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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
9
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pubmed:dateCreated |
2008-2-26
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pubmed:abstractText |
The GRIN3B gene encodes NR3B, a motoneuron-specific member of the NMDA type of ionotropic glutamate receptors. NR3B reduces the Ca(2+)-permeability as well as the overall current of the receptor response and may thereby protect motoneurons against glutamate-mediated excitotoxicity. We tested whether genetic dysfunction of GRIN3B is implicated in the pathogenesis of amyotrophic lateral sclerosis (ALS).
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pubmed:grant |
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
1526-632X
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
26
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pubmed:volume |
70
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
666-76
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pubmed:meshHeading |
pubmed-meshheading:17687115-Alleles,
pubmed-meshheading:17687115-Case-Control Studies,
pubmed-meshheading:17687115-DNA Mutational Analysis,
pubmed-meshheading:17687115-Gene Frequency,
pubmed-meshheading:17687115-Genetic Predisposition to Disease,
pubmed-meshheading:17687115-Genetics, Population,
pubmed-meshheading:17687115-Genotype,
pubmed-meshheading:17687115-Haplotypes,
pubmed-meshheading:17687115-Humans,
pubmed-meshheading:17687115-Linkage Disequilibrium,
pubmed-meshheading:17687115-Motor Neuron Disease,
pubmed-meshheading:17687115-Motor Neurons,
pubmed-meshheading:17687115-Polymorphism, Single Nucleotide,
pubmed-meshheading:17687115-Receptors, N-Methyl-D-Aspartate,
pubmed-meshheading:17687115-Superoxide Dismutase
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pubmed:year |
2008
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pubmed:articleTitle |
Motoneuron-specific NR3B gene: no association with ALS and evidence for a common null allele.
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pubmed:affiliation |
RIKEN-MIT Neuroscience Research Center, The Picower Institute for Learning and Memory, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA, USA. Niemann.Stephan@gmail.com
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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