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Title

High AU content: a signature of upregulated miRNA in cardiac diseases

 

Authors

Richa Gupta, Neha Soni, Purbasa Patnaik, Ishita Sood, Rahul Singh, Kamal Rawal, Vibha Rani*

 

Affiliation

Department of Biotechnology, Jaypee Institute of Information Technology University, Noida, U.P-201307, India.

E-mail*

Vibhasandeep@rediff.com;* Corresponding author

 

Article Type

 

Hypothesis

 

Date

 

Received August 5, 2010; accepted August 26, 2010; published September 20, 2010

 

Abstract

 

MicroRNAs have been implicated for the regulation of gene expression. These miRNA are a class of single stranded non coding RNAs, formed from endogenous transcripts and measure typically about 19-25 nucleotides in length. They are important regulators of the various biological and metabolic functions taking place in humans. Many miRNAs show tissue specific expression. Human heart is a complex organ which during various diseased and developed conditions shows differential expression of miRNA. Here, we overview the recent findings on miRNA in cardiac diseases and report the presence of high AU content in differentially expressed miRNA in developed and diseased condition of heart as compared to all the miRNA present in the human. A total of 905 human miRNA sequences taken from miRBase were computationally analyzed. Trend analysis was performed to study the influence of positional frequency of the nucleotides. This study will help us in understanding the significance of AU rich elements in miRNA during the development of cardiac diseases.

 

Keywords

 

Cardiac, miRNAs, Regulation, miRBase, AU content, Bioinformatics

 

Citation

 

Gupta et al. Bioinformation 5(3): 132-135 (2010)

Edited by

 

P. Kangueane

 

ISSN

 

0973-2063

 

Publisher

 

Biomedical Informatics

 

License

 

This is an Open Access article which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. This is distributed under the terms of the Creative Commons Attribution License.