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SQSTM1, a protective factor of SOD1-linked motor neuron disease, regulates the accumulation and distribution of ubiquitinated protein aggregates in neuron.
Neurochem Int
September 2022
Molecular Neuropathobiology Laboratory, Department of Molecular Life Sciences, Tokai University School of Medicine, Isehara, Kanagawa, 259-1193, Japan; The Institute of Medical Sciences, Tokai University, Isehara, Kanagawa, 259-1193, Japan; Micro/Nano Technology Center, Tokai University, Hiratsuka, Kanagawa, 259-1292, Japan; Research Center for Brain and Nervous Diseases, Tokai University Graduate School of Medicine, Isehara, Kanagawa, 259-1193, Japan. Electronic address:
Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease characterized by selective loss of motor neurons in the brain and spinal cord. Recent studies have shown that mutations in SQSTM1 are linked to ALS. It has also been demonstrated that a systemic loss of SQSTM1 exacerbates disease phenotypes in an ALS mouse model.
View Article and Find Full Text PDFHigh-throughput quantitative analysis of axonal transport in cultured neurons from SOD1 ALS mice by using a microfluidic device.
Neurosci Res
January 2022
Molecular Neuropathobiology Laboratory, Department of Molecular Life Sciences, Tokai University School of Medicine, Isehara, Kanagawa, 259-1193, Japan; Micro/Nano Technology Center, Tokai University, Hiratsuka, Kanagawa, 259-1292, Japan; The Institute of Medical Sciences, Tokai University, Isehara, Kanagawa, 259-1193, Japan; Research Center for Brain and Nervous Diseases, Tokai University Graduate School of Medicine, Isehara, Kanagawa, 259-1193, Japan. Electronic address:
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by selective loss of motor neurons. We have previously shown that autophagosome-like vesicular structures are progressively accumulated in the spinal axons of an ALS mouse model, overexpressing human Cu/Zn superoxide dismutase (SOD1) mutant, prior to the onset of motor symptoms. This suggests that axonal transport perturbation can be an early sign of neuronal dysfunction.
View Article and Find Full Text PDFMonitoring the autophagy-endolysosomal system using monomeric Keima-fused MAP1LC3B.
PLoS One
August 2020
Molecular Neuropathobiology Laboratory, Department of Molecular Life Sciences, Tokai University School of Medicine, Isehara, Kanagawa, Japan.
The autophagy-endolysosomal pathway is an evolutionally conserved degradation system that is tightly linked to a wide variety of physiological processes. Dysfunction of this system is associated with many pathological conditions such as cancer, inflammation and neurodegenerative diseases. Therefore, monitoring the cellular autophagy-endolysosomal activity is crucial for studies on the pathogenesis as well as therapeutics of such disorders.
View Article and Find Full Text PDFBicaudal-D1 regulates the intracellular sorting and signalling of neurotrophin receptors.
EMBO J
July 2014
Molecular NeuroPathobiology Laboratory, Cancer Research UK London Research Institute, London, UK Sobell Department of Motor Neuroscience & Movement Disorders, UCL-Institute of Neurology, University College London, London, UK
We have identified a new function for the dynein adaptor Bicaudal D homolog 1 (BICD1) by screening a siRNA library for genes affecting the dynamics of neurotrophin receptor-containing endosomes in motor neurons (MNs). Depleting BICD1 increased the intracellular accumulation of brain-derived neurotrophic factor (BDNF)-activated TrkB and p75 neurotrophin receptor (p75(NTR)) by disrupting the endosomal sorting, reducing lysosomal degradation and increasing the co-localisation of these neurotrophin receptors with retromer-associated sorting nexin 1. The resulting re-routing of active receptors increased their recycling to the plasma membrane and altered the repertoire of signalling-competent TrkB isoforms and p75(NTR) available for ligand binding on the neuronal surface.
View Article and Find Full Text PDFLinks between progressive HIV-1 infection of humanized mice and viral neuropathogenesis.
Am J Pathol
December 2010
Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE 68198-5880, USA.
Few rodent models of human immunodeficiency virus type one (HIV-1) infection can reflect the course of viral infection in humans. To this end, we investigated the relationships between progressive HIV-1 infection, immune compromise, and neuroinflammatory responses in NOD/scid-IL-2Rγ(c)(null) mice reconstituted with human hematopoietic CD34(+) stem cells. Human blood-borne macrophages repopulated the meninges and perivascular spaces of chimeric animals.
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