Nietert, Manuel Manfred

[["dc.bibliographiccitation.artnumber","12351"],["dc.bibliographiccitation.firstpage","12351"],["dc.bibliographiccitation.issue","20"],["dc.bibliographiccitation.journal","International Journal of Molecular Sciences"],["dc.bibliographiccitation.volume","23"],["dc.contributor.affiliation","Vinhoven, Liza; 1Department of Medical Bioinformatics, University Medical Center Göttingen, Goldschmidtstraße 1, 37077 Göttingen, Germany"],["dc.contributor.affiliation","Stanke, Frauke; 2Clinic for Pediatric Pneumology, Allergology and Neonatology, Hannover Medical School, Carl-Neuberg-Strasse 1, 30625 Hannover, Germany"],["dc.contributor.affiliation","Hafkemeyer, Sylvia; 4Mukoviszidose Institut, In den Dauen 6, 53117 Bonn, Germany"],["dc.contributor.affiliation","Nietert, Manuel Manfred; 1Department of Medical Bioinformatics, University Medical Center Göttingen, Goldschmidtstraße 1, 37077 Göttingen, Germany"],["dc.contributor.author","Vinhoven, Liza"],["dc.contributor.author","Stanke, Frauke"],["dc.contributor.author","Hafkemeyer, Sylvia"],["dc.contributor.author","Nietert, Manuel Manfred"],["dc.contributor.editor","Guerrini, Gabriella"],["dc.contributor.editor","Giovannoni, Maria P."],["dc.date.accessioned","2022-12-01T08:31:41Z"],["dc.date.available","2022-12-01T08:31:41Z"],["dc.date.issued","2022"],["dc.date.updated","2022-11-11T13:12:17Z"],["dc.description.abstract","Cystic fibrosis is a genetic disease caused by mutation of the CFTR gene, which encodes a chloride and bicarbonate transporter in epithelial cells. Due to the vast range of geno- and phenotypes, it is difficult to find causative treatments; however, small-molecule therapeutics have been clinically approved in the last decade. Still, the search for novel therapeutics is ongoing, and thousands of compounds are being tested in different assays, often leaving their mechanism of action unknown. Here, we bring together a CFTR-specific compound database (CandActCFTR) and systems biology model (CFTR Lifecycle Map) to identify the targets of the most promising compounds. We use a dual inverse screening approach, where we employ target- and ligand-based methods to suggest targets of 309 active compounds in the database amongst 90 protein targets from the systems biology model. Overall, we identified 1038 potential target–compound pairings and were able to suggest targets for all 309 active compounds in the database."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft DFG"],["dc.identifier.doi","10.3390/ijms232012351"],["dc.identifier.pii","ijms232012351"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/118235"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-621"],["dc.publisher","MDPI"],["dc.relation.eissn","1422-0067"],["dc.relation.isreplacedby","hdl:2/118235"],["dc.rights","Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/)."],["dc.title","Complementary Dual Approach for In Silico Target Identification of Potential Pharmaceutical Compounds in Cystic Fibrosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]