Bioinformatics evaluation of targetom has- miR-۵۱۳a-۳p signaling pathways and related function of SOD۱ in patients with amyotrophic lateral sclerosis
محل انتشار: کنفرانس بین المللی ژنتیک و ژنومیکس انسانی
سال انتشار: 1400
نوع سند: مقاله کنفرانسی
زبان: انگلیسی
مشاهده: 85
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شناسه ملی سند علمی:
CHGGE01_245
تاریخ نمایه سازی: 13 مهر 1401
چکیده مقاله:
Backgrounds: Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder thattargets motor neurons, leading to paralysis and death within a few years of disease onset. Whileseveral genes have been linked to the inheritable or familial form of ALS, some familial cases(FALS) are linked to mutations of superoxide dismutase ۱ (SOD۱), an antioxidant enzymewhose activity is preserved in most mutant forms.Materials and Methods: For finding more bioinformatics information we used NCBI, miRbase,miRWALK۲.۰, Target scan, DAVID database and KEGG pathway.Results: Mutant SOD۱ promotes apoptosis. Considering that changes in SOD۱ mRNA levelshave been associated with sporadic ALS (SALS), a molecular understanding of the processesinvolved in the regulation of SOD۱ gene expression could not only unravel novel regulatorypathways that may govern cellular phenotypes and changes in diseases but also might revealtherapeutic targets and treatments. The latest SOD۱ gene expression study demonstrated thatSOD۱ mRNA level is elevated in specific nervous areas typically affected by ALS disease.Moreover, increased SOD۱ mRNA expression has been detected in peripheral system aslymphocytes from SALS patients compared to healthy people.Conclusion: In the present project, if according to bioinformatics predictions, the binding site ofthis microRNA is precisely SOD۱ and negative regulatory function of microRNAs, theexpression of has- miR-۵۱۳a-۳p is expected to decrease and consequently increase theexpression of the target gene (SOD۱), miR-۵۱۳a-۳p may be a tumor suppressor cancer. HasmiR-۵۱۳a-۳p expression is predicted to decrease, resulting in less binding to SOD۱ mRNA andincreasing SOD۱ gene expression, leading to ALS.
کلیدواژه ها:
نویسندگان
Payam Baziyar
Department of Molecular and Cellular Biology, Faculty of Basic Science, University of Mazandaran, Mazandaran, Iran
Bagher Seyedalipour
Department of Molecular and Cellular Biology, Faculty of Basic Science, University of Mazandaran, Mazandaran, Iran
Saman Hosseinkhani
Department of Biochemistry, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran