Overexpression Of Mirna

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.

In order to obtain relevant information to support this topic, databases including PubMed, Medline, UpToDate, and Google Scholar were used. Terms used in each search included and combined the following: mesenchymal stem cell, cardiac stem cells, HF, heart repair, ejection fraction, cardiac output, cardiac index, mortality.

Trying to find a cure is hard some virus can help but are they to deadly. Scientist are saying that this virus helps but the immune system does not allow it. The Lassa-VSV virus carries a gene that causes it to produce a fluorescent protein that helps researchers track which

Regarding the compromised capability of Aβ clearance in AD, we suspected that miR34a may be an indispensable player. To validate this, Aβ42 fibrils were prepared from Aβ42 monomer ex vivo and used to treat glioma A172 and U251 cells. Aβ uptake was blocked by both transient transfection of a miR34a mimic and stable miR34a overexpression (Supplementary Fig. 1B, Fig. 1A), but enhanced by anti-miR34a (Fig. 1B), indicating that miR34a suppressed Aβ phagocytosis in these cells. The fact that enhanced and decreased levels of miR34a correlated with corresponding changes in intracellular Aβ supports the notion that miR34a may slow down Aβ clearance by affecting its Aβ uptake and degradation.

Habibi, E., Masoudi-Nejad, A., Abdolmaleky, H. M., & Haggarty, S. J. (2011). Emerging roles of epigenetic mechanisms in Parkinson's disease. Functional & Integrative Genomics, 11(4), 523-537.

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

VPS35 is a gene that plays a huge role in the membrane protein-recycling retromer complex. There are three genes that are known to be associated with Parkinson’s disease, SNCA and LRRK2, which are similar to each other, and one that is different. VPS35 is the third gene associated with Parkinson’s disease that causes an increase in the degrading of DML 1 complexes. The authors of this article want to know why mutation of the VPS35 gene leads to neurodegeneration. The researchers used mice for their experiment that housed the VPS35 mutant gene.

Parkinson’s disease is the second most common neurodegenerative disease known to humans, characterized by loss of control of the central nervous system, and has been studied extensively by the scientific community (Hering et al. 2004). One gene loci identified as PARK7 or DJ-1, has been mapped to chromosome 1p36 and contains the DJ-1 protein (Bonifati et al. 2003). Mutations on the DJ-1 gene are shown to reduce the function of this gene, subsequently leading to the early onset Parkinson’s disease (Bonifati et al. 2003).

The Lassa Virus is a spherical or pleomorphic structured virus. It is enveloped by a lipid membrane as seen in (Figure 1) and has a diameter that ranges between 60-300 nanometres (nm). Imbedded in the surface of the lipid membrane are the Lassa virus matrix proteins (Z) which are responsible for the release of the virus particle into the host cell. Additionally, peplomers, a glycoprotein spike on the viral capsid, attach themselves onto the host cell and fuse protein into it. The Lassa Virus also contains an ambisense single stranded RNA (Ribonucleic Acid) genome, meaning that its genetic information consists of a single-strand of RNA (positive) which encodes the glycoprotein precursor GP-C, the nucleoprotein NP, the polymerase L, and the

P16 is a tumor suppressor protein, which in humans is encoded by the CDKN2A gene. The protein has a key job in regulating the cell cycle. It helps to decelerate cell progression from G1 phase to S phase, so it acts as a tumor suppressor that is linked to the prevention of cancers, particularly cervical cancer, esophageal cancer, and melanoma. P16 can be helpful to increase the histological diagnostic precision of cervical intraepithelial neoplasia, which is a possibly premalignant transformation and atypical growth of squamous cells on the surface of the cervix. In a multitude of tumors, the CDKN2A gene is deleted or mutated. P16 also inhibits cyclin dependent kinases like CDK6 and CDK4. These kinases help phosphorylate retinoblastoma protein

Primary research for this proposal suggests SDF-1α and VEGF play a key role in stem cell recruitment and myocardial regeneration. Increased expression of of SDF-1α through Ad-SDF-1alpha (adenoviral vector containing human SDF-1alpha gene under the control of the rous sarcoma virus (RSV) promoter) through injection into myocardial tissue promotes angiogenesis in damaged tissue. It is suggested that SDF-1 gene expression is regulated by the transcription factor hypoxia-inducible factor-1 (HIF-1) in endothelial cells, resulting in selective in vivo expression of SDF-1 in ischemic tissue in direct proportion to reduced oxygen tension (Ceradini DJ, 2004). VEGF secreted by MSC’s is thought to enhance expression of SDF-1α. Increased expression of SDF-1α in the presence of transplanted MSC’s could potentially promote differentiation of MSC’s into myocytes, leading to regeneration of myocardial tissue leading to improved heart function.

The simple classification of the endothelial cells themselves pose challenges. The endothelium is, anatomically speaking, the inner lining of the blood and lymphatic vessels.3 However, many characteristic structures such as fenestrae are not present on every endothelial cell, and other features, e.g. caveolae, are not specific to the endothelium. There are also other cells that form the inner lining of the blood vessels, and therefore molecular markers are instead being used to differentiate. Furthermore, endothelial cells arise from the mesoderm via hemangioblasts, however they may differentiate instead into hematopoietic stem cells, and the endothelial progenitors may themselves differentiate into other cell lineages. Due to these difficulties endothelial cells are instead recognized with endothelium-specific markers such as vascular endothelial (VE)-cadherin, E-selectin, and vascular endothelial growth factor receptors (VEGFR)-1 and -2.4 Even so, endothelial cells are typically considered “quiescent” at the same time as the endothelium of the corpus luteum undergoes cycles of intense physiological

Recently we have became aware of the microRNAs (miRNAs) which seem to play a role in oncogenesis. Some of these miRNAs have the potential to become very promising targets for developing cancer therapies. In this study we have taken a look at some of the promising candidates identified in breast cancer; specifically miR-155 and the miR-17-92 cluster. We have examined the potential of these targets to be effected by miRNA silencing techniques. The specific technique we have employed in this study relies on the use of antigomirs, or anti-sense miRNA molecules that were shown to be effective in inhibiting miRNA. We have observed the effects of this prospective therapy in the mouse model of breast cancer. The results indicate that for the

A single pri-miRNA often contains sequences for several different miRNAs. Pri-miRNAs fold into hairpin structures containing imperfectly base-paired stems and are processed in two steps, catalyzed by the RNase III type endonucleases Drosha and Dicer. Both Drosha and Dicer function in complexes with proteins containing dsRNA-binding domains (dsRBDs). The Drosha–DGCR8 complex processes pri-miRNAs to ∼70-nucleotide hairpins known as pre-miRNAs. In animals, pre-miRNAs are transported to the cytoplasm by exportin5, where they are cleaved by Dicer (complexed with TAR RNA binding protein (TRBP) in mammals to yield ∼20-bp miRNA duplexes. One strand is then selected to function as a mature miRNA, while the other strand is degraded. Occasionally, both arms of the pre-miRNA hairpin give rise to mature miRNA.

Sponging and subsequently controlling the levels of miRNAs are some of the functions attributed to circRNAs. Hence, we conducted a detailed analysis of the miRNA binding sites in the five TBI-responsive circRNAs that were altered after TBI compared with the sham. These five circRNAs were observed to be altered after TBI showed >30 miRNA binding sites each (Additional file 2:Supplemental Fig.1); this indicates that circRNAs altered after TBI can significantly change the miRNA function and thus the translation of a multitude of proteins that those miRNAs control.