The nuclear exosome cofactors Mpp6 and Rrp47 can stimulate exoribonuclease activities of the nuclear RNA exosome and recruit the Mtr4 helicase to promote helicase dependent RNA decay.

Combined inhibition of oncogenic and epigenetic pathways results in a substantial decrease in the viability and growth of H3-K27M pediatric glioma models.

During development, lateral processes of retinal Müller glia are highly motile, and this motility persists when retinal waves and calcium transients are blocked, suggesting that Müller glial morphology is established independent of neuronal activity.

BMP2 and 7 synergize with H3.3K27M epigenetic context to establish a quiescent but invasive state in pediatric diffuse midline gliomas.

NMNAT is genetically required for glioma development and promotes glioma growth by allowing a higher tolerance to DNA damage and inhibiting DNA damage-p53-caspase-3 apoptosis signaling pathway by enhancing NAD⁺-dependent posttranslational modifications (PTMs) poly(ADP-ribosyl)ation (PARylation) and deacetylation of p53.

Findings challenge the neural noise hypothesis of dyslexia, showing no differences in excitatory/inhibitory balance between individuals with dyslexia and controls.

The analysis of injury-reactivated tectal radial glia in zebrafish reveals a stochastic cell-cycle entry and cell-state-dependent regulation of the balance between neurogenesis and gliogenesis.

The expression of the lipoprotein lipase (LPL) transporter GPIHBP1 in glioma capillaries promotes the LPL-mediated processing of triglyceride-rich lipoproteins, thereby providing lipid nutrients for glioma cells.

Inflammatory S1P signaling is dynamically regulated in chick Müller glia after retinal injury and suppresses Müller glia reprogramming into neuron-like cells.

Deposition of mutant oncohistones by alternative nucleosome assembly pathways results in dramatic local differences in histone methylation in pediatric diffuse midline gliomas.