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In JoVE (1)
- Monitoring Equilibrium veranderingen in RNA structuur door 'Peroxidative' en 'Oxidatieve' hydroxyl radicaal Footprinting
Other Publications (3)
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Articles by Sara Rouhanifard in JoVE
Monitoring Equilibrium veranderingen in RNA structuur door 'Peroxidative' en 'Oxidatieve' hydroxyl radicaal Footprinting
Ravichandra Bachu*1, Frances-Camille S. Padlan*2, Sara Rouhanifard2, Michael Brenowitz2, Jörg C. Schlatterer2
1Department of Chemistry, Hunter College, 2Department of Biochemistry, Albert Einstein College of Medicine
Dit protocol beschrijft hoe het kwantificeren van de Mg (II)-afhankelijke vorming van RNA tertiaire structuur door twee methoden van hydroxyl-radicaal voetafdruk.
Other articles by Sara Rouhanifard on PubMed
Nature. Dec, 2008 | Pubmed ID: 19043405
MicroRNAs comprise a broad class of small non-coding RNAs that control expression of complementary target messenger RNAs. Dysregulation of microRNAs by several mechanisms has been described in various disease states including cardiac disease. Whereas previous studies of cardiac disease have focused on microRNAs that are primarily expressed in cardiomyocytes, the role of microRNAs expressed in other cell types of the heart is unclear. Here we show that microRNA-21 (miR-21, also known as Mirn21) regulates the ERK-MAP kinase signalling pathway in cardiac fibroblasts, which has impacts on global cardiac structure and function. miR-21 levels are increased selectively in fibroblasts of the failing heart, augmenting ERK-MAP kinase activity through inhibition of sprouty homologue 1 (Spry1). This mechanism regulates fibroblast survival and growth factor secretion, apparently controlling the extent of interstitial fibrosis and cardiac hypertrophy. In vivo silencing of miR-21 by a specific antagomir in a mouse pressure-overload-induced disease model reduces cardiac ERK-MAP kinase activity, inhibits interstitial fibrosis and attenuates cardiac dysfunction. These findings reveal that microRNAs can contribute to myocardial disease by an effect in cardiac fibroblasts. Our results validate miR-21 as a disease target in heart failure and establish the therapeutic efficacy of microRNA therapeutic intervention in a cardiovascular disease setting.
Nature Methods. Feb, 2009 | Pubmed ID: 19137005
MicroRNAs are small regulatory RNAs with many biological functions and disease associations. We showed that in situ hybridization (ISH) using conventional formaldehyde fixation results in substantial microRNA loss from mouse tissue sections, which can be prevented by fixation with 1-ethyl-3-(3-dimethylaminopropyl) carbodiimide that irreversibly immobilizes the microRNA at its 5' phosphate. We determined optimal hybridization parameters for 130 locked nucleic acid probes by recording nucleic acid melting temperature during ISH.
The PTEN-regulating MicroRNA MiR-26a is Amplified in High-grade Glioma and Facilitates Gliomagenesis in Vivo
Genes & Development. Jun, 2009 | Pubmed ID: 19487573
Activated oncogenic signaling is central to the development of nearly all forms of cancer, including the most common class of primary brain tumor, glioma. Research over the last two decades has revealed the particular importance of the Akt pathway, and its molecular antagonist PTEN (phosphatase and tensin homolog), in the process of gliomagenesis. Recent studies have also demonstrated that microRNAs (miRNAs) may be responsible for the modulation of cancer-implicated genes in tumors. Here we report the identification miR-26a as a direct regulator of PTEN expression. We also show that miR-26a is frequently amplified at the DNA level in human glioma, most often in association with monoallelic PTEN loss. Finally, we demonstrate that miR-26a-mediated PTEN repression in a murine glioma model both enhances de novo tumor formation and precludes loss of heterozygosity and the PTEN locus. Our results document a new epigenetic mechanism for PTEN regulation in glioma and further highlight dysregulation of Akt signaling as crucial to the development of these tumors.