Explore the Potential with AI-Driven Innovation
This comprehensive focused library is produced on demand with state-of-the-art virtual screening and parameter assessment technology driven by Receptor.AI drug discovery platform. This approach outperforms traditional methods and provides higher-quality compounds with superior 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 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.
Our high-tech, dedicated method is applied to construct targeted 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 is unique due to several crucial aspects:
partner
Reaxense
upacc
Q8WXG6
UPID:
MADD_HUMAN
Alternative names:
Differentially expressed in normal and neoplastic cells; Insulinoma glucagonoma clone 20; Rab3 GDP/GTP exchange factor; Rab3 GDP/GTP exchange protein
Alternative UPACC:
Q8WXG6; A8K8S7; B5MEE5; D3DQR4; O15065; O15293; Q15732; Q15741; Q8IWD7; Q8WXG3; Q8WXG4; Q8WXG5; Q8WZ63
Background:
The MAP kinase-activating death domain protein, also known as Rab3 GDP/GTP exchange factor, plays a pivotal role in cellular processes. It regulates small GTPases of the Rab family, crucial for synaptic vesicle exocytosis and vesicle secretion. This protein is involved in synaptic vesicle formation, trafficking at the neuromuscular junction, and up-regulating synaptic exocytosis in central synapses. It also mediates TNFA-mediated activation of the MAPK pathway, including ERK1/2, and may link TNFRSF1A with MAP kinase activation.
Therapeutic significance:
Linked to DEEAH syndrome and a neurodevelopmental disorder with dysmorphic facies, impaired speech, and hypotonia, understanding the role of MAP kinase-activating death domain protein could open doors to potential therapeutic strategies.