Heterozygous Nf1 knockout mice exhibit distinct dopaminergic phenotypes in vivo, as revealed by the genetically encoded dopamine sensor dLight1, patch clamp electrophysiology, optogenetics, and novel viral tools for morphological analysis.

Nf1 is required during early, but not late, cerebellar development to facilitate neuronal lamination, providing a potential therapeutic prevention strategy for NF1-associated developmental abnormalities.

In a mouse model of neurofibromatosis type 1, the purinergic receptor P2RY14 is a key regulator of Schwann cell precursor self-renewal and proliferation, of neurofibroma tumor initiation and of mouse survival.

Detection of aneuploidy and/or mutations in ctDNA may represent a promising approach to detecting patients with MPNST.

Ras-GAP activity suppresses the hemogenic potential of the embryonic heart.

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.

Biochemical and genetic analysis of the functional relationship between RIT1 and its regulatory protein, LZTR1, across various model organisms helps define the substrate specificity of LZTR1 for RAS GTPases.

Inactivation of the Dictyostelium orthologue of the tumour suppressor Neurofibromin (NF1) enables amoebae to ingest dissolved nutrients using macropinocytosis more rapidly, and to prey on larger organisms using phagocytosis.

Giant ankyrin-B enables the transduction of Sema 3A repelling cues and is important for normal axonal connectivity.

PAK1 regulates inhibitory synaptic transmission in mice through a cyclooxygenase-2 dependent restriction in tonic, but not phasic, secretion of endocannabinoids.