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Agnieszka Rybak

Researcher at Charité

Publications -  5
Citations -  1382

Agnieszka Rybak is an academic researcher from Charité. The author has contributed to research in topics: Regulation of gene expression & Gene silencing. The author has an hindex of 4, co-authored 5 publications receiving 1337 citations.

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Journal ArticleDOI

A feedback loop comprising lin-28 and let-7 controls pre-let-7 maturation during neural stem-cell commitment.

TL;DR: It is demonstrated that the pluripotency factor Lin-28 binds the pre-let-7 RNA and inhibits processing by the Dicer ribonuclease in ES and EC cells, suggesting that let-7, mir-125 and lin-28 participate in an autoregulatory circuit that controls miRNA processing during NS-cell commitment.
Journal ArticleDOI

Post-transcriptional regulation of the let-7 microRNA during neural cell specification

TL;DR: Comparison of primary, precursor, and mature let‐7 RNA levels during both embryonic brain development and neural differentiation of embryonic stem cells and embryocarcinoma (EC) cells suggest post‐transcriptional regulation ofLet‐7 accumulation.
Journal ArticleDOI

The let-7 target gene mouse lin-41 is a stem cell specific E3 ubiquitin ligase for the miRNA pathway protein Ago2.

TL;DR: In this article, an additional let-7 target, mLin41 (mouse homologue of lin-41), was investigated as a potential contributor to the regulatory circuit controlling pluripotency.
Book ChapterDOI

miRNAs Need a Trim : Regulation of miRNA Activity by Trim-NHL Proteins.

TL;DR: Trim-NHL proteins are defined by RING, B-Box and Coiled-coil protein motifs (referred to collectively as the Trim domain) coupled to an NHL domain, which is a scaffold for the assembly of a translational repressor complex by the Brat proto-oncogene, a wellstudied family member in Drosophila as discussed by the authors.

Dependent on TLR7 Viral RNA Causes Neurodegeneration Extracellularly Delivered Single-Stranded

TL;DR: It is reported that ssRNA causes neurodegeneration and neuroinflammation dependent on TLR7 in the CNS and a possible mechanism through which extracellularly delivered ssRNA contributes to CNS damage is pointed to, which would determine an obligatory role for TLR 7 in this pathway.