Competition between neurons for postsynaptic ephrin-B3 controls distribution of a limited pool of synapses and defines a novel trans-synaptic mechanism enabling neurons to set the number of synapses they receive.

Soluble amyloid-β precursor peptide has no functional effects at recombinant and native GABA_B receptors.

Neurofibromatosis type 1 gene (NF1) signaling is causally linked to the acquisition of a mesenchymal gene expression program in gliomas through the regulation of the AP-1 transcription factor FOSL1.

Globotriaosylcermide directly impacts neuronal integrity and ion channel function as potential mechanism underlying small fiber pathology in Fabry disease.

Deletion of the ATM cofactor ATMIN reduces PDGFRA expression and strongly suppresses tumorigenesis in a TP53-deficient mouse model of glioblastoma.

In neurodegeneration of Gaucher disease, glucosylceramides trigger neuroinflammation via attrition of homeostatic microglia and transition to lipid-laden damage-associated microglia concurrently with infiltration of diverse immune cells including activated NK cells and CCR2⁺ macrophages, ameliorated by substrate reduction therapy.

Chromatin-based cancer stem cell heterogeneity typifies primary glioblastoma and includes an invasive subtype associated with a lower survival.

Human blood derived macrophage polarisation can be classified by proxy of their metabolism, using advanced microscopy techniques generating single-cell parameters that are clustered and validated using machine learning classification models.

A regionally resolved single-cell RNA-sequencing analysis of GBM-associated leukocytes reveals distinct activation states of the main immune populations between tumor center, peripheral infiltration zone and blood.

PITAR interaction with TRIM28 mRNA, which encodes a p53 targeting E3 ubiquitin ligase, keeps p53 levels low for cancer cells to divide and attenuates the DNA damage response by p53.