Ciliogenesis requires a gap junction protein (GJA1) mediated ciliary vesicle deposition and CP110 removal.

Src phosphorylates GBF1, promoting binding of the Sec7 domain to Arf1 and the formation of GALNTs containing tubules emanating from the Golgi.

In vivo dopamine neuron imaging-based neuroprotective small molecule screen in larval zebrafish and mechanistic investigation using conditional CRISPR knockout and cell-type-specific RNA-seq analysis, coupled with cross-species analyses including human clinical data interrogation, uncover potential disease-modifying therapeutics for Parkinson's disease (PD).

Gab1 is a key downstream effector of PDGF signaling and essential to oligodendrocyte differentiation by linking PDGF signaling with GSK3β/β-catenin module.

Stress-induced alternative translation of an otherwise common gap junction protein generates an isoform that orchestrates protective mitochondrial fission and organ protection during anticipated ischemia.

Enhancing the management of Gaucher disease patients through multidimensional risk assessment serves as a roadmap towards personalized medicine in the context of a rare disease.

The calibration of decision thresholds will provide evidence for the optimal use of in silico predictors for the standardised classification of globin gene variants under the American College of Medical Genetics and Genomics/Association for Molecular Pathology framework.

Spontaneous remyelination is a common phenomenon in the marmoset experimental autoimmune encephalomyelitis model, reliably detected using in vivo magnetic resonance imaging, rendering this an indispensable model to further investigate the pathobiology of remyelination in multiple sclerosis.

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.

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