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Network theory to u...
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Benson, Mikael,1954Gothenburg University,Göteborgs universitet,Institutionen för kliniska vetenskaper,Institute of Clinical Sciences,Department of Pediatrics, Queen Silvia Children's Hospital, Gothenburg, Sweden
(author)
Network theory to understand microarray studies of complex diseases.
- Article/chapterEnglish2006
Publisher, publication year, extent ...
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Bentham Science Publishers,2006
Numbers
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LIBRIS-ID:oai:gup.ub.gu.se/120009
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https://gup.ub.gu.se/publication/120009URI
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https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-99937URI
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https://doi.org/10.2174/156652406778195044DOI
Supplementary language notes
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Classification
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Subject category:ref swepub-contenttype
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Subject category:art swepub-publicationtype
Notes
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Complex diseases, such as allergy, diabetes and obesity depend on altered interactions between multiple genes, rather than changes in a single causal gene. DNA microarray studies of a complex disease often implicate hundreds of genes in the pathogenesis. This indicates that many different mechanisms and pathways are involved. How can we understand such complexity? How can hypotheses be formulated and tested? One approach is to organize the data in network models and to analyze these in a top-down manner. Globally, networks in nature are often characterized by a small number of highly connected nodes, while the majority of nodes have few connections. The highly connected nodes serve as hubs that affect many other nodes. Such hubs have key roles in the network. In yeast cells, for example, deletion of highly connected proteins is associated with increased lethality, compared to deletion of less connected proteins. This suggests the biological relevance of networks. Moving down in the network structure, there may be sub-networks or modules with specific functions. These modules may be further dissected to analyze individual nodes. In the context of DNA microarray studies of complex diseases, gene-interaction networks may contain modules of co-regulated or interacting genes that have distinct biological functions. Such modules may be linked to specific gene polymorphisms, transcription factors, cellular functions and disease mechanisms. Genes that are reliably active only in the context of their modules can be considered markers for the activity of the modules and may thus be promising candidates for biomarkers or therapeutic targets. This review aims to give an introduction to network theory and how it can be applied to microarray studies of complex diseases.
Subject headings and genre
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Humans
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Models
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Biological
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Oligonucleotide Array Sequence Analysis
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Research Design
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Systems Biology
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DNA microarray; Gene A; Repressor Molecule Z; co-expression; hub proteins
Added entries (persons, corporate bodies, meetings, titles ...)
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Breitling, RainerGroningen Bioinformatics Centre, University of Groningen, The Netherlands
(author)
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Göteborgs universitetInstitutionen för kliniska vetenskaper
(creator_code:org_t)
Related titles
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In:Current molecular medicine: Bentham Science Publishers6:6, s. 695-7011566-52401875-5666
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