Integrative Analysis of Transcriptional Regulation of the ATG4D, an Autophagy-Related Gene, Using JASPAR and STRING databases.

Muna A. Abdal Rhida

doi:10.31185/wjps.414

Authors

Muna A. Abdal Rhida Wasit University/Iraq

DOI:

https://doi.org/10.31185/wjps.414

Keywords:

Autophagy, ATG4D, JASPAR, STRING, TF, TFBS

Abstract

Autophagy is a catabolic cellular process that is conserved and plays an important role in sustaining cellular stability, adjusting to malnourishment, and responding to cellular stress. ATG4D is a gene that involves the formation of the autophagosome and is considered a key player in autophagy. Inclusive knowledge of how the ATG4D gene is regulated may provide insights into the gene's role in different cellular aspects. In this research, bioinformatics tools were utilized, specifically the JASPAR database, to predict the transcription factor binding sites (TFBS) and transcription factors (TFs) binding to the ATG4D promoter region. Multiple TFs were identified, and among these identified TFs, we focused on eight that were well-known for their established roles in regulating autophagy, responding to cellular stress, and promoting transcriptional regulation of ATG4D. These TFs include FOXO3, TFEB, TP53, SP1, STAT3, NF-κB, E2F1, and CREB1. To discover the functional interactions of these TFs, the STRING database was utilized to conduct protein-protein interaction analysis and functional enrichment. This analysis helped us to better comprehend the complicated regulatory network linked to autophagy and the precise role of ATG4D. Functional enrichment analysis revealed significant gene ontology terms and pathways linked with autophagy, cellular stress response, apoptosis, and transcriptional regulation. These findings indicate that the regulation of ATG4D gene expression is shaped by a complicated network of transcription factors that play significant roles in autophagy and sustaining cellular balance. Using a combination of bioinformatics tools such as JASPAR and STRING gave a thorough insight into the regulatory atmosphere of ATG4D, providing opportunities for treating diseases associated with autophagy dysregulation.

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