AI-ACCELERATED DRUG DISCOVERY
Available from Reaxense
This protein is integrated into the Receptor.AI ecosystem as a prospective target with high therapeutic potential. We performed a comprehensive characterization of Deformed epidermal autoregulatory factor 1 homolog including:
1. LLM-powered literature research
Our custom-tailored LLM extracted and formalized all relevant information about the protein from a large set of structured and unstructured data sources and stored it in the form of a Knowledge Graph. This comprehensive analysis allowed us to gain insight into Deformed epidermal autoregulatory factor 1 homolog therapeutic significance, existing small molecule ligands, relevant off-targets, and protein-protein interactions.
Fig. 1. Preliminary target research workflow
2. AI-Driven Conformational Ensemble Generation
Starting from the initial protein structure, we employed advanced AI algorithms to predict alternative functional states of Deformed epidermal autoregulatory factor 1 homolog, including large-scale conformational changes along "soft" collective coordinates. Through molecular simulations with AI-enhanced sampling and trajectory clustering, we explored the broad conformational space of the protein and identified its representative structures. Utilizing diffusion-based AI models and active learning AutoML, we generated a statistically robust ensemble of equilibrium protein conformations that capture the receptor's full dynamic behavior, providing a robust foundation for accurate structure-based drug design.
Fig. 2. AI-powered molecular dynamics simulations workflow
3. Binding pockets identification and characterization
We employed the AI-based pocket prediction module to discover orthosteric, allosteric, hidden, and cryptic binding pockets on the protein’s surface. Our technique integrates the LLM-driven literature search and structure-aware ensemble-based pocket detection algorithm that utilizes previously established protein dynamics. Tentative pockets are then subject to AI scoring and ranking with simultaneous detection of false positives. In the final step, the AI model assesses the druggability of each pocket enabling a comprehensive selection of the most promising pockets for further targeting.
Fig. 3. AI-based binding pocket detection workflow
4. AI-Powered Virtual Screening
Our ecosystem is equipped to perform AI-driven virtual screening on Deformed epidermal autoregulatory factor 1 homolog. With access to a vast chemical space and cutting-edge AI docking algorithms, we can rapidly and reliably predict the most promising, novel, diverse, potent, and safe small molecule ligands of Deformed epidermal autoregulatory factor 1 homolog. This approach allows us to achieve an excellent hit rate and to identify compounds ready for advanced lead discovery and optimization.
Fig. 4. The screening workflow of Receptor.AI
Receptor.AI, in partnership with Reaxense, developed a next-generation technology for on-demand focused library design to enable extensive target exploration.
The focused library for Deformed epidermal autoregulatory factor 1 homolog 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.
Deformed epidermal autoregulatory factor 1 homolog
partner:
Reaxense
upacc:
O75398
UPID:
DEAF1_HUMAN
Alternative names:
Nuclear DEAF-1-related transcriptional regulator; Suppressin; Zinc finger MYND domain-containing protein 5
Alternative UPACC:
O75398; A8K1F8; A8K5R8; C7T5V5; O15152; O75399; O75510; O75511; O75512; O75513; Q9UET1
Background:
Deformed epidermal autoregulatory factor 1 homolog (DEAF-1), also known as Nuclear DEAF-1-related transcriptional regulator, Suppressin, and Zinc finger MYND domain-containing protein 5, plays a pivotal role in transcription regulation. It binds to specific DNA sequences, down-regulating transcription of certain genes, including its own. DEAF-1 is crucial for processes such as neural tube closure, skeletal patterning, and epithelial cell proliferation in the mammary gland. It also influences the expression of peripheral tissue antigens in pancreatic lymph nodes.
Therapeutic significance:
DEAF-1's involvement in Vulto-van Silfout-de Vries syndrome and Neurodevelopmental disorder with hypotonia suggests its potential as a therapeutic target. Understanding DEAF-1's role could open doors to novel treatments for these disorders, emphasizing the importance of further research into its functions and mechanisms.
