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.
We pick out particular compounds from an extensive virtual database of more than 60 billion molecules. The preparation and shipment of these compounds are facilitated by our associate 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.
Fig. 1. The sreening workflow of Receptor.AI
Our methodology employs molecular simulations to explore a wide array of proteins, capturing their dynamic states both individually and within complexes. Through ensemble virtual screening, we address conformational mobility, uncovering binding sites within functional regions and remote allosteric locations. This thorough exploration ensures no potential mechanism of action is overlooked, aiming to discover novel therapeutic targets and lead compounds across an extensive spectrum of biological functions.
Our library stands out due to several important features:
partner
Reaxense
upacc
Q9UKC9
UPID:
FBXL2_HUMAN
Alternative names:
F-box and leucine-rich repeat protein 2; F-box protein FBL2/FBL3
Alternative UPACC:
Q9UKC9; B4DQV0; E9PD06; Q6IAN3; Q9NVQ8; Q9UK27; Q9UKA5; Q9Y3Y9
Background:
F-box/LRR-repeat protein 2, also known as F-box and leucine-rich repeat protein 2 or F-box protein FBL2/FBL3, plays a crucial role in cellular processes. It is a key component of the SCF (SKP1-cullin-F-box protein) E3 ubiquitin-protein ligase complex, SCF(FBXL2), which targets proteins for ubiquitination and proteasomal degradation. This protein is unique in targeting calmodulin-binding motifs instead of phosphodegron, regulating the degradation of cyclins CCND2 and CCND3, and thus influencing cell cycle arrest. Additionally, it is involved in PIK3R2 degradation, affecting phosphatidylinositol 3-kinase signaling and autophagy, and regulates phosphatidylcholine synthesis crucial for membrane formation.
Therapeutic significance:
Understanding the role of F-box/LRR-repeat protein 2 could open doors to potential therapeutic strategies.