Analysis of predicted single nucleotide mutations in functional hot spots of aconitate decarboxylase enzyme in inflammatory and metabolic processes of cancer and various diseases using bioinformatics tools
محل انتشار: نشریه مراقبت سرطان، دوره: 2، شماره: 3
سال انتشار: 1400
نوع سند: مقاله ژورنالی
زبان: انگلیسی
مشاهده: 57
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شناسه ملی سند علمی:
JR_IJCA-2-3_006
تاریخ نمایه سازی: 30 بهمن 1402
چکیده مقاله:
Introduction: Inhibition of inflammatory processes in various diseases can have effective therapeutic applications. The effective function of cis-aconitate decarboxylase (CAD) enzyme, a product of IRG۱ gene, in the inflammatory processes of various diseases has been recently proven in clinical studies. In humans, the enzyme (CAD) catalyzes cis-aconitic acid to itaconic acid. Methods: In this work, with the help of bioinformatics tools, functional hotspots were identified and their position in ACOD۱ structure was investigated. Then, the effects of all mutation modes at these points were investigated and more dangerous mutations were selected. Interactions of selected mutant enzymes with other proteins were evaluated and visualized. Results: During the analysis of different mutations in functional hotspots of ACOD۱ enzyme, it was found that ۹ mutations (A۲۴۷C, A۲۴۸T, A۱۰۱C, L۱۵۶P, A۲۴۴P, N۲۴۸C, N۲۴۸F, E۱۵۰Y, E۱۵۰W) in the seven predicted hotspots had the most destructive effects in terms of function. And decreased the stability and interaction of ACOD۱ enzyme with other proteins. Conclusions: From the bioinformatic analysis of the results of the predicted SNPs of the functional hot spots of the human ACOD۱ gene, finally, among all the studied mutations, ۹ mutations were obtained that had more destructive effects on the ACOD۱ enzyme function. which researchers can use to investigate their role and effectiveness in clinical processes and as diagnostic markers in cancer diseases related to inflammation or as possible drug targets. This insilico study provides a possible path to clarify the study of molecular mechanisms involved in inflammatory processes caused by IRG۱ gene mutation and its protein product (ACOD۱).
کلیدواژه ها:
نویسندگان
سعید پیرمرادی
shahid Chamran Ahwaz University
محمد درویش خادم
shahid Chamran Ahwaz University
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