| http://purl.uniprot.org/citations/16009496 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/16009496 | http://www.w3.org/2000/01/rdf-schema#comment | "The presence and regulation of basic fibroblast growth factor and its high-affinity tyrosine kinase receptor FGFR3 in sensory neurons during development and after peripheral nerve injury suggest a physiological role of the fibroblast growth factor-2 system for survival and maintenance of sensory neurons. Here we investigated L5 spinal ganglia of intact and lesioned fibroblast growth factor-2 knock-out and FGFR3 knock-out mice. Quantification of sensory neurons in intact L5 spinal ganglia revealed no differences between wild-types and mutant mice. After sciatic nerve axotomy, the normally occurring neuron loss in wild-type mice was significantly reduced in both knock-out strains suggesting that fibroblast growth factor-2 is involved in neuronal death mediated via FGFR3. In addition, the number of chromatolytic and eccentric cells was significantly increased in fibroblast growth factor-2 knock-out mice indicating a transient protection of injured spinal ganglia neurons in the absence of fibroblast growth factor-2. The expression of the neuropeptide calcitonin gene-related peptide in sensory neurons of intact fibroblast growth factor-2 knock-out and FGFR3 knock-out mice was not changed in comparison to adequate wild-types. Fibroblast growth factor-2 wild-type and FGFR3 wild-type mice showed a lesion-induced decrease of calcitonin gene-related peptide-positive neurons in ipsilateral L5 spinal ganglia whereas the loss of calcitonin gene-related peptide-immunoreactive sensory neurons is reduced in the absence of fibroblast growth factor-2 or FGFR3, respectively. In addition, FGFR3 wild-type and knock-out mice displayed a contralateral reduction of the neuropeptide after axotomy. These results suggest that endogenous fibroblast growth factor-2 and FGFR3 are crucially involved in the regulation of survival and calcitonin gene-related peptide expression of lumbar sensory neurons after lesion, but not during development."xsd:string |
| http://purl.uniprot.org/citations/16009496 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.neuroscience.2005.04.066"xsd:string |
| http://purl.uniprot.org/citations/16009496 | http://purl.uniprot.org/core/author | "Meyer K."xsd:string |
| http://purl.uniprot.org/citations/16009496 | http://purl.uniprot.org/core/author | "Grothe C."xsd:string |
| http://purl.uniprot.org/citations/16009496 | http://purl.uniprot.org/core/author | "Jungnickel J."xsd:string |
| http://purl.uniprot.org/citations/16009496 | http://purl.uniprot.org/core/author | "Guhr S."xsd:string |
| http://purl.uniprot.org/citations/16009496 | http://purl.uniprot.org/core/author | "Klutzny A."xsd:string |
| http://purl.uniprot.org/citations/16009496 | http://purl.uniprot.org/core/date | "2005"xsd:gYear |
| http://purl.uniprot.org/citations/16009496 | http://purl.uniprot.org/core/name | "Neuroscience"xsd:string |
| http://purl.uniprot.org/citations/16009496 | http://purl.uniprot.org/core/pages | "1343-1350"xsd:string |
| http://purl.uniprot.org/citations/16009496 | http://purl.uniprot.org/core/title | "Regulation of neuronal death and calcitonin gene-related peptide by fibroblast growth factor-2 and FGFR3 after peripheral nerve injury: evidence from mouse mutants."xsd:string |
| http://purl.uniprot.org/citations/16009496 | http://purl.uniprot.org/core/volume | "134"xsd:string |
| http://purl.uniprot.org/citations/16009496 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/16009496 |
| http://purl.uniprot.org/citations/16009496 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/16009496 |
| http://purl.uniprot.org/uniprot/P15655#attribution-F99DE2288E7F748FDD819CE37AB2B7A4 | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/16009496 |
| http://purl.uniprot.org/uniprot/Q61851#attribution-F99DE2288E7F748FDD819CE37AB2B7A4 | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/16009496 |
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| http://purl.uniprot.org/uniprot/#_A0A0J9YTQ5-mappedCitation-16009496 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16009496 |
| http://purl.uniprot.org/uniprot/#_A0A0J9YU04-mappedCitation-16009496 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16009496 |
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| http://purl.uniprot.org/uniprot/#_F6TK14-mappedCitation-16009496 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16009496 |