Fischer, André

[["dc.bibliographiccitation.artnumber","16913"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Mandad, Sunit"],["dc.contributor.author","Rahman, Raza-Ur"],["dc.contributor.author","Centeno, Tonatiuh Pena"],["dc.contributor.author","Vidal, Ramon O."],["dc.contributor.author","Wildhagen, Hanna"],["dc.contributor.author","Rammner, Burkhard"],["dc.contributor.author","Keihani, Sarva"],["dc.contributor.author","Opazo, Felipe"],["dc.contributor.author","Urban, Inga"],["dc.contributor.author","Ischebeck, Till"],["dc.contributor.author","Kirli, Koray"],["dc.contributor.author","Benito, Eva"],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Yousefi, Roya Y."],["dc.contributor.author","Dennerlein, Sven"],["dc.contributor.author","Rehling, Peter"],["dc.contributor.author","Feußner, Ivo"],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Bonn, Stefan"],["dc.contributor.author","Rizzoli, Silvio O."],["dc.contributor.author","Fornasiero, Eugenio F."],["dc.date.accessioned","2019-07-09T11:50:21Z"],["dc.date.available","2019-07-09T11:50:21Z"],["dc.date.issued","2018"],["dc.description.abstract","The homeostasis of the proteome depends on the tight regulation of the mRNA and protein abundances, of the translation rates, and of the protein lifetimes. Results from several studies on prokaryotes or eukaryotic cell cultures have suggested that protein homeostasis is connected to, and perhaps regulated by, the protein and the codon sequences. However, this has been little investigated for mammals in vivo. Moreover, the link between the coding sequences and one critical parameter, the protein lifetime, has remained largely unexplored, both in vivo and in vitro. We tested this in the mouse brain, and found that the percentages of amino acids and codons in the sequences could predict all of the homeostasis parameters with a precision approaching experimental measurements. A key predictive element was the wobble nucleotide. G-/C-ending codons correlated with higher protein lifetimes, protein abundances, mRNA abundances and translation rates than A-/U-ending codons. Modifying the proportions of G-/C-ending codons could tune these parameters in cell cultures, in a proof-of-principle experiment. We suggest that the coding sequences are strongly linked to protein homeostasis in vivo, albeit it still remains to be determined whether this relation is causal in nature."],["dc.identifier.doi","10.1038/s41598-018-35277-8"],["dc.identifier.pmid","30443017"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15918"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59754"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/209"],["dc.identifier.url","https://sfb1190.med.uni-goettingen.de/production/literature/publications/44"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/339580/EU//MITRAC"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/614765/EU//NEUROMOLANATOMY"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","SFB 1190: Transportmaschinen und Kontaktstellen zellulärer Kompartimente"],["dc.relation","SFB 1190 | P09: Proteinsortierung in der Synapse: Prinzipien und molekulare Organisation"],["dc.relation.issn","2045-2322"],["dc.relation.workinggroup","RG A. Fischer (Epigenetics and Systems Medicine in Neurodegenerative Diseases)"],["dc.relation.workinggroup","RG Rehling (Mitochondrial Protein Biogenesis)"],["dc.relation.workinggroup","RG Rizzoli (Quantitative Synaptology in Space and Time)"],["dc.relation.workinggroup","RG Urlaub (Bioanalytische Massenspektrometrie)"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","The codon sequences predict protein lifetimes and other parameters of the protein life cycle in the mouse brain"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Molecular Neurobiology"],["dc.bibliographiccitation.lastpage","14"],["dc.contributor.author","Weise, Stefan C."],["dc.contributor.author","Arumugam, Ganeshkumar"],["dc.contributor.author","Villarreal, Alejandro"],["dc.contributor.author","Videm, Pavankumar"],["dc.contributor.author","Heidrich, Stefanie"],["dc.contributor.author","Nebel, Nils"],["dc.contributor.author","Dumit, Verónica I."],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.contributor.author","Reimann, Viktoria"],["dc.contributor.author","Craske, Madeline"],["dc.contributor.author","Schilling, Oliver"],["dc.contributor.author","Hess, Wolfgang R."],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Backofen, Rolf"],["dc.contributor.author","Vogel, Tanja"],["dc.date.accessioned","2019-07-09T11:51:06Z"],["dc.date.available","2019-07-09T11:51:06Z"],["dc.date.issued","2018"],["dc.description.abstract","Rett syndrome is a complex neurodevelopmental disorder that is mainly caused by mutations in MECP2. However, mutations in FOXG1 cause a less frequent form of atypical Rett syndrome, called FOXG1 syndrome. FOXG1 is a key transcription factor crucial for forebrain development, where it maintains the balance between progenitor proliferation and neuronal differentiation. Using genome-wide small RNA sequencing and quantitative proteomics, we identified that FOXG1 affects the biogenesis of miR200b/a/429 and interacts with the ATP-dependent RNA helicase, DDX5/p68. Both FOXG1 and DDX5 associate with the microprocessor complex, whereby DDX5 recruits FOXG1 to DROSHA. RNA-Seq analyses of Foxg1cre/+ hippocampi and N2a cells overexpressing miR200 family members identified cAMP-dependent protein kinase type II-beta regulatory subunit (PRKAR2B) as a target of miR200 in neural cells. PRKAR2B inhibits postsynaptic functions by attenuating protein kinase A (PKA) activity; thus, increased PRKAR2B levels may contribute to neuronal dysfunctions in FOXG1 syndrome. Our data suggest that FOXG1 regulates PRKAR2B expression both on transcriptional and posttranscriptional levels."],["dc.identifier.doi","10.1007/s12035-018-1444-7"],["dc.identifier.pmid","30539330"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16050"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59877"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","FOXG1 Regulates PRKAR2B Transcriptionally and Posttranscriptionally via miR200 in the Adult Hippocampus"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]