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 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 includes a list of the most promising modulators annotated with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Also, each compound is presented with its optimal docking poses, affinity scores, and activity scores, providing a comprehensive overview.
Our top-notch dedicated system is used to design specialised libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
It includes comprehensive molecular simulations of the catalytic and allosteric binding pockets and the ensemble virtual screening accounting for their conformational mobility. In the case of designing modulators, the structural changes induced by reaction intermediates are taken into account to leverage activity and selectivity.
Key features that set our library apart include:
partner
Reaxense
upacc
Q6EMB2
UPID:
TTLL5_HUMAN
Alternative names:
SRC1 and TIF2-associated modulatory protein; Tubulin--tyrosine ligase-like protein 5
Alternative UPACC:
Q6EMB2; B9EGH8; B9EGH9; Q9BUB0; Q9H0G4; Q9H7W2; Q9P1V5; Q9UPZ4
Background:
Tubulin polyglutamylase TTLL5, also known as SRC1 and TIF2-associated modulatory protein, plays a crucial role in modifying tubulin. This enzyme generates polyglutamate side chains on tubulin, essential for proper cellular function. It shows a preference for initiating over elongating the polyglutamylation reaction and modifies alpha-tubulin more than beta-tubulin. TTLL5 is vital for CCSAP localization to microtubules and enhances NCOA2/TIF2's effects in hormone receptor signaling.
Therapeutic significance:
TTLL5's mutation is linked to Cone-rod dystrophy 19, a retinal dystrophy leading to severe vision loss. Understanding TTLL5's role could unveil new therapeutic strategies for this and potentially other related diseases.