Research Topics
Genomes and GenesSpecies | Niels H GehringSummaryAffiliation: University of Heidelberg Country: Germany Publications
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Detail Information
Publications
The hierarchy of exon-junction complex assembly by the spliceosome explains key features of mammalian nonsense-mediated mRNA decayNiels H Gehring
Molecular Medicine Partnership Unit, University of Heidelberg and European Molecular Biology Laboratory, Heidelberg, Germany
PLoS Biol 7:e1000120. 2009..Based on this systematic analysis of EJC assembly by the spliceosome, we propose a model of how a functional EJC is assembled in a strictly sequential and hierarchical fashion, including nuclear splicing-dependent and cytoplasmic steps...
Disassembly of exon junction complexes by PYMNiels H Gehring
University of Heidelberg and European Molecular Biology Laboratory, Germany
Cell 137:536-48. 2009..In cells depleted of PYM, EJCs accumulate on spliced mRNAs and EJC protein recycling is impaired. Hence, PYM is an EJC disassembly factor that acts both in vitro and in living cells, and that antagonizes important EJC functions...
A chemiluminescence-based reporter system to monitor nonsense-mediated mRNA decayStephanie Boelz
Molecular Medicine Partnership Unit, University of Heidelberg and European Molecular Biology Laboratory, Im Neuenheimer Feld 156, 69120 Heidelberg, Germany
Biochem Biophys Res Commun 349:186-91. 2006..Wortmannin treatment enhanced NMD reporter expression in our system in a dose-dependent way, illustrating its utility for small molecule screening...
Interactions between UPF1, eRFs, PABP and the exon junction complex suggest an integrated model for mammalian NMD pathwaysPavel V Ivanov
Department of Pediatric Oncology, Hematology and Immunology, University of Heidelberg, Heidelberg, Germany
EMBO J 27:736-47. 2008..The EJC, with UPF2 or UPF3b as a cofactor, interferes with physiological termination through UPF1. This model integrates previously competing models of NMD and suggests a mechanistic basis for alternative NMD pathways...
Mechanism of escape from nonsense-mediated mRNA decay of human beta-globin transcripts with nonsense mutations in the first exonGabriele Neu-Yilik
Department of Pediatric Oncology, Hematology and Immunology, University of Heidelberg, Heidelberg, Germany
RNA 17:843-54. 2011..Furthermore, our data uncover a reason why the position of a nonsense mutation alone does not suffice to predict the fate of the affected mRNA and its effect on protein expression...
Exon-junction complex components specify distinct routes of nonsense-mediated mRNA decay with differential cofactor requirementsNiels H Gehring
Molecular Medicine Partnership Unit, University of Heidelberg and European Molecular Biology Laboratory, Heidelberg 69120, Germany
Mol Cell 20:65-75. 2005..These results are integrated into a nonlinear model for mammalian NMD involving alternative routes of entry that converge at a common requirement of UPF1...
Internal ribosome entry sequence-mediated translation initiation triggers nonsense-mediated decayJill A Holbrook
European Molecular Biology Laboratory, University Hospital Heidelberg, Molecular Medicine Partnership Unit, University of Heidelberg, Im Neuenheimer Feld 150, Heidelberg 69120, Germany
EMBO Rep 7:722-6. 2006..These data generalize the previous model and suggest that translation per se, irrespective of how it is initiated, can mediate NMD...
3' end processing of the prothrombin mRNA in thrombophiliaSven Danckwardt
Department of Pediatric Oncology, Hematology and Immunology, University of Heidelberg, Heidelberg, Germany
Acta Haematol 115:192-7. 2006....
Tethering assays to investigate nonsense-mediated mRNA decay activating proteinsNiels H Gehring
Department of Pediatric Oncology, Hematology and Immunology, University of Heidelberg, Heidelberg, Germany
Methods Enzymol 448:467-82. 2008..In this chapter we explicate the cloning of appropriate reporter plasmids and the setup of a tethering experiment with the necessary control experiments. Advantages of the different systems and tags are discussed...
The prothrombin 3'end formation signal reveals a unique architecture that is sensitive to thrombophilic gain-of-function mutationsSven Danckwardt
Molecular Medicine Partnership Unit, Im Neuenheimer Feld 153, 69120 Heidelberg, Germany
Blood 104:428-35. 2004..This balance appears to be highly susceptible to being disturbed by clinically relevant gain-of-function mutations...
