Explore the Potential with AI-Driven Innovation
The specialised, focused library is developed on demand with the most recent virtual screening and parameter assessment technology, guided by the Receptor.AI drug discovery platform. This approach exceeds the capabilities of traditional methods and offers compounds with higher 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.
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 utilise our cutting-edge, exclusive workflow to develop focused libraries.
Fig. 1. The sreening workflow of Receptor.AI
Our strategy employs molecular simulations to explore an extensive range of proteins, capturing their dynamics both individually and within complexes with other proteins. Through ensemble virtual screening, we address proteins' conformational mobility, uncovering key binding sites at both functional regions and remote allosteric locations. This comprehensive investigation ensures a thorough assessment of all potential mechanisms of action, with the goal of discovering innovative therapeutic targets and lead molecules across across diverse biological functions.
Our library is unique due to several crucial aspects:
partner
Reaxense
upacc
O95297
UPID:
MPZL1_HUMAN
Alternative names:
Protein zero-related
Alternative UPACC:
O95297; B2REB9; B2REC0; Q5R332; Q8IX11; Q9BWZ3; Q9NYK4; Q9UL20
Background:
Myelin protein zero-like protein 1, alternatively known as Protein zero-related, plays a pivotal role in cell surface receptor signaling. It facilitates the recruitment of PTPN11/SHP-2 to the cell membrane and acts as a substrate for PTPN11/SHP-2. This protein is a key receptor for concanavalin-A (ConA), engaging in cellular signaling pathways initiated by ConA, which likely involve Src family tyrosine-protein kinases. Notably, isoform 3 of this protein exerts a dominant negative effect by inhibiting tyrosine phosphorylation of MPZL1 induced by ConA, whereas isoform 1 is implicated in the regulation of integrin-mediated cell motility.
Therapeutic significance:
Understanding the role of Myelin protein zero-like protein 1 could open doors to potential therapeutic strategies.