William C. Mobley

Affiliations: 
Neurology University of California, San Diego, La Jolla, CA 
Area:
neurodegneration, Down syndrome
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"William Mobley"
Bio:

William C. Mobley, MD, PhD is a clinician and researcher who is internationally known for his work on degenerative diseases of the central nervous system and the neurobiology of Down syndrome.

Mean distance: 15.07 (cluster 40)
 
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Publications

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Kaplan DR, Mobley WC. (2020) (H)Elping nerve growth factor: Elp1 inhibits TrkA's phosphatase to maintain retrograde signaling. The Journal of Clinical Investigation
Rafii MS, Kleschevnikov AM, Sawa M, et al. (2019) Down syndrome. Handbook of Clinical Neurology. 167: 321-336
Chen XQ, Fang F, Florio JB, et al. (2018) TRiC enhances retrograde axonal transport by modulating tau phosphorylation. Traffic (Copenhagen, Denmark)
Sung K, Ferrari LF, Yang W, et al. (2018) Swedish Nerve Growth Factor Mutation (NGF) Defines a Role for TrkA and p75in Nociception. The Journal of Neuroscience : the Official Journal of the Society For Neuroscience
Kleschevnikov AM, Yu J, Kim J, et al. (2017) Evidence that increased Kcnj6 gene dose is necessary for deficits in behavior and dentate gyrus synaptic plasticity in the Ts65Dn mouse model of Down syndrome. Neurobiology of Disease
Xing Z, Li Y, Pao A, et al. (2016) Mouse-based genetic modeling and analysis of Down syndrome. British Medical Bulletin
Mojabi FS, Fahimi A, Moghadam S, et al. (2016) GABAergic Hyperinnervation of Dentate Granule Cells in the Ts65Dn Mouse Model of Down Syndrome Exploring the Role of App. Hippocampus
Zhao X, Chen XQ, Han E, et al. (2016) TRiC subunits enhance BDNF axonal transport and rescue striatal atrophy in Huntington's disease. Proceedings of the National Academy of Sciences of the United States of America
Peiris H, Duffield MD, Fadista J, et al. (2016) A Syntenic Cross Species Aneuploidy Genetic Screen Links RCAN1 Expression to β-Cell Mitochondrial Dysfunction in Type 2 Diabetes. Plos Genetics. 12: e1006033
Xu W, Weissmiller AM, White JA, et al. (2016) Amyloid precursor protein-mediated endocytic pathway disruption induces axonal dysfunction and neurodegeneration. The Journal of Clinical Investigation
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