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  • Articles  (933)
  • American Institute of Physics  (626)
  • Oxford University Press  (307)
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  • Articles  (933)
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  • 11
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    Identifying novel associations between small molecules and miRNAs based on integrated molecular networks (2015)
    Oxford University Press
    Details
    Publication Date: 2015-11-05
    Description: Motivation: miRNAs play crucial roles in human diseases and newly discovered could be targeted by small molecule (SM) drug compounds. Thus, the identification of small molecule drug compounds (SM) that target dysregulated miRNAs in cancers will provide new insight into cancer biology and accelerate drug discovery for cancer therapy. Results: In this study, we aimed to develop a novel computational method to comprehensively identify associations between SMs and miRNAs. To this end, exploiting multiple molecular interaction databases, we first established an integrated SM-miRNA association network based on 690 561 SM to SM interactions, 291 600 miRNA to miRNA associations, as well as 664 known SM to miRNA targeting pairs. Then, by performing Random Walk with Restart algorithm on the integrated network, we prioritized the miRNAs associated to each of the SMs. By validating our results utilizing an independent dataset we obtained an area under the ROC curve greater than 0.7. Furthermore, comparisons indicated our integrated approach significantly improved the identification performance of those simple modeled methods. This computational framework as well as the prioritized SM-miRNA targeting relationships will promote the further developments of targeted cancer therapies. Contact: yxli@sibs.ac.cn , lixia@hrbmu.edu.cn or jiangwei@hrbmu.edu.cn Supplementary information: Supplementary data are available at Bioinformatics online.
    Print ISSN: 1367-4803
    Electronic ISSN: 1460-2059
    Topics: Biology , Computer Science , Medicine
    Published by Oxford University Press
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  • 12
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    The 2-Extra Connectivity and 2-Extra Diagnosability of Bubble-Sort Star Graph Networks (2016)
    Oxford University Press
    Details
    Publication Date: 2016-12-10
    Description: Connectivity plays an important role in measuring the fault tolerance of interconnection networks G=(V,E) . A faulty set FV is called a g -extra faulty set if every component of G – F has more than g nodes. A g -extra cut of G is a g -extra faulty set F such that G – F is disconnected. The minimum cardinality of g -extra cuts is said to be the g -extra connectivity of G . Diagnosability is an important metric for measuring the reliability of G . A new measure for fault diagnosis of G restrains that every fault-free component has at least (g+1) fault-free nodes, which is called the g -extra diagnosability of G . As a favorable topology structure of interconnection networks, the n -dimensional bubble-sort star graph BS n has many good properties. In this paper, we prove that 2-extra connectivity of BS n is 6n–15 for n≥5 and the 2-extra connectivity of BS 4 is 8; the 2-extra diagnosability of BS n is 6n–13 under the PMC model for n≥5 and the 2-extra diagnosability of BS n is 6n–13 under the MM * model for n≥6 .
    Print ISSN: 0010-4620
    Electronic ISSN: 1460-2067
    Topics: Computer Science
    Published by Oxford University Press
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  • 13
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    Multi-hierarchical profiling: an emerging and quantitative approach to characterizing diverse biological networks (2017)
    Oxford University Press
    Details
    Publication Date: 2017-01-10
    Description: Multi-hierarchical profiling may offer valuable insights into the structural stability and functional direction of biological networks in cellular development, pathological process and disease variation. Owing to the emergence of several new techniques, such as bioinformatics for omics data, structural biology and structural bioinformatics, the pace of network hierarchical research has accelerated a lot in recent years. Here, we discuss and compare the techniques available for quantifying multilevel hierarchies, with a focus on their features, capabilities and drawbacks when used for different applications. Then, we classify these methods into three types: topological spatial-scales, multilevel hierarchical control and feature ordering. We observe that challenges and limitations do exist in functional hierarchical identification. And, we also provide useful suggestions on how to analyze the dynamic data of complex network studies.
    Print ISSN: 1467-5463
    Electronic ISSN: 1477-4054
    Topics: Biology , Computer Science
    Published by Oxford University Press
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  • 14
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    GWASdb v2: an update database for human genetic variants identified by genome-wide association studies (2016)
    Oxford University Press
    Details
    Publication Date: 2016-01-07
    Description: Genome-wide association studies (GWASs), now as a routine approach to study single-nucleotide polymorphism (SNP)-trait association, have uncovered over ten thousand significant trait/disease associated SNPs (TASs). Here, we updated GWASdb (GWASdb v2, http://jjwanglab.org/gwasdb ) which provides comprehensive data curation and knowledge integration for GWAS TASs. These updates include: (i) Up to August 2015, we collected 2479 unique publications from PubMed and other resources; (ii) We further curated moderate SNP-trait associations ( P -value 〈 1.0 x 10 –3 ) from each original publication, and generated a total of 252 530 unique TASs in all GWASdb v2 collected studies; (iii) We manually mapped 1610 GWAS traits to 501 Human Phenotype Ontology (HPO) terms, 435 Disease Ontology (DO) terms and 228 Disease Ontology Lite (DOLite) terms. For each ontology term, we also predicted the putative causal genes; (iv) We curated the detailed sub-populations and related sample size for each study; (v) Importantly, we performed extensive function annotation for each TAS by incorporating gene-based information, ENCODE ChIP-seq assays, eQTL, population haplotype, functional prediction across multiple biological domains, evolutionary signals and disease-related annotation; (vi) Additionally, we compiled a SNP-drug response association dataset for 650 pharmacogenetic studies involving 257 drugs in this update; (vii) Last, we improved the user interface of website.
    Print ISSN: 0305-1048
    Electronic ISSN: 1362-4962
    Topics: Biology
    Published by Oxford University Press
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  • 15
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    MDC1 functionally identified as an androgen receptor co-activator participates in suppression of prostate cancer (2015)
    Oxford University Press
    Details
    Publication Date: 2015-05-29
    Description: Mediator of DNA damage checkpoint protein 1 (MDC1) is essential for DNA damage response. However, the role of MDC1 in modulating gene transcription independently of DNA damage and the underlying mechanisms have not been fully defined. Androgen receptor (AR) is the central signaling pathway in prostate cancer (PCa) and its target genes are involved in both promotion and suppression of PCa. Here, we functionally identified MDC1 as a co-activator of AR. We demonstrate that MDC1 facilitates the association between AR and histone acetyltransferase GCN5, thereby increasing histone H3 acetylation level on cis-regulatory elements of AR target genes. MDC1 knockdown promotes PCa cells growth and migration. Moreover, depletion of MDC1 results in decreased expression of a subset of the endogenous androgen-induced target genes, including cell cycle negative regulator p21 and PCa metastasis inhibitor Vinculin, in AR positive PCa cell lines. Finally, the expression of MDC1 and p21 correlates negatively with aggressive phenotype of clinical PCa. These studies suggest that MDC1 as an epigenetic modifier regulates AR transcriptional activity and MDC1 may function as a tumor suppressor of PCa, and provide new insight into co-factor-AR-signaling pathway mechanism and a better understanding of the function of MDC1 on PCa.
    Print ISSN: 0305-1048
    Electronic ISSN: 1362-4962
    Topics: Biology
    Published by Oxford University Press
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  • 16
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    Dicer interacts with SIRT7 and regulates H3K18 deacetylation in response to DNA damaging agents (2016)
    Oxford University Press
    Details
    Publication Date: 2016-05-06
    Description: Dicer participates in heterochromatin formation in fission yeast and plants. However, whether it has a similar role in mammals remains controversial. Here we showed that the human Dicer protein interacts with SIRT7, an NAD + -dependent H3K18Ac (acetylated lysine 18 of histone H3) deacetylase, and holds a proportion of SIRT7 in the cytoplasm. Dicer knockdown led to an increase of chromatin-associated SIRT7 and simultaneously a decrease of cytoplasmic SIRT7, while its overexpression induced SIRT7 reduction in the chromatin-associated fraction and increment in the cytoplasm. Furthermore, DNA damaging agents promoted Dicer expression, leading to decreased level of chromatin-associated SIRT7 and increased level of H3K18Ac, which can be alleviated by Dicer knockdown. Taken together with that H3K18Ac was exclusively associated with the chromatin, our findings suggest that Dicer induction by DNA damaging treatments prevents H3K18Ac deacetylation, probably by trapping more SIRT7 in the cytoplasm.
    Keywords: Protein-protein interaction, Repair
    Print ISSN: 0305-1048
    Electronic ISSN: 1362-4962
    Topics: Biology
    Published by Oxford University Press
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  • 17
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    Coronary heart disease is associated with a mutation in mitochondrial tRNA (2013)
    Oxford University Press
    Details
    Publication Date: 2013-09-25
    Description: Coronary heart disease (CHD) is the leading cause of death worldwide. Mitochondrial genetic determinant for the development of CHD remains poorly explored. We report there the clinical, genetic, molecular and biochemical characterization of a four-generation Chinese family with maternally inherited CHD. Thirteen of 32 adult members in this family exhibited variable severity and age-at-onset of CHD. Mutational analysis of their mitochondrial genomes identified the tRNA Thr 15927G〉A mutation belonging to the Eastern Asian haplogroup B5. The anticipated destabilization of a highly conserved base-pairing (28C-42G) by the 15927G〉A mutation affects structure and function of tRNA Thr . Northern analysis revealed 80% decrease in the steady-state level of tRNA Thr in the mutant cell lines carrying the 15927G〉A mutation. The 15927G〉A mutation changed the conformation of tRNA Thr , as suggested by slower electrophoretic mobility of mutated tRNA with respect to the wild-type molecule. In addition, ~39% reduction in aminoacylated efficiency of tRNA Thr was observed in mutant cells derived from this Chinese family. An in vivo mitochondrial protein labeling analysis showed ~53% reduction in the rate of mitochondrial translation in mutant cells. The impaired mitochondrial protein synthesis leads to defects in overall respiratory capacity or malate/glutamate-promoted respiration or succinate/glycerol-3-phosphate-promoted respiration, or N,N,N',N '-tetramethyl-pphenylenediamine/ascorbate-promoted respiration in mutant cells. An increasing production of reactive oxygen species was observed in the mutant cells carrying the 15927G〉A mutation. These results provide the direct evidence that the tRNA Thr 15927G〉A mutation is associated with CHD. Our findings may provide new insights into pathophysiology and intervention targets of this disorder.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
    Published by Oxford University Press
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  • 18
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    MiR-10a* up-regulates coxsackievirus B3 biosynthesis by targeting the 3D-coding sequence (2013)
    Oxford University Press
    Details
    Publication Date: 2013-04-02
    Description: MicroRNAs (miRNAs) are small non-coding RNAs that can posttranscriptionally regulate gene expression by targeting messenger RNAs. During miRNA biogenesis, the star strand (miRNA*) is generally degraded to a low level in the cells. However, certain miRNA* express abundantly and can be recruited into the silencing complex to regulate gene expression. Most miRNAs function as suppressive regulators on gene expression. Group B coxsackieviruses (CVB) are the major pathogens of human viral myocarditis and dilated cardiomyopathy. CVB genome is a positive-sense, single-stranded RNA. Our previous study shows that miR-342-5p can suppress CVB biogenesis by targeting its 2C-coding sequence. In this study, we found that the miR-10a duplex could significantly up-regulate the biosynthesis of CVB type 3 (CVB3). Further study showed that it was the miR-10a star strand (miR-10a*) that augmented CVB3 biosynthesis. Site-directed mutagenesis showed that the miR-10a* target was located in the nt6818–nt6941 sequence of the viral 3D-coding region. MiR-10a* was detectable in the cardiac tissues of suckling Balb/c mice, suggesting that miR-10a* may impact CVB3 replication during its cardiac infection. Taken together, these data for the first time show that miRNA* can positively modulate gene expression. MiR-10a* might be involved in the CVB3 cardiac pathogenesis.
    Print ISSN: 0305-1048
    Electronic ISSN: 1362-4962
    Topics: Biology
    Published by Oxford University Press
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  • 19
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    A Formal Analytic Approach to Credible Potential Path and Mining Algorithms for Multimedia Social Networks (2015)
    Oxford University Press
    Details
    Publication Date: 2015-03-27
    Description: Multimedia social networks (MSNs) services and tools provide a convenient platform for users to share multimedia contents, such as electronic book, digital image, audio and video, with each other. However, in an open network, uncontrolled sharing and transmission mode of digital content between users create considerable problems regarding digital rights management (DRM). This paper aims to explore potential paths on the propagation of copyrighted contents. An approach to mining credible potential paths is proposed for MSNs. The formal descriptions were primarily based on rough set theory for mining potential paths. Trust was also measured to find credible potential paths. We presented related algorithms for mining two kinds of paths between any two nodes. Finally, we conducted an experiment based on three non-overlapped sharing communities multiplied by 150 nodes. In the communities found by using a representative real-world MSN YouTube dataset, we further mine the general and credible potential paths based on the simulated trust assessment values. The proposed method could effectively and accurately mine two kinds of potential paths of copyrighted digital content distribution and sharing, which can help to resolve critical DRM issues.
    Print ISSN: 0010-4620
    Electronic ISSN: 1460-2067
    Topics: Computer Science
    Published by Oxford University Press
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  • 20
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    F-box protein 7 mutations promote protein aggregation in mitochondria and inhibit mitophagy (2015)
    Oxford University Press
    Details
    Publication Date: 2015-10-23
    Description: The mutations of F-box protein 7 (FBXO7) gene (T22M, R378G and R498X) are associated with a severe form of autosomal recessive juvenile-onset Parkinson's disease (PD) (PARK 15). Here we demonstrated that wild-type (WT) FBXO7 is a stress response protein and it can play both cytoprotective and neurotoxic roles. The WT FBXO7 protein is vital to cell mitophagy and can facilitate mitophagy to protect cells, whereas mutant FBXO7 inhibits mitophagy. Upon stress, the endogenous WT FBXO7 gets up-regulated, concentrates into mitochondria and forms FBXO7 aggregates in mitochondria. However, FBXO7 mutations aggravate deleterious FBXO7 aggregation in mitochondria. The FBXO7 aggregation and toxicity can be alleviated by Proline, glutathione (GSH) and coenzyme Q10, whereas deleterious FBXO7 aggregation in mitochondria can be aggravated by prohibitin 1 (PHB1), a mitochondrial protease inhibitor. The overexpression of WT FBXO7 could lead to FBXO7 protein aggregation and dopamine neuron degeneration in transgenic Drosophila heads. The elevated FBXO7 expression and aggregation were identified in human fibroblast cells from PD patients. FBXO7 can also form aggregates in brains of PD and Alzheimer's disease. Our study provides novel pathophysiologic insights and suggests that FBXO7 may be a potential therapeutic target in FBXO7-linked neuron degeneration in PD.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
    Published by Oxford University Press
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