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 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 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 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.
Our library is unique due to several crucial aspects:
partner
Reaxense
upacc
Q8IW41
UPID:
MAPK5_HUMAN
Alternative names:
p38-regulated/activated protein kinase
Alternative UPACC:
Q8IW41; B3KVA5; O60491; Q86X46; Q9BVX9; Q9UG86
Background:
MAP kinase-activated protein kinase 5, also known as p38-regulated/activated protein kinase, plays a pivotal role in mTORC1 signaling and post-transcriptional regulation. It phosphorylates several key proteins including FOXO3, ERK3/MAPK6, and p53/TP53, acting as a tumor suppressor and mediating Ras-induced senescence. Its involvement in the atypical MAPK signaling pathway underscores its complex regulatory functions in cellular processes.
Therapeutic significance:
Given its role in tumor suppression and regulation of critical signaling pathways, MAP kinase-activated protein kinase 5 holds significant therapeutic potential. Understanding its mechanisms could lead to novel interventions for Neurocardiofaciodigital syndrome, characterized by developmental delay and congenital defects, and potentially other diseases linked to dysregulated mTORC1 signaling and cellular senescence.