scispace - formally typeset
W

Witold Filipowicz

Researcher at Friedrich Miescher Institute for Biomedical Research

Publications -  130
Citations -  32510

Witold Filipowicz is an academic researcher from Friedrich Miescher Institute for Biomedical Research. The author has contributed to research in topics: RNA & Gene silencing. The author has an hindex of 66, co-authored 129 publications receiving 30281 citations. Previous affiliations of Witold Filipowicz include University of Basel.

Papers
More filters
Journal ArticleDOI

Mechanisms of post-transcriptional regulation by microRNAs: are the answers in sight?

TL;DR: This Review summarizes the current understanding of the mechanistic aspects of microRNA-induced repression of translation and discusses some of the controversies regarding different modes of micro RNA function.
Journal ArticleDOI

The widespread regulation of microRNA biogenesis, function and decay.

TL;DR: This work has shown that the regulation of miRNA metabolism and function by a range of mechanisms involving numerous protein–protein and protein–RNA interactions has an important role in the context-specific functions of miRNAs.
Journal ArticleDOI

Regulation of mRNA Translation and Stability by microRNAs

TL;DR: In this article, the authors describe principles of miRNA-mRNA interactions and proteins that interact with miRNAs and function in miRNA mediated repression, and discuss the multiple, often contradictory, mechanisms that miRNA have been reported to use, which cause translational repression and mRNA decay.
Journal ArticleDOI

Inhibition of translational initiation by Let-7 MicroRNA in human cells.

TL;DR: It is demonstrated that endogenous let-7 microribonucleoproteins (miRNPs) or the tethering of Argonaute proteins to reporter mRNAs in human cells inhibit translation initiation, suggesting that miRNPs interfere with recognition of the cap.
Journal ArticleDOI

Relief of microRNA-Mediated Translational Repression in Human Cells Subjected to Stress

TL;DR: This work shows that cationic amino acid transporter 1 (CAT-1) mRNA and reporters bearing its 3'UTR can be relieved from the microRNA miR-122-induced inhibition in human hepatocarcinoma cells subjected to different stress conditions and proposes that proteins interacting with the 3'utR will generally act as modifiers altering the potential of miRNAs to repress gene expression.