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Robert J. Dunn

Researcher at Montreal General Hospital

Publications -  62
Citations -  5360

Robert J. Dunn is an academic researcher from Montreal General Hospital. The author has contributed to research in topics: Myelin-associated glycoprotein & Gene expression. The author has an hindex of 35, co-authored 62 publications receiving 5257 citations. Previous affiliations of Robert J. Dunn include University of Toronto & Montreal Neurological Institute and Hospital.

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Identification of myelin-associated glycoprotein as a major myelin-derived inhibitor of neurite growth.

TL;DR: It is established that MAG is a significant, and possibly the major, inhibitor in CNS myelin; this has broad implications for axonal regeneration in the injured mammalian CNS.
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RasGRP, a Ras Guanyl Nucleotide- Releasing Protein with Calcium- and Diacylglycerol-Binding Motifs

TL;DR: Sustained ligand-induced signaling and membrane partitioning were absent when the DAG-binding domain was deleted and RasGRP is expressed in the nervous system, where it may couple changes in DAG and possibly calcium concentrations to Ras activation.
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Ceruloplasmin Regulates Iron Levels in the CNS and Prevents Free Radical Injury

TL;DR: The results indicate that ceruloplasmin plays an important role in maintaining iron homeostasis in the CNS and in protecting the CNS from iron-mediated free radical injury and could have important implications for various neurodegenerative diseases such as Parkinson's disease and Alzheimer's disease.
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A rat brain na + channel α subunit with novel gating properties

TL;DR: A full-length rat brain Na + channel α subunit cDNA is constructed that differs from the previously reported a subunit of Noda et al. at 6 amino acid positions indicating the presence of a component, either a structural sub unit of the channel complex or a modifying enzyme, necessary for normal gating of the channels.
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Gene encoding the beta subunit of S100 protein is on chromosome 21: implications for Down syndrome.

TL;DR: The gene for the beta subunit of S100 protein was identified as a candidate sequence which, when expressed in the trisomic state, may underlie the neurologic disturbances in Down syndrome.