Emily Banks
A5011150477- Parkinson's Disease Mechanisms and Treatments
- Microtubule and mitosis dynamics
- Cellular transport and secretion
- Autophagy in Disease and Therapy
- Calcium signaling and nucleotide metabolism
- Lysosomal Storage Disorders Research
- Alzheimer's disease research and treatments
- Nerve injury and regeneration
- Nuclear Receptors and Signaling
- Hippo pathway signaling and YAP/TAZ
- Retinal Development and Disorders
- Botulinum Toxin and Related Neurological Disorders
- Genetics and Neurodevelopmental Disorders
- RNA Research and Splicing
- Epigenetics and DNA Methylation
Montreal Neurological Institute and Hospital
2022-2024
McGill University
2022-2024
The nervous system spread of alpha-synuclein fibrils is thought to cause Parkinson's disease (PD) and other synucleinopathies; however, the mechanisms underlying internalization cellular are enigmatic. Here, we use confocal superresolution microscopy, subcellular fractionation, electron microscopy (EM) immunogold-labeled α-synuclein preformed (PFFs) demonstrate that this form protein undergoes rapid targeted directly lysosomes in as little 2 min. Uptake PFFs disrupted by macropinocytic...
Lysosomes help maintain cellular proteostasis, and defects in lysosomal positioning function can cause disease, including neurodegenerative disorders. The spatiotemporal distribution of lysosomes is regulated by small GTPases Rabs, which are activated guanine nucleotide exchange factors (GEFs). DENN domain proteins the largest family Rab GEFs. Using a cell-based assay, we screened DENND6A, member protein against all known Rabs identified it as potential GEF for 20 Rab34. Here, demonstrate...
Cytokinesis relies on membrane trafficking pathways regulated by Rabs and guanine nucleotide exchange factors (GEFs). During cytokinesis, the intercellular cytokinetic bridge (ICB) connecting daughter cells undergoes abscission, which requires actin depolymerization. Rab35 recruits MICAL1 to oxidize depolymerize filaments. We show that DENND2B, a protein linked cancer congenital disorders, functions as GEF, recruiting activating at ICB. DENND2B's N-terminal region also interacts with an...
SUMMARY Lewy bodies (LBs), rich in α-synuclein, are a hallmark of Parkinson’s disease (PD). Understanding their biogenesis is likely to provide insight into the pathophysiology PD, yet cellular model for LB formation remains elusive. The realization that immune challenge trigger neurodegenerative diseases has been breakthrough understanding PD. Here, iPSC-derived human dopaminergic (DA) neurons from multiple healthy donors were found form LB-like inclusions following treatment with α-...
Developmental and epileptic encephalopathies (DEEs) feature altered brain development, developmental delay seizures, with seizures exacerbating delay. Here we identify a cohort biallelic variants in DENND5A, encoding membrane trafficking protein, develop animal models phenotypes like the human syndrome. We demonstrate that DENND5A interacts Pals1/MUPP1, components of Crumbs apical polarity complex required for symmetrical division neural progenitor cells. Human induced pluripotent stem cells...
Abstract Cytokinesis is the final stage of cell division. Successful cytokinesis requires membrane trafficking pathways regulated by Rabs, molecular switches activated guanine nucleotide exchange factors (GEFs). Late in cytokinesis, an intercellular cytokinetic bridge (ICB) connecting two daughter cells undergoes abscission, which depolymerization actin. Rab35 recruits MICAL1 to oxidate and depolymerize actin filaments. We report that DENND2B, a protein previously implicated cancer, mental...
SUMMARY The nervous system spread of alpha-synuclein fibrils is thought to cause Parkinson’s disease (PD) and other synucleinopathies, yet the mechanisms underlying internalization cellular are enigmatic. Here we use confocal super-resolution microscopy, subcellular fractionation electron microscopy (EM) immunogold labelled preformed (PFF) demonstrate that this fibril form undergoes rapid targeted directly lysosomes in as little 2 minutes. Uptake PFF disrupted by macropinocytic inhibitors...
Abstract Developmental and epileptic encephalopathies (DEEs) are a heterogenous group of epilepsies in which altered brain development leads to developmental delay seizures, with the activity further negatively impacting neurodevelopment. Identifying underlying cause DEEs is essential for progress toward precision therapies. Here we describe individuals biallelic variants DENND5A determine that variant type correlated disease severity. We demonstrate interacts MUPP1 PALS1, components Crumbs...