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.
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.
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
Q15750
UPID:
TAB1_HUMAN
Alternative names:
Mitogen-activated protein kinase kinase kinase 7-interacting protein 1; TGF-beta-activated kinase 1-binding protein 1
Alternative UPACC:
Q15750; Q2PP09; Q8IZW2
Background:
TGF-beta-activated kinase 1 and MAP3K7-binding protein 1, also known as Mitogen-activated protein kinase kinase kinase 7-interacting protein 1, is a pivotal adapter protein. It plays a crucial role in the activation of JNK and NF-kappa-B, leading to the production of proinflammatory cytokines upon stimulation with TLRs and cytokines. This protein facilitates the autophosphorylation and full activation of MAP3K7/TAK1, and similarly, it activates MAPK14 through autophosphorylation. Additionally, it participates in a feedback mechanism by recruiting MAPK14 to the TAK1 complex for phosphorylation of TAB2 and TAB3.
Therapeutic significance:
Understanding the role of TGF-beta-activated kinase 1 and MAP3K7-binding protein 1 could open doors to potential therapeutic strategies.