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.
We carefully select specific compounds from a vast collection of over 60 billion molecules in virtual chemical space. Our partner Reaxense helps in synthesizing and delivering these compounds.
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.
Our high-tech, dedicated method is applied to construct targeted libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
It includes in-depth molecular simulations of both the catalytic and allosteric binding pockets, with ensemble virtual screening focusing on their conformational flexibility. For modulators, the process includes considering the structural shifts due to reaction intermediates to boost activity and selectivity.
Key features that set our library apart include:
partner
Reaxense
upacc
Q86YT6
UPID:
MIB1_HUMAN
Alternative names:
DAPK-interacting protein 1; Mind bomb homolog 1; RING-type E3 ubiquitin transferase MIB1; Zinc finger ZZ type with ankyrin repeat domain protein 2
Alternative UPACC:
Q86YT6; B0YJ38; Q2TB37; Q68D01; Q6YI51; Q8NBY0; Q8TCB5; Q8TCL7; Q9P2M3
Background:
E3 ubiquitin-protein ligase MIB1, known as Mind bomb homolog 1, plays a crucial role in Notch signaling by mediating the ubiquitination of Delta receptors. This process enhances Notch signaling, pivotal for cell fate determination. MIB1 also regulates apoptosis through ubiquitination and degradation of DAPK1, and inhibits primary cilium formation by targeting centriolar satellite proteins for ubiquitination.
Therapeutic significance:
MIB1's involvement in left ventricular non-compaction 7, a cardiomyopathy with variable clinical manifestations, underscores its potential as a therapeutic target. Understanding MIB1's role could open doors to novel strategies for treating heart conditions.