Their patterns may appear to be similar to those of weak redox inhibitors based on the slow phase of the reaction curve

potential candidate disease-related 1198097-97-0 miRNAs for guiding further biological experiments. However, until now, only several computational methods have been developed to meet the requirement. Therefore, comparing miRNAs is still a challenging and a badly needed task with the availability of various biological data resources. Many studies have shown that the functions of miRNAs can be predicted or inferred by analyzing the properties of miRNA targets. It has been reported that the targeting propensity of miRNA can be largely explained by the XY1 functional behavior of protein connectivity in the protein-protein interaction network. With the rapid advances in biotechnology, largescale PPIN is currently available and is already rich enough to evaluate the relationship between miRNAs based on their targeting propensity in PPIN. Here, based on the above notion, we proposed a novel computational method, called miRFunSim, to quantify the associations between miRNAs in the context of protein interaction network. We evaluated and validated the performance of our miRFunSim method on miRNA family, miRNA cluster data and experimentally verified miRNA-disease associations. Further comparison analysis showed that our method is more effective and reliable as compared to other existing similar methods, and offers a significant advance in measuring the associations between miRNAs. The high throughput protein-protein interaction data were obtained from Wang��s study consisting of 69,331 interactions between 11,305 proteins, which integrated BioGRID, IntAct, MINT, HPRD and by the Co-citation of text mining databases and made further filtering to improve coverage and quality of PPIN and reduce false-positives produced by different prediction algorithms in different databases. To date no mutants for Drosophila Mkk4 have been identified and its functional relevance towards JNK activation therefore remains elusive. Based on the embryonic lethality of hep mutants it is obvious that Mkk4, which is expressed during embryonic development, cannot substitute for Hep function in this process. Although it has been reported that in mammals Mkk4 and Mkk7 may synergistically activate JNK, it does not seem to be the case for Hep-mediated Bsk activ

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