AutDB is an evolving database for the autism research community that is centered on genes implicated in autism susceptibility. The AutDB web portal seamlessly integrates different kinds of genetic data that are being generated by research studies, and in so doing encourages the generation of new hypotheses.
AutDB utilizes a systems biology approach, linking information on autism candidate genes within its original "Human Gene" module to corresponding data within diverse modules such as Animal Model, Protein Interaction (PIN), Gene Scoring, and Copy Number Variant (CNV).
Our database is envisioned to have immediate application for network biology analysis of molecular pathways involved in ASD pathogenesis.
An article describing this resource was published in the 2009 database issue of Nucleic Acids Research.
AutDB: a gene reference resource for autism research.
Who is citing AutDB?
Human Gene: thoroughly annotated list of genes that have been studied in the context of autism, with information on the genes themselves, relevant references from the literature, and the nature of the evidence. Uniquely, AutDB incorporates information on both common and rare variants.
Animal Model: information about lines of genetically modified mice that represent potential models of autism. This information includes the nature of the targeting construct, the background strain and, most importantly, a thorough summary of the phenotypic features of the mice that are most relevant to autism.
Protein Interaction (PIN): compilation of all known direct protein interactions for those gene products implicated in autism. It presents both graphical and tabular views of interactomes, highlighting connections between autism candidate genes. Each protein interaction is manually verified by consultation with the primary reference.
Copy Number Variant (CNV): a parallel resource providing genetic information about all known copy number variants linked to autism.
Gene Scoring: includes a 'score' for each autism candidate gene, based on an assessment of the strength of human genetic evidence.