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13 results on '"Cooper, Jonathan"'

2. Tyrosine O-sulfation proteoforms affect HIV-1 monoclonal antibody potency

Author

Cai, Cindy X., Doria-Rose, Nicole A., Schneck, Nicole A., Ivleva, Vera B., Tippett, Brad, Shadrick, William R., O’Connell, Sarah, Cooper, Jonathan W., Schneiderman, Zachary, Zhang, Baoshan, Gowetski, Daniel B., Blackstock, Daniel, Demirji, Jacob, Lin, Bob C., Gorman, Jason, Liu, Tracy, Li, Yile, McDermott, Adrian B., Kwong, Peter D., Carlton, Kevin, Gall, Jason G., and Lei, Q. Paula

Published
2022
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3. Proteomic mapping of differentially vulnerable pre-synaptic populations identifies regulators of neuronal stability in vivo.

Author

Llavero Hurtado, Maica, Fuller, Heidi R, Wong, Andrew MS, Eaton, Samantha L, Gillingwater, Thomas H, Pennetta, Giuseppa, Cooper, Jonathan D, and Wishart, Thomas M

Subjects
Neurons, Synapses, Animals, Mice, Inbred C57BL, Humans, Drosophila, Disease Models, Animal, Membrane Glycoproteins, Drosophila Proteins, Membrane Proteins, Proteomics, Neuronal Ceroid-Lipofuscinoses, Mice, Inbred C57BL, Disease Models, Animal, Brain Disorders, Dementia, Batten Disease, Acquired Cognitive Impairment, Neurodegenerative, Pediatric, Neurosciences, Biotechnology, Rare Diseases, 2.1 Biological and endogenous factors, Generic Health Relevance, Neurological, Biochemistry and Cell Biology, Other Physical Sciences
Abstract

Synapses are an early pathological target in many neurodegenerative diseases ranging from well-known adult onset conditions such as Alzheimer and Parkinson disease to neurodegenerative conditions of childhood such as spinal muscular atrophy (SMA) and neuronal ceroid lipofuscinosis (NCLs). However, the reasons why synapses are particularly vulnerable to such a broad range of neurodegeneration inducing stimuli remains unknown. To identify molecular modulators of synaptic stability and degeneration, we have used the Cln3 -/- mouse model of a juvenile form of NCL. We profiled and compared the molecular composition of anatomically-distinct, differentially-affected pre-synaptic populations from the Cln3 -/- mouse brain using proteomics followed by bioinformatic analyses. Identified protein candidates were then tested using a Drosophila CLN3 model to study their ability to modify the CLN3-neurodegenerative phenotype in vivo. We identified differential perturbations in a range of molecular cascades correlating with synaptic vulnerability, including valine catabolism and rho signalling pathways. Genetic and pharmacological targeting of key 'hub' proteins in such pathways was sufficient to modulate phenotypic presentation in a Drosophila CLN3 model. We propose that such a workflow provides a target rich method for the identification of novel disease regulators which could be applicable to the study of other conditions where appropriate models exist.

Published
2017

12. Microrheology with Optical Tweezers: Measuring the relative viscosity of solutions ‘at a glance’

Author

Tassieri, Manlio, primary, Giudice, Francesco Del, additional, Robertson, Emma J., additional, Jain, Neena, additional, Fries, Bettina, additional, Wilson, Rab, additional, Glidle, Andrew, additional, Greco, Francesco, additional, Netti, Paolo Antonio, additional, Maffettone, Pier Luca, additional, Bicanic, Tihana, additional, and Cooper, Jonathan M., additional

Published
2015
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