Nucleic Acids Research Advance Access originally published online on November 10, 2008
Nucleic Acids Research 2009 37(Database issue):D832-D836; doi:10.1093/nar/gkn835
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Nucleic Acids Research, 2009, Vol. 37, Database issue D832-D836
© 2008 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
This article appears in the following Nucleic Acids Research issue: Database issue [View the issue table of contents]
Articles |
AutDB: a gene reference resource for autism research
MindSpec Inc., 9656 Blake Lane, Fairfax, VA 22031
* To whom correspondence should be addressed. Tel: +1 703 938 0161; Fax: +1 703 938 5325; Email: sharmila{at}mindspec.org
Received August 15, 2008. Revised October 8, 2008. Accepted October 14, 2008.
Recent advances in studies of Autism Spectrum Disorders (ASD) has uncovered many new candidate genes and continues to do so at an accelerated pace. To address the genetic complexity of ASD, we have developed AutDB (http://www.mindspec.org/autdb.html), a publicly available web-portal for on-going collection, manual annotation and visualization of genes linked to the disorder. We present a disease-driven database model in AutDB where all genes connected to ASD are collected and classified according to their genetic variation: candidates identified from genetic association studies, rare single gene mutations and genes linked to syndromic autism. Gene entries are richly annotated for their relevance to autism, along with an in-depth view of their molecular functions. The content of AutDB originates entirely from the published scientific literature and is organized to optimize its use by the research community. The main focus of this resource is to provide an up-to-date, annotated list of ASD candidate genes in the form of reference dataset for interrogating molecular mechanisms underlying the disorder. Our model for consolidated knowledge representation in genetically complex disorders could be replicated to study other such disorders.
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