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. 2006 Jan 1;34(Database issue):D546-51.
doi: 10.1093/nar/gkj107.

TRANSPATH: an information resource for storing and visualizing signaling pathways and their pathological aberrations

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TRANSPATH: an information resource for storing and visualizing signaling pathways and their pathological aberrations

Mathias Krull et al. Nucleic Acids Res. .

Abstract

TRANSPATH is a database about signal transduction events. It provides information about signaling molecules, their reactions and the pathways these reactions constitute. The representation of signaling molecules is organized in a number of orthogonal hierarchies reflecting the classification of the molecules, their species-specific or generic features, and their post-translational modifications. Reactions are similarly hierarchically organized in a three-layer architecture, differentiating between reactions that are evidenced by individual publications, generalizations of these reactions to construct species-independent 'reference pathways' and the 'semantic projections' of these pathways. A number of search and browse options allow easy access to the database contents, which can be visualized with the tool PathwayBuildertrade mark. The module PathoSign adds data about pathologically relevant mutations in signaling components, including their genotypes and phenotypes. TRANSPATH and PathoSign can be used as encyclopaedia, in the educational process, for vizualization and modeling of signal transduction networks and for the analysis of gene expression data. TRANSPATH Public 6.0 is freely accessible for users from non-profit organizations under http://www.gene-regulation.com/pub/databases.html.

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Figures

Figure 1
Figure 1
Hierarchical relations between the different molecule types and their assignment to the three-layer reaction hierarchy. Lines indicate links between items. Modified forms are represented with the ending _mod, e.g. basic_mod, orthocomplex_mod. This can be applied to any type. Relations between the gene and molecule table are shown with dashed lines.
Figure 2
Figure 2
PathoSign mutated molecule view. Depicted is one of 14 mutations of the ribosomal S6 kinase 2 gene (RSK2) which are presently annotated. The Coffin–Lowry syndrome is caused by mutations in the RSK2 gene. Linked to the mutated molecule entry is the respective genotype (see ‘Internal Links’ in figure), wherefrom the phenotype entry referring to the Coffin–Lowry syndrome (PathoSign entry no. PTS00210) can be accessed.

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