Background. HNF-1a is a transcription factor that regulates glucose metabolism by expression in various tissues. Aim. To dock potential ligands of HNF-1a using docking software in silico. Methods. We performed in silico studies using HNF-1a protein 2GYP·pdb and the following softwares: ISIS/Draw 2.5SP4, ARGUSLAB 4.0.1, and HEX5.1. Observations. The docking distances (in angstrom units: 1 angstrom unit (？)？=？0.1 nanometer or ？metres) with ligands in decreasing order are as follows: resveratrol (3.8？？), aspirin (4.5？？), stearic acid (4.9？？), retinol (6.0？？), nitrazepam (6.8？？), ibuprofen (7.9？？), azulfidine (9.0？？), simvastatin (9.0？？), elaidic acid (10.1？？), and oleic acid (11.6？？). Conclusion. HNF-1a domain interacted most closely with resveratrol and aspirin 1. Introduction Hepatic nuclear factor 1 alpha (HNF-1a) is a liver enriched transcription factor that was first discovered in studies aimed at identifying proteins that were responsible for tissue-specific regulation of gene expression in the human liver [1]. These transcription factors were also found in tissues other than liver, including pancreatic islets and kidneys, suggesting they could have a more widespread role in physiological processes [2]. Together, the HNF family is part of a network of transcription factors that together control gene expression during embryogenic development and during adulthood [1]. Genes regulated by HNF-1a also encode products involved in the synthesis of seroproteins, carbohydrates and in detoxification [2]. HNF encoding genes arose by duplication of an ancestral gene at the onset of vertebrate evolution, an evolutionary mechanism for the generation of novel functions [3]. Mutations of HNF transcription family are well known to cause the autosomal dominant maturity onset diabetes of young (MODY), a clinically heterogeneous form of early onset of diabetes resulting from a primary defect in pancreatic beta cell function [4]. Some consider diabetes to be “a disorder of abnormal transcription factors” [4]. However it is now established that MODY results from a dysfunction of transcription factors [5] that regulate beta cell function by controlling downstream targets [6]. Protein-ligand interactions are increasingly employed to derive three dimensional structures of protein complexes. Computational techniques have become important to understand the molecular mechanisms of biological systems, as well as in obtaining leads for therapeutic agent identification. Considering the wide ranging effects of transcription factors in beta cell physiology, and the diverse
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