Stress granules are dispensable for mRNA stabilization during cellular stress.

During cellular stress, protein synthesis is severely reduced and bulk mRNA is recruited to stress granules (SGs). Previously, we showed that the SG-recruited IGF2 mRNA-binding protein 1 (IGF2BP1) interferes with target mRNA degradation during cellular stress. Whether this requires the formation of SGs remained elusive.

Extraction of protein profiles from primary neurons using active contour models and wavelets.

The function of complex networks in the nervous system relies on the proper formation of neuronal contacts and their remodeling. To decipher the molecular mechanisms underlying these processes, it is essential to establish unbiased automated tools allowing the correlation of neurite morphology and the subcellular distribution of molecules by quantitative means. We developed NeuronAnalyzer2D, a plugin for ImageJ, which allows the extraction of neuronal cell morphologies from two dimensional high resolution images, and in particular their correlation with protein profiles determined by indirect immunostaining of primary neurons.

IGF2BP1 promotes cell migration by regulating MK5 and PTEN signaling.

In primary neurons, the oncofetal RNA-binding protein IGF2BP1 (IGF2 mRNA-binding protein 1) controls spatially restricted β-actin (ACTB) mRNA translation and modulates growth cone guidance. In cultured tumor-derived cells, IGF2BP1 was shown to regulate the formation of lamellipodia and invadopodia. However, how and via which target mRNAs IGF2BP1 controls the motility of tumor-derived cells has remained elusive.

ZBP1 regulates mRNA stability during cellular stress.

An essential constituent of the integrated stress response (ISR) is a reversible translational suppression. This mRNA silencing occurs in distinct cytoplasmic foci called stress granules (SGs), which transiently associate with processing bodies (PBs), typically serving as mRNA decay centers. How mRNAs are protected from degradation in these structures remains elusive.

Aluminium in over-the-counter drugs: risks outweigh benefits?

In the early 1970s, aluminium toxicity was first implicated in the pathogenesis of clinical disorders in patients with chronic renal failure involving bone (renal osteomalacia) or brain tissue (dialysis encephalopathy). Before that time the toxic effects of aluminium ingestion were not considered to be a major concern because absorption seemed unlikely to occur. Meanwhile, aluminium toxicity has been investigated in countless epidemiological and clinical studies as well as in animal experiments and many papers have been published on the subject.