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MicroRNA Gene Interaction in Amyotrophic Lateral Sclerosis Dataset

DOI: 10.1155/2014/780726

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Abstract:

All microRNAs (miRNAs) in amyotrophic lateral sclerosis (ALS) study were collected from public databases such as miRBase, mir2Disease, and Human miRNA and Disease Database (HMDD). These miRNA datasets were used for target identification; these sets of miRNAs were expressed in brain specific parts of brain such as midbrain, cerebellum, frontal cortex, and hippocampus. Gene’s information and sequences were collected from NCBI and KEGG databases. All miRNAs were used for target prediction against 35 ALS associated genes. Three programs were used for target identification, namely, miRanda, TargetScan, and PicTar. The dataset contained information about miRNA targets sites identified by each program. Intersection studies of three programs such as miRanda versus TargetScan, miRanda versus PicTar, and TargetScan versus PicTar were carried out with all datasets. Target sites identified by each program were further explored for distribution of target sites across 35 genes in 5′ UTR, CDS, and 3′ UTR for miRNAs expressed in midbrain, cerebellum, frontal cortex, and hippocampus as predicted. Dataset was also used for calculation of multiplicity and coopretivity; this information was then used for construction of complex gene-microRNA interaction map. 1. Introduction Neurological disorders are major health problems in recent years and it is projected that the number of people affected by these disorders will double every 20 years [1]. The burden associated with these diseases is especially very high in low income and developing countries. The most assuring approaches must be used for rehabilitation and reduction of the burden of neurological disorders. This needs promising healthcare policies which will strengthen neurological care within the existing healthcare system. ALS is the most common neuromuscular disease which affects younger and older people of all races and ethnic background. It is caused due to mutations in SOD1 and other associated genes which lead to ALS-related motor neuron degeneration. There is no specific cure for ALS disease. However, FDA has approved first drug treatment for the disease riluzole (Rilutek), which is believed to reduce damage of motor neurons [2]. It increases survival in ALS patients, but it is not a very effective treatment for ALS patients. Thus there is a major challenge to search novel therapeutics for treatment of ALS; new promising technologies such as RNAi are the boon for healthcare. miRNAs are the small potent regulators which are effective noncoding RNA, which control almost 60% of human gene and several diseases.

References

[1]  WHO Library Cataloguing-in-Publication Data, Neurological Disorders: Public Health Challenges, World Health Organization, 2007.
[2]  V. B. Tripathi and A. Al-Chalabi, “Molecular insights and therapeutic targets in amyotrophic lateral sclerosis,” CNS & Neurological Disorders Drug Targets, vol. 7, no. 1, pp. 11–19, 2008.
[3]  G. M. Schratt, F. Tuebing, E. A. Nigh et al., “A brain-specific microRNA regulates dendritic spine development,” Nature, vol. 439, no. 7074, pp. 283–289, 2006.
[4]  M. Costa-Mattioli, W. S. Sossin, E. Klann, and N. Sonenberg, “Translational control of long-lasting synaptic plasticity and memory,” Neuron, vol. 61, no. 1, pp. 10–26, 2009.
[5]  A. M. Krichevsky, K. S. King, C. P. Donahue, K. Khrapko, and K. S. Kosik, “A microRNA array reveals extensive regulation of microRNAs during brain development,” RNA, vol. 9, no. 10, pp. 1274–1281, 2003.
[6]  E. A. Miska, E. Alvarez-Saavedra, M. Townsend et al., “Microarray analysis of microRNA expression in the developing mammalian brain,” Genome Biology, vol. 5, no. 9, article R68, 2004.
[7]  P. Kaur, A. Armugam, and K. Jeyaseelan, “MicroRnas in neurotoxicity,” Journal of Toxicology, vol. 2012, Article ID 870150, 15 pages, 2012.
[8]  C. Lagier-Tourenne and D. W. Cleveland, “Rethinking ALS: the FUS about TDP-43,” Cell, vol. 136, no. 6, pp. 1001–1004, 2009.
[9]  A. H. Williams, G. Valdez, V. Moresi et al., “MicroRNA-206 delays ALS progression and promotes regeneration of neuromuscular synapses in mice,” Science, vol. 326, no. 5959, pp. 1549–1554, 2009.
[10]  Z. Li, Y. Lu, X. L. Xu, and F. B. Gao, “The FTD/ALS-associated RNA-binding protein TDP-43 regulates the robustness of neuronal specification through microRNA-9a in Drosophila,” Human Molecular Genetics, vol. 22, no. 2, pp. 218–225, 2013.
[11]  O. C. Maes, H. M. Chertkow, E. Wang, and H. M. Schipper, “MicroRNA: implications for Alzheimer disease and other human CNS disorders,” Current Genomics, vol. 10, no. 3, pp. 154–168, 2009.
[12]  M. Lu, Q. Zhang, M. Deng et al., “An analysis of human microRNA and disease associations,” PLoS ONE, vol. 3, no. 10, article e3420, 2008.
[13]  Q. Jiang, Y. Wang, Y. Hao et al., “miR2Disease: a manually curated database for microRNA deregulation in human disease,” Nucleic Acids Research, vol. 37, pp. D98–D104, 2009.
[14]  S. Griffiths-Jones, H. K. Saini, S. van Dongen, and A. J. Enright, “miRBase: tools for microRNA genomics,” Nucleic Acids Research, vol. 36, no. 1, pp. D154–D158, 2008.
[15]  M. Kanehisa, M. Araki, S. Goto et al., “KEGG for linking genomes to life and the environment,” Nucleic Acids Research, vol. 36, no. 1, pp. D480–D484, 2008.
[16]  B. John, A. J. Enright, A. Aravin, T. Tuschl, C. Sander, and D. S. Marks, “Human microRNA targets,” PLoS Biology, vol. 2, no. 11, article e363, 2004.
[17]  A. J. Enright, B. John, U. Gaul, T. Tuschl, C. Sander, and D. S. Marks, “MicroRNA targets in Drosophila,” Genome Biology, vol. 5, article R1, 2003.
[18]  B. P. Lewis, C. B. Burge, and D. P. Bartel, “Conserved seed pairing, often flanked by adenosines, indicates that thousands of human genes are microRNA targets,” Cell, vol. 120, no. 1, pp. 15–20, 2005.
[19]  A. Krek, D. Grün, M. N. Poy et al., “Combinatorial microRNA target predictions,” Nature Genetics, vol. 37, no. 5, pp. 495–500, 2005.
[20]  Y. Tay, J. Zhang, A. M. Thomson, B. Lim, and I. Rigoutsos, “MicroRNAs to Nanog, Oct4 and Sox2 coding regions modulate embryonic stem cell differentiation,” Nature, vol. 455, no. 7216, pp. 1124–1128, 2008.
[21]  A. M. Duursma, M. Kedde, M. Schrier, C. Le Sage, and R. Agami, “miR-148 targets human DNMT3b protein coding region,” RNA, vol. 14, no. 5, pp. 872–877, 2008.
[22]  J. J. Forman, A. Legesse-Miller, and H. A. Coller, “A search for conserved sequences in coding regions reveals that the let-7 microRNA targets Dicer within its coding sequence,” Proceedings of the National Academy of Sciences of the United States of America, vol. 105, no. 39, pp. 14879–14884, 2008.
[23]  X. Zhou, X. Duan, J. Qian, and F. Li, “Abundant conserved microRNA target sites in the 5′-untranslated region and coding sequence,” Genetica, vol. 137, no. 2, pp. 159–164, 2009.
[24]  A. Lal, H. H. Kim, K. Abdelmohsen et al., “p16INK4a translation suppressed by miR-24,” PLoS ONE, vol. 3, no. 3, article e1864, 2008.

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