Call for papers for an open special issue on small/microRNAs:
Small RNAs: Revolutionizing the Genomics Landscape
The editors invite researchers to contribute original research articles as well as review articles focused on the use, development, or the application of genomics tools for investigating the role of small RNAs at the whole-genome level. The editors will be interested in review manuscripts that describe biology of noncoding RNAs as well as bioinformatics and computational biology based approaches for analyzing small RNAs datasets.
Potential topics include, but are not limited to:
- Small RNAs and microRNAs next-generation sequencing data analysis
- Identification and classification of miRNA genes and targets
- Small RNAs regulatory networksSoftware and tool development for small RNA data analysis
- Comparative evolution of small RNAs
- Small RNAs players in cancer and plant stress responses
Before submission authors should carefully read over the journal’s Author Guidelines, which are located at http://www.hindawi.com/journals/ijg/guidelines/.
Prospective authors should submit an electronic copy of their complete manuscript through the journal Manuscript Tracking System at http://mts.hindawi.com/submit/journals/ijg/rnas/ according to the following timetable:
- Manuscript Due: Friday, 2 August 2013
- First Round of Reviews: Friday, 25 October 2013
- Publication Date: Friday, 20 December 2013
For the full details please see:
http://www.hindawi.com/journals/ijg/si/431758/cfp/
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Dr. Lucrecia Alvarez is currently editing one of the Springer Book Series on Methods in Molecular Biology entitled “Structural and Functional RNA Mapping” and is looking for contributions:
“All I am asking the authors to do is to present their routinely laboratory protocols in a define format and, therefore, there is not too much work involved. I am looking for potential authors interested in writing a book chapter on experimental or in silico methods related to the study of microRNA and long non-coding RNAs. Each chapter will appear indexed in PubMed and on Web of Science.”
If you are interested, please contact her at lalvarez@tgen.org and state the title and a brief summary of the book chapter that you would like to contribute. You will receive the Instructions for Authors and a sample of a book chapter. Thanks!
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Researchers at the University of Texas Southwestern Medical Center and Baylor Institute for Immunology Research have identified a novel expression signature in patients with DiGeorge Syndrome. DiGeorge Syndrome occurs because of a chromosomal deletion in 22q11.2, resulting in the hemizygous deletion of > 60 genes and 4 microRNAs. Peripheral blood taken from 31 DiGeorge Syndrome patients and 22 normal controls was analyzed for microRNA expression signatures. Van Oers’ group identified a panel of microRNA that is deregulated in the peripheral blood of DiGeorge patients as compared to controls, and in particular, miR-185 was observed to have reduced expression (<60%) in DiGeorge patients. miR-185 is a microRNA gene located within the 22q11.2 gene locus.
The authors note that evaluating miR-185 expression levels in blood may be a faster and more reliable method to diagnose patients with DiGeorge Syndrome and can be used as a marker for 22q11.2 deletions. Several patients presenting with DiGeorge-like symptoms had normal expression levels of miR-185, and follow-up FISH analysis confirmed these patients had no deletion of 22q11.2. Considering DiGeorge patients can present with several different clinical symptoms, the use of association studies and mosaic cluster analyses has provided evidence for the first time that miR-185 expression can distinguish patients with true DiGeorge 22q11.2 deletions and patients with other genetic abnormalities presenting with similar symptoms. The study concludes by noting that microRNA profiling can be useful in helping researchers and clinicians identify important biomarkers for other abnormal chromosomal diseases presenting with heterogeneous symptoms like DiGeorge Syndrome.
M. Teresa de la Morena, Jennifer L. Eitson, Igor M. Dozmorov, Serkan Belkaya, Ashley R. Hoover, Esperanza Anguiano, M. Virginia Pascual, Nicolai S.C. van Oers, Signature MicroRNA Expression Patterns Identified in Humans with 22q11.2 Deletion/DiGeorge Syndrome, Clinical Immunology (2013), doi:10.1016/j.clim.2013.01.011
Article Link: http://www.sciencedirect.com/science/article/pii/S1521661613000223
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Researchers have identified a microRNA liver gene, miR-27b, which regulates lipid (cholesterol or fat) levels in the blood. This regulator gene controls multiple genes involved in dyslipidemia—abnormal blood cholesterol levels that can contribute to heart disease. Study details published in the February issue of Hepatology, a journal of the American Association for the Study of Liver Diseases (AASLD), describe a new in silico approach to identify the significance of microRNAs in regulating disease-related gene pathways.
The Human Genome Project (HGP) was completed in April, 2003 and the world had a map of the 3 billion DNA letters making up the human genome. One of the HGP leaders was Dr. Francis Collins, currently NIH Director and contributor to the present study. “The HGP provided the basic instruction book for human biology,” explains Dr. Collins. “Further genomic studies, such as the investigation of microRNAs, have built upon the efforts of the HGP to explain how the genome carries out its functions, and helps identify genes involved in the development of disease.”
For the present study, lead author Dr. Kasey Vickers from the NIH/NHLBI Lipoprotein Metabolism Section (presently at Vanderbilt University School of Medicine) and colleagues performed high-throughput small RNA sequencing of mouse liver and detected roughly 150 microRNAs. The team used a novel in silico approach to identify microRNA regulatory hub genes involved in lipid metabolism. In human and mouse livers miR-27b was determined to be the strongest hub with 27 predicted targets.
“We found liver miR-27b levels to be sensitive to high triglycerides (hyperlipidemia) in the blood and liver,” said Dr. Vickers. The team reported a nearly 3-fold increase in miR-27b levels in [click to continue…]
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NOTE: hsa-miR-29c* mentioned in the following paper is the retired name for what is now hsa-miR-29c-5p: http://www.mirbase.org/cgi-bin/mature.pl?mature_acc=MIMAT0004673
PHILADELPHIA and REHOVOT, Israel, Feb. 7, 2013 /PRNewswire/ — Rosetta Genomics Ltd. (NASDAQ: ROSG), a leading developer and provider of microRNA-based molecular diagnostics, today announced that data from a study demonstrating the ability of microRNA expression to serve as a biomarker to predict the progression of bladder urothelial carcinoma were published online in the British Journal of Urology International, in an article entitled, “Predicting progression of bladder urothelial carcinoma using microRNA expression.” The article can be accessed online at http://onlinelibrary.wiley.com/doi/10.1111/j.1464-410X.2012.11748.x/abstract and is expected to be published in the print edition of the British Journal of Urology International.
In the study, formalin-fixed, paraffin-embedded samples of 108 non-muscle invasive (“NMI”) bladder carcinomas, and 29 muscle invasive tumors, were collected and highly specific microRNA expression levels were measured by Rosetta Genomics’ microarray technology. Using micro-dissection, specific tumor microRNAs were chosen to be included in the study in order to avoid background contamination derived from surrounding tissue. The study found that the expression level of one microRNA, miR-29c*, was significantly under-expressed in tumors that progressed and could be used to stratify bladder cancer patients into risk groups.
The study showed that significantly higher expression of miR-29c* was detected in NMI bladder tumors that did not progress compared with lesions that did progress. The lower expression of miR-29c* in patients that later progressed was similar to the expression levels seen in patients with muscle invasive disease.
Prediction of recurrence and progression is currently based upon clinical and pathological factors such as: tumor grade, tumor stage, number of lesions, tumor size, prior recurrence rate and presence of concomitant carcinoma in-situ (“CIS”). These factors are not [click to continue…]
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