Topic: park2

Membrane trafficking defects are one of the core components of Parkinson’s Disease (PD), a progressive neurodegenerative disorder that results in severe motor deficits. Several genes associated with Clathrin-Mediated Endocytosis (CME) have been identified as PD risk genes, suggesting a putative link between trafficking defects and early nigrostriatal dysfunction. Intriguingly, recent work on endocytosis-defective mutants has implicated a renowned PD protein: Parkin (or PARK2), an E3 Ubiquitin ligase conventionally involved in mitochondrial quality control, in CME. Parkin is reported to mono-ub

Parkinson’s disease (PD) is a progressive disorder of the nervous system, affecting 1% of the ageing population. Common motor symptoms include tremor and bradykinesia, while non-motor symptoms range from constipation to sleep disturbances. The neuropathological hallmarks involve the loss of dopaminergic neurons in the substantia nigra and abnormal intra-neuronal accumulation of Lewy bodies. Here, the zebrafish model is used to investigate the behavioural defects associated with PD. Mutations of PARK2, PINK1, PARK7, LRRK2 and SNCA genes cause different forms of PD in humans. Using CRISPR/Cas9