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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6274
|
pubmed:dateCreated |
1990-6-28
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pubmed:abstractText |
The dominant mutation deg-1(u38) results in a toxic gene product that leads to the late-onset degeneration of a small number of neurons in the nematode Caenorhabditis elegans. Both intragenic and extragenic mutations as well as changes in wild-type gene dosage can delay or block the time of onset of the neuronal deaths. The deg-1 gene has been cloned and a partial complementary DNA reveals that the gene encodes a novel protein that may act as a membrane receptor. Because the late-onset loss of specific sets of neurons, often as a result of dominant mutations, is characteristic of several human neurodegenerative diseases, the analysis of the deg-1 gene and its suppressors may provide a means of understanding the mechanisms underlying some of these human diseases.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0028-0836
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
31
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pubmed:volume |
345
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
410-6
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:2342572-Age Factors,
pubmed-meshheading:2342572-Amino Acid Sequence,
pubmed-meshheading:2342572-Animals,
pubmed-meshheading:2342572-Base Sequence,
pubmed-meshheading:2342572-Caenorhabditis,
pubmed-meshheading:2342572-Cloning, Molecular,
pubmed-meshheading:2342572-Gene Expression,
pubmed-meshheading:2342572-Genes,
pubmed-meshheading:2342572-Genes, Dominant,
pubmed-meshheading:2342572-Membrane Proteins,
pubmed-meshheading:2342572-Molecular Sequence Data,
pubmed-meshheading:2342572-Nerve Degeneration,
pubmed-meshheading:2342572-Phenotype,
pubmed-meshheading:2342572-Suppression, Genetic
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pubmed:year |
1990
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pubmed:articleTitle |
The identification and suppression of inherited neurodegeneration in Caenorhabditis elegans.
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pubmed:affiliation |
Department of Biological Sciences, Columbia University, New York, New York 10027.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|