HECT E3s and human disease

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SCHEFFNER, Martin, Oliver STAUB, 2007. HECT E3s and human disease. In: BMC Biochemistry. 8(Suppl 1), S6. ISSN 1471-2091. eISSN 1471-2091

@article{Scheffner2007human-7704, title={HECT E3s and human disease}, year={2007}, doi={10.1186/1471-2091-8-S1-S6}, number={Suppl 1}, volume={8}, issn={1471-2091}, journal={BMC Biochemistry}, author={Scheffner, Martin and Staub, Oliver}, note={Article Number: S6} }

<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:bibo="http://purl.org/ontology/bibo/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:xsd="http://www.w3.org/2001/XMLSchema#" > <rdf:Description rdf:about="https://kops.uni-konstanz.de/rdf/resource/123456789/7704"> <dcterms:issued>2007</dcterms:issued> <dc:creator>Scheffner, Martin</dc:creator> <dc:contributor>Staub, Oliver</dc:contributor> <dc:creator>Staub, Oliver</dc:creator> <dcterms:available rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2011-03-24T17:36:30Z</dcterms:available> <dc:format>application/pdf</dc:format> <dc:language>eng</dc:language> <dcterms:bibliographicCitation>BMC Biochemistry ; 8 (2007), Suppl. 1. - S6</dcterms:bibliographicCitation> <dcterms:title>HECT E3s and human disease</dcterms:title> <bibo:uri rdf:resource="http://kops.uni-konstanz.de/handle/123456789/7704"/> <dcterms:rights rdf:resource="http://nbn-resolving.org/urn:nbn:de:bsz:352-20140905103416863-3868037-7"/> <dcterms:abstract xml:lang="eng">In a simplified view, members of the HECT E3 family have a modular structure consisting of the C-terminal HECT domain, which is catalytically involved in the attachment of ubiquitin to substrate proteins, and N-terminal extensions of variable length and sequence that mediate the substrate specificity of the respective HECT E3. Although the physiologically relevant substrates of most HECT E3s have remained elusive, it is becoming increasingly clear that HECT E3s play an important role in sporadic and hereditary human diseases including cancer, cardiovascular (Liddle's syndrome) and neurological (Angelman syndrome) disorders, and/or in disease-relevant processes including bone homeostasis, immune response and retroviral budding. Thus, molecular approaches to target the activity of distinct HECT E3s, regulators thereof, and/or of HECT E3 substrates could prove valuable in the treatment of the respective diseases.</dcterms:abstract> <dc:rights>deposit-license</dc:rights> <dc:contributor>Scheffner, Martin</dc:contributor> <dc:date rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2011-03-24T17:36:30Z</dc:date> </rdf:Description> </rdf:RDF>

Dateiabrufe seit 01.10.2014 (Informationen über die Zugriffsstatistik)

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