Search Results - "Fraser, Paul E."
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ALS/FTD Mutation-Induced Phase Transition of FUS Liquid Droplets and Reversible Hydrogels into Irreversible Hydrogels Impairs RNP Granule Function
Published in Neuron (Cambridge, Mass.) (18-11-2015)“…The mechanisms by which mutations in FUS and other RNA binding proteins cause ALS and FTD remain controversial. We propose a model in which low-complexity (LC)…”
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Inflammation and Oxidative Stress: The Molecular Connectivity between Insulin Resistance, Obesity, and Alzheimer's Disease
Published in Mediators of Inflammation (01-01-2015)“…Type 2 diabetes (T2DM), Alzheimer’s disease (AD), and insulin resistance are age-related conditions and increased prevalence is of public concern. Recent…”
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The Link Between Tau and Insulin Signaling: Implications for Alzheimer's Disease and Other Tauopathies
Published in Frontiers in cellular neuroscience (05-02-2019)“…The microtubule-associated protein tau (MAPT) is mainly identified as a tubulin binding protein essential for microtubule dynamics and assembly and for neurite…”
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α-Synuclein Regulates Peripheral Insulin Secretion and Glucose Transport
Published in Frontiers in aging neuroscience (30-07-2021)“…Aim Population based studies indicate a positive association between type 2 diabetes (T2D) and Parkinson’s disease (PD) where there is an increased risk of…”
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The Adult Mouse and Human Pancreas Contain Rare Multipotent Stem Cells that Express Insulin
Published in Cell stem cell (04-03-2011)“…The search for putative precursor cells within the pancreas has been the focus of extensive research. Previously, we identified rare pancreas-derived…”
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SUMO1 Modification of Tau in Progressive Supranuclear Palsy
Published in Molecular neurobiology (01-07-2022)“…Small ubiquitin-like modifiers (SUMO) have been implicated in several neurodegenerative diseases. SUMO1 conjugation has been shown to promote aggregation and…”
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SARS-CoV-2 Nucleocapsid Protein Induces Tau Pathological Changes That Can Be Counteracted by SUMO2
Published in International journal of molecular sciences (01-07-2024)“…Neurologic manifestations are an immediate consequence of SARS-CoV-2 infection, the etiologic agent of COVID-19, which, however, may also trigger long-term…”
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Combination of human tau and islet amyloid polypeptide exacerbates metabolic dysfunction in transgenic mice
Published in The Journal of pathology (01-07-2021)“…Amyloid plaques and neurofibrillary tangles composed of hyperphosphorylated tau are important contributors to Alzheimer's disease (AD). Tau also impacts…”
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Behavioral Abnormalities in Knockout and Humanized Tau Mice
Published in Frontiers in endocrinology (Lausanne) (12-03-2020)“…Microtubule-associated protein tau assists in stabilizing microtubules and has been particularly implicated in Alzheimer's disease (AD). Given the importance…”
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SUMO1 impact on Alzheimer disease pathology in an amyloid-depositing mouse model
Published in Neurobiology of disease (01-02-2018)“…Small ubiquitin-related modifiers (SUMOs) conjugated or bound to target proteins can affect protein trafficking, processing and solubility. SUMOylation has…”
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Brain‐Penetrating and Disease Site‐Targeting Manganese Dioxide‐Polymer‐Lipid Hybrid Nanoparticles Remodel Microenvironment of Alzheimer's Disease by Regulating Multiple Pathological Pathways
Published in Advanced science (01-04-2023)“…Finding effective disease‐modifying treatment for Alzheimer's disease remains challenging due to an array of factors contributing to the loss of neural…”
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SUMO1 Affects Synaptic Function, Spine Density and Memory
Published in Scientific reports (29-05-2015)“…Small ubiquitin-like modifier-1 (SUMO1) plays a number of roles in cellular events and recent evidence has given momentum for its contributions to neuronal…”
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SUMOylation Is an Inhibitory Constraint that Regulates the Prion-like Aggregation and Activity of CPEB3
Published in Cell reports (Cambridge) (23-06-2015)“…Protein synthesis is crucial for the maintenance of long-term-memory-related synaptic plasticity. The prion-like cytoplasmic polyadenylation element-binding…”
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Retraction Note to: Differential regulation of wild-type and mutant alpha-synuclein binding to synaptic membranes by cytosolic factors
Published in BMC neuroscience (03-06-2021)“…This article has been retracted. Please see the Retraction Notice for more detail: https://doi.org/10.1186/s12868-021-00644-1…”
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Structural Interactions between Inhibitor and Substrate Docking Sites Give Insight into Mechanisms of Human PS1 Complexes
Published in Structure (London) (07-01-2014)“…Presenilin-mediated endoproteolysis of transmembrane proteins plays a key role in physiological signaling and in the pathogenesis of Alzheimer disease and some…”
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Mixed pathologies in pancreatic β cells from subjects with neurodegenerative diseases and their interaction with prion protein
Published in Acta neuropathologica communications (08-04-2021)“…Protein misfolding diseases refer to a variety of disorders that develop as a consequence of the misfolding of proteins in various organs. The etiologies of…”
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The in Vivo Brain Interactome of the Amyloid Precursor Protein
Published in Molecular & cellular proteomics (01-01-2008)“…Despite intense research efforts, the physiological function and molecular environment of the amyloid precursor protein has remained enigmatic. Here we…”
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Aβ43 aggregates exhibit enhanced prion-like seeding activity in mice
Published in Acta neuropathologica communications (10-05-2021)“…When injected into genetically modified mice, aggregates of the amyloid-β (Aβ) peptide from the brains of Alzheimer's disease (AD) patients or transgenic AD…”
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Structural biology of presenilin 1 complexes
Published in Molecular neurodegeneration (18-12-2014)“…The presenilin genes were first identified as the site of missense mutations causing early onset autosomal dominant familial Alzheimer's disease. Subsequent…”
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Amyloid inhibitors enhance survival of cultured human islets
Published in Biochimica et biophysica acta (01-06-2009)“…Amyloid fibrils created by misfolding and aggregation of proteins are a major pathological feature in a variety of degenerative diseases. Therapeutic…”
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