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Journal of Neuropathology & Experimental Neurology
Article . 2024 . Peer-reviewed
License: CC BY
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https://dx.doi.org/10.60692/n0...
Other literature type . 2024
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https://dx.doi.org/10.60692/82...
Other literature type . 2024
Data sources: Datacite
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Revealing the potential role of hsa-miR-663a in modulating the PI3K-Akt signaling pathway via miRNA microarray in spinal muscular atrophy patient fibroblast-derived iPSCs

الكشف عن الدور المحتمل لـ hsa - miR -663a في تعديل مسار إشارات PI3K - Akt عبر مصفوفة miRNA الدقيقة في iPSCs المستمدة من الضمور العضلي الشوكي للمريض
Authors: Gayatri Gandhi; Radha Kodiappan; Saifollah Abdullah; Hoon Koon Teoh; L. Tai; Soon Keng Cheong; Wendy Wai Yeng Yeo;

Revealing the potential role of hsa-miR-663a in modulating the PI3K-Akt signaling pathway via miRNA microarray in spinal muscular atrophy patient fibroblast-derived iPSCs

Abstract

Abstract Spinal muscular atrophy (SMA) is an autosomal recessive neuromuscular disorder due to deletion or mutation of survival motor neuron 1 (SMN1) gene. Although survival motor neuron 2 (SMN2) gene is still present in SMA patients, the production of full-length survival motor neuron (SMN) protein is insufficient owing to missing or mutated SMN1. No current disease-modifying therapies can cure SMA. The aim of this study was to explore microRNA (miRNA)-based therapies that may serve as a potential target for therapeutic intervention in delaying SMA progression or as treatment. The study screened for potentially dysregulated miRNAs in SMA fibroblast-derived iPSCs using miRNA microarray. Results from the miRNA microarray were validated using quantitative reverse transcription polymerase chain reaction. Bioinformatics analysis using various databases was performed to predict the potential putative gene targeted by hsa-miR-663a. The findings showed differential expression of hsa-miR-663a in SMA patients in relation to a healthy control. Bioinformatics analysis identified GNG7, IGF2, and TNN genes that were targeted by hsa-miR-663a to be involved in the PI3K-AKT pathway, which may be associated with disease progression in SMA. Thus, this study suggests the potential role of hsa-miR-663a as therapeutic target for the treatment of SMA patients in the near future.

Keywords

Male, FOS: Computer and information sciences, Motor neuron, Microarray, Signal transduction, Gene, Phosphatidylinositol 3-Kinases, Spinal cord, mRNA modification, microRNA, Life Sciences, RNA Methylation and Modification in Gene Expression, PI3K/AKT/mTOR pathway, Medicine, Original Article, Female, Gene Therapy for Spinal Muscular Atrophy, Survival Motor Neuron Protein, Microarray analysis techniques, Gene chip analysis, Signal Transduction, 570, Bioinformatics, Induced Pluripotent Stem Cells, 610, Cancer research, Muscular Atrophy, Spinal, Protein kinase B, Insulin-Like Growth Factor II, SMA*, Biochemistry, Genetics and Molecular Biology, Health Sciences, Genetics, FOS: Mathematics, Humans, Molecular Biology, Biology, Fibroblasts, Spinal muscular atrophy, MicroRNAs, Combinatorics, FOS: Biological sciences, Regulation of RNA Processing and Function, Spinal Muscular Atrophy, Gene expression, Proto-Oncogene Proteins c-akt, SMN1, Mathematics, Neuroscience

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selected citations
These citations are derived from selected sources.
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
1
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