Publications co-authored by Proteomics Core Facility

Bluhm A, Casas-Vila N, Scheibe M and Butter F (2016). Reader interactome of epigenetic histone marks in birds. Proteomics, 16, 427-436

Cicova Z, Dejung M, Skalicky T, Eisenhuth N, Hanselmann S, Morriswood B, Figueiredo LM, Butter F# and Janzen CJ# (2016). Two flagellar BAR domain proteins in Trypanosoma brucei with stage-specific regulation. Sci Rep, 6, 35826

Dejung M, Subota I, Brucerius F, Dindar G, Freiwald A, Engstler M, Boshart M, Butter F and Janzen CJ (2016). Quantitative proteomics uncovers novel factors involved in developmental differentiation of Trypanosoma brucei. PLoS Pathog, 12, e1005439

Klassen R, Ciftci A, Funk J, Bruch A, Butter F and Schaffrath R (2016). tRNA anticodon loop modifications ensure protein homeostasis and cell morphogenesis in yeast. Nucleic Acids Res, 44, 10946-10959

Wagner SA, Oehler H, Voigt A, Dalic D, Freiwald A, Serve H and Beli P (2016). ATR inhibition rewires cellular signaling networks induced by replication stress. Proteomics, 16, 402-416

Casas-Vila N, Scheibe M, Freiwald A, Kappei D and Butter F (2015). Identification of TTAGGG-binding proteins in Neurospora crassa, a fungus with vertebrate-like telomere repeats. BMC Genomics, 16, 965

Roovers EF, Rosenkranz D, Mahdipour M, Han CT, He N, Chuva de Sousa Lopes SM, van der Westerlaken LAJ, Zischler H, Butter F, Roelen BAJ and Ketting RF (2015). Piwi proteins and piRNAs in mammalian oocytes and early embryos. Cell Rep, 10, 2069-2082

Wagner SA, Oehler H, Voigt A, Dalic D, Freiwald A, Serve H and Beli P (2016). ATR inhibition rewires cellular signaling networks induced by replication stress. Proteomics, 16, 402-416

Machyna M, Kehr S, Straube K, Kappei D, Buchholz F, Butter F, Ule J, Hertel J, Stadler PF and Neugebauer KM (2014). Global identification of coilin binding partners reveals hundreds of small non-coding RNAs that traffic through Cajal bodies. Mol Cell, 56, 389-399

Hornburg D, Drepper C, Butter F, Meissner F, Sendtner M and Mann M (2014). Deep proteomic evaluation of primary and cell line motoneuron disease models delineates major differences in neuronal characteristics. Mol Cell Proteomics, 13, 3410-3420