Gene regulation network fitting of genes involved in the pathophysiology of fatty liver in the mice by promoter mining

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Article Type:
Research/Original Article (دارای رتبه معتبر)
Abstract:
Background and Aim
Non-Alcoholic Fatty Liver Disease (NAFLD) is the major cause of chronic liver disease in developed countries. In this study, we identified the most important transcription factors and biological mechanisms affecting the incidence of fatty liver disease using the promoter region data mining.
Materials and Methods
In this study, at first, the marker genes associated with this disease were detected and the pattern of transcription factors was examined by the Genomatix software.  In the whole of genome, genes with a similar binding pattern for transcription factors in the promoter region were identified as potentially effective genes on the fatty liver. By using the Cytoscape software (3.6.0), the network of transcription factors and target genes was mapped. Finally, the most important biological pathways associated with genes derived from fatty liver were studied using the DAVID database.
Results
The protein network fitting showed Creb1, Jun and Max transcription factors and  Sfpi1, Ddit3 and Gsk3b genes play an important role in the development of this disease. Gene ontology analysis revealed that biological pathways including apoptosis, intracellular signals, and biosynthesis of aromatic compounds and signaling pathways of circadian rhythm, non-alcoholic fatty liver, and chemokine signals contributed to the occurrence of fatty liver disease.
Conclusion
Increasing the expression of transcription factors and genes produced can be one of the most factors affecting the onset of the disease, also, biological pathways including apoptosis, intracellular signals, and biosynthesis of aromatic compounds and signaling pathways of circadian rhythm, non-alcoholic fatty liver, and chemokine signals are important in fatty liver phenomenon.
Language:
Persian
Published:
Birjand University of Medical Sciences, Volume:26 Issue: 2, 2019
Pages:
118 to 127
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