Selected Publications
For detailed publication lists please refer to each research group
Publication by Markus Holzner et al.: The scramblases VMP1 and TMEM41B are required for primitive endoderm specification by targeting WNT signaling.
Findings of Holzner et al. identify the role of the lipid scramblases VMP1 and TMEM41B in WNT signaling during extra-embryonic endoderm development and characterize their distinct and overlapping functions.
Publication by Grégoire Cullot et al.: Genome editing with the HDR-enhancing DNA-PKcs inhibitor AZD7648 causes large-scale genomic alterations.
Cullot et al. shows that genome editing with the DNA-PKcs inhibitor AZD7648, which enhances CRISPR-Cas9 directed homology-directed repair efficiencies, causes frequent large-scale genomic alterations. This promtes caution in deploying AZD7648, and reinforces the need to investigate multiple type of potential editig outcomes.
Publication by Stefanova et al.: FGF receptor kinase inhibitors exhibit broad antiviral activity by targeting Src family kinases.
Stefanova et al. identified FGF receptor kinase inhibitors as broad-spectrum antiviral agents, which inhibit the early phase of the viral life cycle. Unexpectedly, their antiviral activity was largely independent of FGF receptor kinase inhibition. Rather, blockade of Src family kinases, in particular Lyn, is mainly responsible for their antiviral effect. These results suggest the poorly studied Lyn kinase as a promising target for the treatment of viral infections.
Publication by Kevin Halter & Jingyi Chen et al.: Cdk8 and Hira mutations trigger X chromosome elimination in naive female hybrid mouse embryonic stem cells.
Here we report that Hira and Cdk8 mutations induce rapid loss of one X chromosome in a Mus musculus castaneus hybrid female ESC line that originally maintains two X chromosomes. Our analysis shows that X chromosome loss is not explained by selection of XO cells, but likely driven by a process of chromosome elimination.
Publication by Luca Ferrarese & Michael Koch et al.: Inflammatory mediators suppress FGFR2 expression in human keratinocytes to promote inflammation.
Ferrarese/Koch show that loss of FGFR2 in human keratinocytes promotes the expression of pro-inflammatory genes and that expression of FGFR2 itself is downregulated in keratinocytes exposed to pro-inflammatory stimuli, similarly to lesional skin of atopic dermatitis patients.