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Sheath blight, caused by Rhizoctonia solani AG1-IA, is one of the most destructive disease. Conventional methods of disease control using fungicides may develop new problems. Therefore, understanding molecular mechanisms of plant–pathogen interaction is necessary to adopt effective approaches for managing the disease. Here for the first time, by using bioinformatics tools and RT-PCR analysis and sequencing confirmed the presence of a Magnaporthe oryzae Avr-pita gene orthologous sequence designated as Rhiz-pita1 gene in three different geographic isolates of R. solani AG1- IA( A2,R1 and T2) genome. SignalP program predicted a secretion signal upstream of Rhiz-pita1 gene. Nucleotide sequences of 5' region of Rhiz-pita1 gene from geographical isolates showed 99% identity in exons and 100% in introns which are characteristics of fast evolving effector proteins. Also, 98% homology between Rhiz-pita and M.oryza-pita1gene suggests that Rhiz-pita encodes an effector protein. Howevere, more researchs are necessary to confirm of this suggestion. Keywords: Rhizoctonia solani, signal peptide Rice blast , Effector

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Neurotrophins are a family of secretive growth factors that do their functions via binding to their specific receptors (Trks) or their common receptor (p75ntr). p75ntr has important roles in survival, differentiation and proliferation of several types of cells. MicroRNAs are non-coding small RNAs that regulate post-transcriptional mRNA expression. Recently, a MiRNA named hsa-miR-6165 has been discovered in forth intron of p75ntr. Bioinformatics analysis has revealed that this MiRNA has important roles on regulation of several cellular signaling pathways and signaling pathway involve in differentiation. Therefore, in the present study, the expression of hsa-miR-6165 in neuronal differentiation of NT2 human embryonic carcinoma stem cell line and non-nervous and nervous human cell lines was analyzed. Our results indicated that hsa-miR-6165 not only has been expressed in differentiation process of NT2 cells and neural cell lines but although significantly expressed in several human non-neural cell lines such as hFSF and Hela. In addition, the expression of this miRNA, unlike its host gene, upregulated at the end of the differentiation. These results indicate the probable presence of independent promoter for this MiRNA and revealed that hsa-mir-6165 maybe has roles in cellular differentiation which needs more investigation.

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MiRNAs are known as regulatory genes in eukaryotic genomes, regulating their target genes expression. Here, we have investigated five pathogen responsive miRNAs; tae-miR156, tae-miR159, tae-miR167, tae-miR171 and tae-miR393 expression pattern in wheat Taichung 29 cultivar between day 10 to 20th of the seedling life. Since plant seedlings are mostly used for plant-pathogene interaction analysis, this research was committed to analyze the expression pattern of these miRNAs independent of pathogenesis and in 10 to 20 days old seedlings. Plants were grown in soil in greenhouse condition, and 10, 11, 13, 17 and 20 days old seedlings were harvested for RNA extraction and cDNA synthesis. QRT-PCR analysis of candidate miRNAs expression indicated that, tae-miR156 and tae-miR159 expression level has been sharply increased between day 13th to 17th and then after, decreased to the minimum level before day 20th. On the other hand, tae-miR167, tae-miR171 and tae-miR393 expression level has been gradually increased since day 13th of the growth. These data suggest that day 13th to 17th of the wheat seedling life, is crucial period of life in terms of drastic physiological changes which are affected by miRNAs expression. Since majority of the target genes of these candidate miRNAs are not known yet, their expression alterations is only suggested to be consistent with the expression of some known target genes, belong to the signaling pathway like auxin signaling. Considering sequence conservation pattern of miRNA precursors, here we suggested functional miR*s for tae-miR156, tae-miR159, and tae-miR393.

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Breast cancer is the leading cause of cancer-related mortality among women worldwide. In Iran, breast cancer ranks first among cancers diagnosed in women comprising 24.4% of all malignancies. Currently, the large number of etiological factors and the complexity of breast cancer present challenge for prevention and treatment. Breast cancer tumorigenesis can be described as a multi-step process in which a normal cell undergoes malignant transformation to a fully developed tumor through accumulations of genetic and epigenetic changes, on the other hand, Several studies indicated the signaling pathways role in Breast cancer. EGFR gene has been shown to be overexpressed in breast cancer .Dimerization of EGFR/HER2 induces breast cancer progression via activation of PI3K/AKT signaling cascade
MicroRNAs are endogenous, small non-coding RNAs that regulate gene expression at the transcriptional and posttranscriptional level. MicroRNAs pair with partially complementary sites in the 3′untranslated regions (UTRs) of target mRNAs, leading to translational repression and/or mRNA degradation. They play important roles in several cellular processes, such as proliferation, differentiation, apoptosis, and development, by simultaneously controlling the expression level of hundreds of genes. Here we demonstrated the tumor suppression effect of miR-1226-3p in Breast cancer by targeting EGFR oncogene.
 

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Resistance to chemotherapy drugs always has been an obstacle in the definitive treatment of cancers. Therefore, the discovery of molecular events leading to drug resistance improves therapeutic methods. Non-coding RNAs (ncRNAs) are a group of molecules that regulate intracellular events, including carcinogenesis and drug resistance pathways. For example, the competitive network of endogenous ncRNAs (ceRNA) regulates the mRNA expression of target genes by binding to miRNAs and limiting their regulatory effect. So far, limited studies have been reported on the role of ceRNA in drug resistance in ovarian cancer. In this study, large-scale RNAseq sequencing data obtained from cisplatin-resistant and sensitive cells were used to search for ceRNAs that are possible regulators of drug resistance in ovarian cancer. For this purpose, the A2780 sensitive and resistant cisplatin ovarian cancer cell line was selected, and the SRA data prepared by RNAseq method was screened. During this process, lncRNAs, microRNAs and mRNAs with expression changes were separated and classified. In the bioinformatic analysis of resistant and sensitive cells, 16 mRNAs, 10 lncRNAs, and 149 miRNAs were overexpressed, and 622 mRNAs, 263 lncRNAs, and 177 miRNAs were underexpressed. These genes were involved in 57 cellular pathways, and by mapping the regulatory ceRNA network, ZNRF3-AS1-miR-33-DUSP1 and ZNRF3-AS1-miR33-HSPA2 axes were identified as potential ceRNA networks involved in cisplatin-resistant ovarian cancer.
 

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Objective: Different signaling pathways have been identified that are involved in the cellular response to opiates. The mitogen-activated protein kinase pathway is one of the most important signaling pathways underlying the neuronal response to opiates. MicroRNAs (miRNAs) are considered to be post-transcriptional regulators of gene expression with paramount significance, which plays key roles in modulating cellular processes such as neuronal plasticity and synaptic consolidation. The purpose of this study is to identify miRNAs that are differentially expressed in response to chronic morphine treatment, and predict those genes that have a possible role in this process. Because the MAPK pathway in involved in morphine dependence and participates in hypersensitivity to pain, determining miRNAs that modulate this pathway could be insightful in morphine dependence treatment and pain control. Methods: In this study, the BE(2)-C neuroblastoma cell line was chronically treated with morphine sulphate and the changes in expression of 750 miRNAs were analyzed by real time PCR. Results: Two up- and down- regulated groups of  miRNAs were determined to be differentially expressed in response to morphine: i) has-mir-193a-3p, -212, -181c, -362-3p, -639, -646  and ii) has-mir-412, -937, -558, -552, -943, -628-5p, -593, -555, -636, -643, 566, -571, -642, -653, -611, -31, let7-g. Conclusion: The analysis of differentially expressed miRNAs showed that the MAPK signaling pathway could be regarded as a signaling pathway with utmost significance in chronic morphine response. Due to the role played by MAPK pathway in cellular response to morphine exposure, we can propose that protein phosphorylation has a presumable part in this response.

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Objective: Cardiac cell differentiation with the help of miRNAs has recently opened a promising window for the restoration of myocardial infarction. Independent miR-1-2/133a-1 and miR-206/133b clusters are known to be expressed in cardiac and skeletal muscles, respectively. miR-133b differs from miR-133a by only one nucleotide. The sequence similarity of these two miRNAs suggests that they target the same pathways and similar mRNA targets. The present study seeks to determine if miR-133b is expressed during the cardiac cell differentiation and if its expression is in reverse correlation with the SRF and CCND2 (as potential target genes) expression patterns. Methods: Human cardiac progenitor cells were prepared from Royan Stem Cell Bank (RSCB) and differentiated into cardiomyocytes. To initiate differentiation, cells were treated with 5-azacytidine as a demethylation factor. Then, ascorbic acid and TGFB1 were added every other day and twice per week, respectively. Differentiation into cardiomyocytes was confirmed by immunocytochemistry (ICC), flow cytometry and real-time PCR for some of the cardiac marker genes. The expression profiles of hsa-miR-133b and two of its potential target genes were also analyzed during the cardiac differentiation. Results: Three weeks after the first differentiation induction, expression level of hsa-miR-133b was approximately five times higher than early stage expression (phsa-miR-133b expression. Conclusion: It is known that SRF is critically involved in the cell cycle. Considering increased miR-133b and decreased SRF expression levels during the late stages of heart cell differentiation, here we speculate that elevated expression of miR-133b blocks SRF expression and decreases cardiomyocytes proliferation in order to induce differentiation with direct targeting of SRF. Taken together, our data suggest that miR-133b along with miR-133a may be involved in cardiomyocytes differentiation.

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Although more than 98% of the human genome is transcribed, most of these transcripts are not translated into proteins. Rather, they are considered as non-coding RNAs. MicroRNAs (miRNAs) are very short non-coding RNAs approximately 22 nucleotides in length which regulate many key processes of cells such as growth, proliferation, differentiation, cell cycle, apoptosis (programmed cell death) and metabolism. On the other hand, it is known that these small regulatory molecules are involved in many human diseases such as different cancers and cardiovascular disorders. Therefore, discovery and functional characterization of novel miRNAs is a prominent achievement. Low abundance and spatiotemporal expression of these mediator molecules make their discovery difficult by conventional methods. Therefore, bioinformatics software have been designed for the prediction of stem-loop structures capable of producing miRNA precursors in the human genome. On the other hand, there are several bioinformatics tools for prediction of miRNA target genes. Prediction of miRNA target genes helps to characterize the function of a miRNA. In this paper, we have reviewed some of the common efficient bioinformatics tools and experimental approaches used for prediction and identification of the miRNA genes and their target genes. 

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Objective: A pure nucleotide pool is essential for correct DNA replication in addition to the prevention of mutagenesis and abnormalities in a living cell. Inosine triphosphatase (ITPase) is a critical enzyme for the removal of deaminated rough purine nucleotides such as inosine from the nucleotide pool. It has been shown that abnormal function and expression of the ITPA gene is followed by an increased substitution mutation rate in the genome. This study compares the ITPA gene expression level between human adenocarcinoma tumors and their normal marginal tissues. Method: We examined ITPA gene expression in 24 pairs of gastric adenocarcinoma tumors and their normal adjacent tissues by quantitative real-time PCR. Result: There was reduced ITPA gene expression in tumor tissues compared with the adjacent normal tissues. The decline in ITPA gene expression was more significant in the higher grade samples. Conclusion: ITPA is involved in omitting deaminated purines from the nucleotide pool. Therefore its abnormal function increases the frequency of mutations and causes higher genomic instability. Our data suggest that lower expression of ITPA can be considered a risk factor for the development and progression of gastric cancer.