عنوان
پدید آورنده
موضوع
رده
کتابخانه
محل استقرار
TL58204
انگلیسی
İnsanda apoptozu düzenleyen uzun kodlamayan RNA'ların moleküler karakterizasyonu
[Thesis]
Sweef, Osama
Akgül, Bünyamin
Izmir Institute of Technology (Turkey)
2019
149 p.
Ph.D.
Izmir Institute of Technology (Turkey)
2019
Apoptosis is an evolutionarily form of programmed cell death for development and tissue homeostasis. Apoptosis is regulated by protein-coding genes and plays an important role in a wide range of biological processes. We aimed to identify and characterize differentially expressed lncRNAs in apoptosis. HeLa cells were used as a model system to identify the lncRNAs. The total RNAs was subjected to deep sequencing by next-generation sequencing. OmicsBOX Bioinformatics tools were used for differential expression analysis of lncRNAs that are apoptosis-induced. Gene set enrichment analysis (GSEA) was used to profile the miRNAs targeting lncRNAs. Cytoscape software was used to reconstruct lncRNA-miRNA targeting networks. RT-qPCR was used to validate miRNAs and their targets of lncRNAs and it was found that the overexpression of miR-519d-3p causes downregulation of lncRNAs RAB22A-202, PARD3-211, and AC027237.1-210. Also, the overexpression of miR-124-3p down-regulates the expression level of APEX2-202 and CD59-209. GTF2A1-AS, TNFRSF10B-AS, and CAMTA1-DT were detected in the nucleus and have no poly (A) tail and they belong to TATA-less promoter genes. TNFRSF10B-AS has a coding probability of 0.99 and alignment to High-scoring Segment Pair (HSP) clarifies one hit to Q9UBN6 protein. ChIRP clarifies that TNFRSF10B-AS binds to a protein (25 kDa). miR-519d-3p and miR-124-3p interact with lncRNA targets by miRNA-mediated lncRNA degradation pattern under apoptosis conditions. TNFRSF10B-AS has a putative regulatory function in the nucleus during apoptosis via binding specifically to the ribonucleoprotein partner.
Apoptosis
Genetics
Molecular biology
Sweef, Osama
Akgül, Bünyamin
Izmir Institute of Technology (Turkey)
مطالعه متن کتاب p
[Thesis]
276903
a
Y
