| URL: | http://signor.uniroma2.it |
| Full name: | SIGnaling Network Open Resource |
| Description: | SIGNOR is a database of causal relationships between biological entities. |
| Year founded: | 2016 |
| Last update: | 2022 |
| Version: | v3.0 |
| Accessibility: |
Accessible
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| Country/Region: | Italy |
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| Database category: | |
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| University/Institution: | University of Rome Tor Vergata |
| Address: | Rome, Italy |
| City: | Rome |
| Province/State: | |
| Country/Region: | Italy |
| Contact name (PI/Team): | Gianni Cesareni |
| Contact email (PI/Helpdesk): | cesareni@uniroma2.it |
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SIGNOR 3.0, the SIGnaling network open resource 3.0: 2022 update. [PMID: 36243968]
The SIGnaling Network Open Resource (SIGNOR 3.0, https://signor.uniroma2.it) is a public repository that captures causal information and represents it according to an 'activity-flow' model. SIGNOR provides freely-accessible static maps of causal interactions that can be tailored, pruned and refined to build dynamic and predictive models. Each signaling relationship is annotated with an effect (up/down-regulation) and with the mechanism (e.g. binding, phosphorylation, transcriptional activation, etc.) causing the regulation of the target entity. Since its latest release, SIGNOR has undergone a significant upgrade including: (i) a new website that offers an improved user experience and novel advanced search and graph tools; (ii) a significant content growth adding up to a total of approx. 33,000 manually-annotated causal relationships between more than 8900 biological entities; (iii) an increase in the number of manually annotated pathways, currently including pathways deregulated by SARS-CoV-2 infection or involved in neurodevelopment synaptic transmission and metabolism, among others; (iv) additional features such as new model to represent metabolic reactions and a new confidence score assigned to each interaction. |
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SIGNOR 2.0, the SIGnaling Network Open Resource 2.0: 2019 update. [PMID: 31665520]
The SIGnaling Network Open Resource 2.0 (SIGNOR 2.0) is a public repository that stores signaling information as binary causal relationships between biological entities. The captured information is represented graphically as a signed directed graph. Each signaling relationship is associated to an effect (up/down-regulation) and to the mechanism (e.g. binding, phosphorylation, transcriptional activation, etc.) causing the up/down-regulation of the target entity. Since its first release, SIGNOR has undergone a significant content increase and the number of annotated causal interactions have almost doubled. SIGNOR 2.0 now stores almost 23 000 manually-annotated causal relationships between proteins and other biologically relevant entities: chemicals, phenotypes, complexes, etc. We describe here significant changes in curation policy and a new confidence score, which is assigned to each interaction. We have also improved the compliance to the FAIR data principles by providing (i) SIGNOR stable identifiers, (ii) programmatic access through REST APIs, (iii) bioschemas and (iv) downloadable data in standard-compliant formats, such as PSI-MI CausalTAB and GMT. The data are freely accessible and downloadable at https://signor.uniroma2.it/. |
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SIGNOR: A Database of Causal Relationships Between Biological Entities-A Short Guide to Searching and Browsing. [PMID: 28654729]
SIGNOR (http://signor.uniroma2.it), the SIGnaling Network Open Resource, is a database designed to store experimentally validated causal interactions, i.e., interactions where a source entity has a regulatory effect (up-regulation, down-regulation, etc.) on a second target entity. SIGNOR acts both as a source of signaling information and a support for data analysis, modeling, and prediction. A user-friendly interface features the ability to search entries for any given protein or group of proteins and to display their interactions graphically in a network view. At the time of writing, SIGNOR stores approximately 16,000 manually curated interactions connecting more than 4,000 biological entities (proteins, chemicals, protein complexes, etc.) that play a role in signal transduction. SIGNOR also offers a collection of 37 signaling pathways. SIGNOR can be queried by three search tools: "single-entity" search, "multiple-entity" search, and "pathway" search. This manuscript describes two basic protocols detailing how to navigate and search the SIGNOR database and how to download the annotated dataset for local use. Finally, the support protocol reviews the utilities of the graphic visualizer. © 2017 by John Wiley & Sons, Inc. |
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SIGNOR: a database of causal relationships between biological entities. [PMID: 26467481]
Assembly of large biochemical networks can be achieved by confronting new cell-specific experimental data with an interaction subspace constrained by prior literature evidence. The SIGnaling Network Open Resource, SIGNOR (available on line at http://signor.uniroma2.it), was developed to support such a strategy by providing a scaffold of prior experimental evidence of causal relationships between biological entities. The core of SIGNOR is a collection of approximately 12 000 manually-annotated causal relationships between over 2800 human proteins participating in signal transduction. Other entities annotated in SIGNOR are complexes, chemicals, phenotypes and stimuli. The information captured in SIGNOR can be represented as a signed directed graph illustrating the activation/inactivation relationships between signalling entities. Each entry is associated to the post-translational modifications that cause the activation/inactivation of the target proteins. More than 4900 modified residues causing a change in protein concentration or activity have been curated and linked to the modifying enzymes (about 351 human kinases and 94 phosphatases). Additional modifications such as ubiquitinations, sumoylations, acetylations and their effect on the modified target proteins are also annotated. This wealth of structured information can support experimental approaches based on multi-parametric analysis of cell systems after physiological or pathological perturbations and to assemble large logic models. © The Author(s) 2015. Published by Oxford University Press on behalf of Nucleic Acids Research. |