Magdalena Götz

This study identifies RTTN's role in ribosome biogenesis and tRNA modification in human brain organoids, showing mutations disrupt translation and cause cortical malformations.

The paper identifies ECM remodeling differences between slowly and rapidly dividing RGCs that regulate aNSC emergence and pool size through in vivo perturbation and single-cell RNA-sequencing.

The paper shows that ependymal cell cilia beating regulates neural stem cell quiescence through mechanical forces involving PKD1/2 and TRPM3.

The paper identifies age-related changes in cortical astrocytes, including impaired Wnt signaling and Jun transcription factors, using single-cell RNA-seq and multiome analysis in mice.

This study shows that fibrin-containing hydrogels influence human astrocyte states and their ability to reprogram into neurons, with 3D-Fibrin promoting neuronal conversion while 3D-FAR induces an inflammatory state that hinders reprogramming.

The paper shows that Hmgb2 enhances astrocyte-to-neuron conversion by regulating chromatin accessibility of neuronal maturation genes in response to growth factors.

The paper identifies TGIF2 as a key regulator of neural stem cell fate and neurogenic priming through transcriptomic and chromatin analysis in mouse brain development.

This study shows that TREM2 deficiency rescues synaptic integration and functional maturation of transplanted neurons in an inflammatory environment.

This study develops an in vitro model of brain injury that recapitulates key features of injury and regeneration, enabling the study of glia-to-neuron reprogramming and stem cell dynamics.

This study identifies injury-induced plastic astrocytes in mice that exhibit self-renewal and neurosphere-forming capabilities, resembling transit-amplifying progenitors in transcriptional profile.

The paper identifies a shared inflammatory glial cell signature after brain injury using spatial and single-cell transcriptomics in mice, showing common injury-regulated genes across astrocytes, microglia, and oligodendrocyte precursor cells.

This study shows that transplanted neurons in traumatic brain injury environments form excessive but vulnerable connections, while fewer connections are formed in intact or inflamed brains.