Source:http://linkedlifedata.com/resource/pubmed/id/17035534
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rdf:type | |
lifeskim:mentions |
umls-concept:C0004927,
umls-concept:C0009219,
umls-concept:C0011155,
umls-concept:C0015127,
umls-concept:C0023693,
umls-concept:C0028246,
umls-concept:C0030193,
umls-concept:C0065042,
umls-concept:C0162429,
umls-concept:C0337112,
umls-concept:C1314792,
umls-concept:C1419782,
umls-concept:C1442161,
umls-concept:C1524075
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pubmed:issue |
41
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pubmed:dateCreated |
2006-10-12
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pubmed:abstractText |
The S100 family protein p11 (S100A10, annexin 2 light chain) is involved in the trafficking of the voltage-gated sodium channel Na(V)1.8, TWIK-related acid-sensitive K+ channel (TASK-1), the ligand-gated ion channels acid-sensing ion channel 1a (ASIC1a) and transient receptor potential vanilloid 5/6 (TRPV5/V6), as well as 5-hydroxytryptamine receptor 1B (5-HT1B), a G-protein-coupled receptor. To evaluate the role of p11 in peripheral pain pathways, we generated a loxP-flanked (floxed) p11 mouse and used the Cre-loxP recombinase system to delete p11 exclusively from nociceptive primary sensory neurons in mice. p11-null neurons showed deficits in the expression of Na(V)1.8, but not of annexin 2. Damage-sensing primary neurons from these animals show a reduced tetrodotoxin-resistant sodium current density, consistent with a loss of membrane-associated Na(V)1.8. Noxious coding in wide-dynamic-range neurons in the dorsal horn was markedly compromised. Acute pain behavior was attenuated in certain models, but no deficits in inflammatory pain were observed. A significant deficit in neuropathic pain behavior was also apparent in the conditional-null mice. These results confirm an important role for p11 in nociceptor function.
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pubmed:grant | |
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 |
Oct
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pubmed:issn |
1529-2401
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:day |
11
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pubmed:volume |
26
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
10499-507
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pubmed:dateRevised |
2007-8-13
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pubmed:meshHeading |
pubmed-meshheading:17035534-Animals,
pubmed-meshheading:17035534-Annexin A2,
pubmed-meshheading:17035534-Cells, Cultured,
pubmed-meshheading:17035534-Evoked Potentials, Somatosensory,
pubmed-meshheading:17035534-Ganglia, Spinal,
pubmed-meshheading:17035534-Gene Deletion,
pubmed-meshheading:17035534-Mice,
pubmed-meshheading:17035534-Mice, Inbred C57BL,
pubmed-meshheading:17035534-Mice, Knockout,
pubmed-meshheading:17035534-Nociceptors,
pubmed-meshheading:17035534-Pain Measurement,
pubmed-meshheading:17035534-S100 Proteins
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pubmed:year |
2006
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pubmed:articleTitle |
Deletion of annexin 2 light chain p11 in nociceptors causes deficits in somatosensory coding and pain behavior.
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pubmed:affiliation |
Molecular Nociception Group, Department of Biology, University College London, London WC1E 6BT, United Kingdom.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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