Source:http://linkedlifedata.com/resource/pubmed/id/14630342
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
2003-11-21
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pubmed:abstractText |
PC12 cells undergo neuritogenesis upon nerve growth factor (NGF) activation of the TrkA receptor, an effect mimicked by the ganglioside GM1 binding B-subunit of cholera toxin (CTB). Modulation of neuritogenesis by a GM1 ligand indicates a possible pathway for pathophysiological actions of neuropathy-associated anti-GM1 antibodies. Here we examine the ability of GM1 binding toxins and antibodies to induce neuritogenesis, using a PC12 neurite outgrowth assay. Cholera toxin (CT) and commercially prepared CTB (sCTB, contaminated with traces of the adenyl cyclase activating CT A-subunit) were highly neuritogenic. Recombinant cholera toxin B-subunit (rCTB, free from CTA) induced a much smaller effect, suggesting that the potent effects of sCTB are largely due to contaminating CTA. The recombinant GM1 binding B-subunit of Escherichia coli heat-labile enterotoxin (rETxB) exhibited no neuritogenic activity, whilst rETx holotoxin, which activates adenyl cyclase, was highly neuritogenic. Monoclonal anti-GM1 IgM antibodies from human neuropathy subjects induced small neuritogenic effects. These data indicate that GM1/ligand interaction does not necessarily lead to neuritogenesis and suggest that a specialisation of CTB, not shared by anti-GM1 antibodies or rETxB, is required to activate TrkA. Our data also indicate that antibodies are unlikely to exert major modulatory effects on TrkA activity in patients with anti-GM1 antibody-associated peripheral neuropathies.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/Cholera Toxin,
http://linkedlifedata.com/resource/pubmed/chemical/Enterotoxins,
http://linkedlifedata.com/resource/pubmed/chemical/G(M1) Ganglioside,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin M,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, trkA
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0168-0102
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
47
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
383-90
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:14630342-Animals,
pubmed-meshheading:14630342-Antibodies, Monoclonal,
pubmed-meshheading:14630342-Binding, Competitive,
pubmed-meshheading:14630342-Cholera Toxin,
pubmed-meshheading:14630342-Drug Contamination,
pubmed-meshheading:14630342-Enterotoxins,
pubmed-meshheading:14630342-Escherichia coli,
pubmed-meshheading:14630342-G(M1) Ganglioside,
pubmed-meshheading:14630342-Humans,
pubmed-meshheading:14630342-Immunoglobulin M,
pubmed-meshheading:14630342-Neurites,
pubmed-meshheading:14630342-PC12 Cells,
pubmed-meshheading:14630342-Peripheral Nervous System Diseases,
pubmed-meshheading:14630342-Rats,
pubmed-meshheading:14630342-Receptor, trkA
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pubmed:year |
2003
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pubmed:articleTitle |
Ganglioside GM1 binding toxins and human neuropathy-associated IgM antibodies differentially promote neuritogenesis in a PC12 assay.
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pubmed:affiliation |
University Department of Neurology, Institute of Neurological Sciences, Southern General Hospital, Glasgow G51 4TF, Scotland, UK.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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