J
Javier Martinez
Researcher at Medical University of Vienna
Publications - 55
Citations - 5116
Javier Martinez is an academic researcher from Medical University of Vienna. The author has contributed to research in topics: RNA & RNA splicing. The author has an hindex of 24, co-authored 55 publications receiving 4465 citations. Previous affiliations of Javier Martinez include Austrian Academy of Sciences & Institute of Molecular Biotechnology.
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Journal ArticleDOI
Molecular basis for target RNA recognition and cleavage by human RISC.
TL;DR: It is shown, both in vitro and in vivo, that the accessibility of the target site correlates directly with the efficiency of cleavage, demonstrating that RISC is unable to unfold structured RNA.
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Cleavage of the siRNA passenger strand during RISC assembly in human cells.
TL;DR: It is shown that the passenger strand is cleaved during the course of RISC assembly following the same rules established for the siRNA‐guided cleavage of a target RNA.
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A functional screen implicates microRNA-138-dependent regulation of the depalmitoylation enzyme APT1 in dendritic spine morphogenesis
Gabriele Siegel,Gregor Obernosterer,Roberto Fiore,Martin Oehmen,Silvia Bicker,Mette Christensen,Mette Christensen,Sharof Khudayberdiev,Philipp F Leuschner,Clara J L Busch,Christina G. Kane,Katja Hübel,Frank J. Dekker,Christian Hedberg,Balamurugan Rengarajan,Carsten Drepper,Carsten Drepper,Herbert Waldmann,Sakari Kauppinen,Sakari Kauppinen,Michael E. Greenberg,Andreas Draguhn,Marc Rehmsmeier,Marc Rehmsmeier,Javier Martinez,Gerhard Schratt +25 more
TL;DR: The results uncover a previously unknown miRNA-dependent mechanism in neurons and demonstrate a previously unrecognized complexity of mi RNA-dependent control of dendritic spine morphogenesis.
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Post-transcriptional regulation of microRNA expression
TL;DR: It is shown by Northern blots and in situ hybridization experiments that the expression of mammalian miRNAs can be regulated at the post-transcriptional level, and that differential processing of pre-miRNAs might be an alternative mechanism to control miRNA function.
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miR‐29a suppresses tristetraprolin, which is a regulator of epithelial polarity and metastasis
TL;DR: Overexpression of miR‐29a suppressed the expression of tristetraprolin (TTP), a protein involved in the degradation of messenger RNAs with AU‐rich 3′‐untranslated regions, and led to EMT and metastasis in cooperation with oncogenic Ras signalling.