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.
We pick out particular compounds from an extensive virtual database of more than 60 billion molecules. The preparation and shipment of these compounds are facilitated by our associate Reaxense.
Contained in the library are leading modulators, each labelled with 38 ADME-Tox and 32 physicochemical and drug-likeness qualities. In addition, each compound is illustrated with its optimal docking poses, affinity scores, and activity scores, giving a complete picture.
We use our state-of-the-art dedicated workflow for designing focused libraries.
Fig. 1. The sreening workflow of Receptor.AI
Utilising molecular simulations, our approach thoroughly examines a wide array of proteins, tracking their conformational changes individually and within complexes. Ensemble virtual screening enables us to address conformational flexibility, revealing essential binding sites at functional regions and allosteric locations. Our rigorous analysis guarantees that no potential mechanism of action is overlooked, aiming to uncover new therapeutic targets and lead compounds across diverse biological functions.
Our library is unique due to several crucial aspects:
partner
Reaxense
upacc
O14907
UPID:
TX1B3_HUMAN
Alternative names:
Glutaminase-interacting protein 3; Tax interaction protein 1; Tax-interacting protein 1
Alternative UPACC:
O14907; B2RD53; D3DTJ6; Q7LCQ4
Background:
Tax1-binding protein 3, also known as Glutaminase-interacting protein 3 or Tax interaction protein 1, plays a crucial role in cellular signaling pathways. It regulates protein-protein interactions, inhibits the Wnt signaling pathway by binding to CTNNB1, and influences the Rho signaling pathway. Additionally, it competes with LIN7A for KCNJ4 binding, promoting KCNJ4 internalization, and may be involved in CDC42 activation by HPV16 E6.
Therapeutic significance:
Understanding the role of Tax1-binding protein 3 could open doors to potential therapeutic strategies.