Mrna Synthesis Mirna

RNA interference, or RNAi, is a biological process in which RNA molecules reduce the gene expression of an organism. This is done typically by causing the destruction of specific mRNA molecules. RNAs are direct products of genes, these small RNAs can bind to other mRNA molecules to either increase or decrease their activity like in the example of preventing an mRNA from producing a protein. There are two types of RNA molecules that are central to RNAi, these molecules are, micro RNA (miRNA) and small interfering RNA (siRNA).

Researchers affirm that RNAi exterminated unwanted viral RNA, and RNAi-based drugs are being tested for treating certain conditions. Initially, a good part of our genes is inherited by our parents. Chromatins, a long string of DNA spooled around histones, controls the access to genes. Likewise, the histones in chromatins have “special chemical tags that act like switches to control the access of DNA” (Chapter 2, Page 31). Expressly, an embryo is able to determine which genes came from which parents, so it knows what genes should be turned on or

Expression of mir124 and 184 decreased significantly in old R2 neurons. These results suggest that aging of neurons is associated with specific changes in expression of miRNAs. Furthermore, these results are consistent with our previous finding that aging is associated with neuron specific changes in gene expression [30].

The ability to walk is something that our society seems to take for granted. A neuromuscular disease can take that ability away instantly. As with any neuromuscular disease, the body’s muscles are specifically attacked. Normally that attack is caused by a lack or mutation of a specific gene. Duchenne Muscular Dystrophy (DMD) has a direct relationship with a lack of dystrophin synthesis. It is possible that the dystrophin synthesis can be increased by manipulation of microRNA-31.

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The company ‘Invivogen’ made a transfectable and simple-to-use plasmid, called psiRNA™, that allows the production of siRNAs within the cells. To transfect means to introduce foreign material into eukaryotic cells. psiRNA is an RNA polymerase III-based plasmid that produces ‘short hairpin’ RNAs (shRNAs). shRNAs are more stable than synthetic siRNAs and since they are continuously expressed within the cells rather than having to be injected into the cytoplasm, this method permits long-lasting silencing of the BLG gene.

Structurally, miRNAs are initially transcribed from the genome as a long primary transcript that are cleaved or undergoes sequential processing by the RNAse III endonucleases Drosha and Dicer to yield the 17-23 mature nucleotide species (Kim, 2005). Mature miRNAs enters the RNA-induced silencing complex (RISC), thus a multiprotein complex that separate the mature strand from passenger strand and assists the interaction of mRNAs with miRNA that contain complementary sequences (Bader, 2012). As a result, mRNAs targeted by miRNA loads are either degraded or silenced in order not to be translated into protein. In the genome, a given miRNA can regulate several hundred transcripts whose molecules function within various cellular pathways including cell proliferation and apoptosis. To date, more than 50% of the activities of all protein-coding genes in mammals are controlled by miRNAs and greatly contributes to cell-type specific profiles of protein expression

Introduction: Mutation within cell populations are seldom.1 The mutS gene in E.coli takes part in the repair and recombination of DNA.2 When mutS was deleted from E.coli in a previous study, the mutation rate increased when compared to the wild type strain.2 Rifampicin is known for its inhibition of RNA Polymerase production.3 Without RNA Polymerase, RNA is incapable of production and thus protein synthesis ceases within the cell, resulting in cell death. We hypothesize that since mutS repairs recombinant DNA within E. coli, the deletion of the mutS gene will increase the mutation rate of E. coli.

Pancreatic cancer is one of the most deadliest cancers one can be afflicted with in the United States of America. Within one year of affliction, the survival rate is a mere twenty percent. Within five years of affliction, only six percent of patients will still be alive. Pancreatic cancer has long since been renowned for being caused by epigenetic changes in many cases. One subset of epigenetic a is DNA methylation which can suppress genes and prevent them from being transcribed. Aberrant DNA methylation increases the risk of metastatic pancreatic cancer by silencing tumor-suppressor microRNAs. Although methylation silencing can have disastrous effects, it can help by enabling scientists and doctors to recognize signs of pancreatic cancer early

MiR-21 has been found to be over expressed in 20 pancreatic carcinoma tissues and cell lines compared to normal tissue or cell lines. (15)

In the second paper, “Novel RNA Modifications in the Nervous System: Form and Function,” Lee discusses the role of several novel RNA modification in the physiological setting of the nervous system. RNA editing plays a major role in many pathologies; for example, loss of normal function in an m6a demethylase, FTO, has been connected with cancer, ADHD, and Alzheimer’s. Other RNA modifications are necessary for proper development of the central nervous system. NSUN2 is an m5C RNA modification heavily implicated in embryogenesis, especially in the brain. Mutation of the NSUN2 gene is correlated with intellectual disability, developmental delay, and facial dysmorphism. The aforementioned A-to-I RNA edit is also enriched in the brain, and is necessary for the proper function of genes such as GluA2, which without modification leads to postnatal death. GluA2 is also implicated in glutamate reception by neurons, and consequently in the mechanisms of addiction. Furthermore, A-to-I RNA editing failure been linked with several chronic diseases, including

Recent reports indicate the potential role of miRNAs as both therapeutic targets and biomarkers in IPF (5). MiRNAs are small (approximately 22 nucleotides in length) and stable non-coding molecules, which can regulate gene expression (6). They are important regulators of physiological processes, such as cellular proliferation leading to lung tissue repair. The miR200 family is functionally involved in canonical pathways of immune response and cell-cell communication. Here we propose novel studies using miR200b and miR200c in IPF compared to controls, first, to determine their function in the niche composed of ATII cells and fibroblasts, second, analyze their potential to stimulate ATII cell proliferation and transdifferentation to alveolar type I cells, third to analyze their capacity to inhibit the growth of fibroblasts; and fourth, to use them as early biomarkers of IPF development. The rationale for using 200miRNA family members as curing IPF drug is based on their dysregulated expression observed in IPF (7). Moreover, our

Deciphering MECP2-associated disorders: disrupted circuits and the hope for repair). Recently, Mellios and collaborators identified novel MECP2-regulated miRNAs during the human prenatal neurodevelopment. Utilizing human patient- and MeCP2 knockdown-derived monolayer neuronal culture and organoids models, they found an upregulation of the expression levels of miR-199 and miR-214 and their downstream targets (PAK4 and PTEN, respectively), that differentially regulate extracellular signal regulated kinase (ERK) and mitogen-activated kinase and protein kinase B (PKB/AKT) signalling pathways upstream of neurogenesis. The miR199/214 overexpression was correlated with aberrant neurogenesis and neuronal migration, whereas the inhibition of their expression rescues these effects, suggesting that the neurogenesis may be impacted in RTT via MeCP2-regulated miRNAs that acts as important effectors of neuronal development modulating molecular pathways involved in proliferation and differentiation (Mellios N et al, MeCP2-regulated miRNAs control early human neurogenesis through differential effects on ERK and AKT signaling. Molecular Psychiatry (2017) 00,

In addition to increased DNA methylation, a typical WT response also includes post-transcriptional gene regulation by miRNAs. One of the miRNAs that are upregulated in the WT embryos in response to stress is miR-21c. miR-21c is expected to target Chromodomain Helicase DNA Binding Protein 7 (CHD7). Chd7 is a protein that through chromatin remodeling, regulates the gene expression of several genes. CHARGE syndrome, an ASD syndromic subtype, is the most common result of a CHD7 gene mutation10. This hypermethylation of the CHD7 gene in addition to the increased expression of miR-21c, collaborate and lead to reduced gene expression.

Specific Aim #1. To determine the effect of miR200 family on human primary ATII cell biology and lung regeneration in IPF.