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| http://purl.uniprot.org/citations/17404255 | http://www.w3.org/2000/01/rdf-schema#comment | "Mutations in the gene encoding ataxia-telangiectasia (A-T) mutated (Atm) cause the disease A-T, characterized by immunodeficiency, the molecular basis of which is not known. Following stimulation through the TCR, Atm-deficient T cells and normal T cells in which Atm is inhibited undergo apoptosis rather than proliferation. Apoptosis is prevented by scavenging reactive oxygen species (ROS) during activation. Atm therefore plays a critical role in T cell proliferation by regulating responses to ROS generated following T cell activation. The inability of Atm-deficient T cells to control responses to ROS is therefore the molecular basis of immunodeficiency associated with A-T."xsd:string |
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| http://purl.uniprot.org/citations/17404255 | http://purl.uniprot.org/core/author | "Singh G."xsd:string |
| http://purl.uniprot.org/citations/17404255 | http://purl.uniprot.org/core/author | "Iacomini J."xsd:string |
| http://purl.uniprot.org/citations/17404255 | http://purl.uniprot.org/core/author | "Bagley J."xsd:string |
| http://purl.uniprot.org/citations/17404255 | http://purl.uniprot.org/core/date | "2007"xsd:gYear |
| http://purl.uniprot.org/citations/17404255 | http://purl.uniprot.org/core/name | "J Immunol"xsd:string |
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| http://purl.uniprot.org/citations/17404255 | http://purl.uniprot.org/core/title | "Regulation of oxidative stress responses by ataxia-telangiectasia mutated is required for T cell proliferation."xsd:string |
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