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.
The compounds are cherry-picked from the vast virtual chemical space of over 60B molecules. The synthesis and delivery of compounds is facilitated by our partner Reaxense.
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.
We employ our advanced, specialised process to create targeted libraries.
Fig. 1. The sreening workflow of Receptor.AI
Our methodology leverages molecular simulations to examine a vast array of proteins, capturing their dynamics in both isolated forms and in complexes with other proteins. Through ensemble virtual screening, we thoroughly account for the protein's conformational mobility, identifying critical binding sites within functional regions and distant allosteric locations. This detailed exploration ensures that we comprehensively assess every possible mechanism of action, with the objective of identifying novel therapeutic targets and lead compounds that span a wide spectrum of biological functions.
Key features that set our library apart include:
partner
Reaxense
upacc
Q969V6
UPID:
MRTFA_HUMAN
Alternative names:
MKL/myocardin-like protein 1; Megakaryoblastic leukemia 1 protein; Megakaryocytic acute leukemia protein
Alternative UPACC:
Q969V6; Q8TCL1; Q96SC5; Q96SC6; Q9P2B0
Background:
Myocardin-related transcription factor A (MRTFA), also known as MKL/myocardin-like protein 1, plays a pivotal role in regulating cytoskeletal gene expression. This is achieved through its association with the serum response factor (SRF), responding to Rho GTPase-induced changes in cellular actin dynamics. MRTFA's interaction with globular actin (G-actin) and filamentous actin (F-actin) in the nucleus modulates the activity of the MRTFA-SRF complex, crucial for development, morphogenesis, and cell migration.
Therapeutic significance:
MRTFA's involvement in Immunodeficiency 66, a disorder characterized by recurrent viral infections and impaired neutrophil migration, underscores its therapeutic potential. Understanding the role of MRTFA could open doors to potential therapeutic strategies, particularly in enhancing immune responses and correcting cytoskeletal abnormalities.