.
Therapeutic significance:
Understanding the role of E3 ubiquitin-protein ligase TRIM38 could open doors to potential therapeutic strategies.