Anneke Brümmer
University of Lausanne
19 Papers
111 Citations
Anneke Brümmer is an academic researcher from University of Lausanne. The author has contributed to research in topics: RNA-binding protein & RNA. The author has an hindex of 9, co-authored 18 publications. Previous affiliations of Anneke Brümmer include Swiss Institute of Bioinformatics & University of California, Los Angeles.
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Papers
MicroRNA binding sites in the coding region of mRNAs: extending the repertoire of post-transcriptional gene regulation.
Anneke Brümmer,Jean Hausser +1 more
TL;DR: It is proposed that these domain‐dependent effects of translation inhibition through CDS targeting serve to diversify the functional repertoire of post‐transcriptional gene expression control and generalize to RNA‐binding proteins beyond miRNAs and Argonaute proteins.
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miR-CLIP capture of a miRNA targetome uncovers a lincRNA H19-miR-106a interaction.
Jochen Imig,Andreas Brunschweiger,Anneke Brümmer,Boris Guennewig,Nitish Mittal,Shivendra Kishore,Panagiota Tsikrika,André P. Gerber,Mihaela Zavolan,Jonathan Hall +9 more
TL;DR: It is shown that miR-17-5p family members bind H19 in HeLa cells and myoblasts, suggesting that H19 acts as a 'sponge' for these miRNAs during myoblast differentiation.
186
Regulation of RNA editing by RNA-binding proteins in human cells
Giovanni Quinones-Valdez,Stephen Tran,Hyun-Ik Jun,Jae Hoon Bahn,Ei-Wen Yang,Lijun Zhan,Anneke Brümmer,Xintao Wei,Eric L. Van Nostrand,Gabriel A. Pratt,Gene W. Yeo,Brenton R. Graveley,Xinshu Xiao +12 more
- 14 Jan 2019
TL;DR: This work identifies several RNA-binding proteins that regulate ADAR1 expression, interaction, or binding with Alu elements in a cell type-specific manner, and highlights that editing regulation by Ro60 is consistent with the global up-regulation of RNA editing in systemic lupus erythematosus.
131
Mathematical Modelling of DNA Replication Reveals a Trade-off between Coherence of Origin Activation and Robustness against Rereplication
TL;DR: The model rationalizes how experimentally observed inefficient replication from fewer origins is caused by premature activation of S-Cdk, while premature activity of the S- Cdk targets Sld2 and Sld3 results in DNA rereplication, and demonstrates how kinetic deregulation of the molecular network governing DNA replication may result in genomic instability.
Timing control in regulatory networks by multisite protein modifications
TL;DR: It is suggested that multisite protein modifications provide a molecular mechanism to robustly time cellular events in the cell cycle, the circadian clock and signal transduction.
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