| pubmed-article:15987945 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15987945 | lifeskim:mentions | umls-concept:C0178719 | lld:lifeskim |
| pubmed-article:15987945 | lifeskim:mentions | umls-concept:C0107103 | lld:lifeskim |
| pubmed-article:15987945 | lifeskim:mentions | umls-concept:C0536670 | lld:lifeskim |
| pubmed-article:15987945 | lifeskim:mentions | umls-concept:C1159366 | lld:lifeskim |
| pubmed-article:15987945 | lifeskim:mentions | umls-concept:C2587213 | lld:lifeskim |
| pubmed-article:15987945 | lifeskim:mentions | umls-concept:C1947906 | lld:lifeskim |
| pubmed-article:15987945 | pubmed:issue | 26 | lld:pubmed |
| pubmed-article:15987945 | pubmed:dateCreated | 2005-6-30 | lld:pubmed |
| pubmed-article:15987945 | pubmed:abstractText | Brain-derived neurotrophic factor (BDNF), after activity-dependent secretion from neurons, modulates critical nervous system functions. Recently, a variant in the human bdnf gene, resulting in a valine to methionine substitution in the prodomain, has been shown to lead to defective regulated secretion from neurons and memory impairment. Here, we report a novel function for a Vps10p domain protein, sortilin, in controlling BDNF sorting to the regulated secretory pathway. Sortilin interacts specifically with BDNF in a region encompassing the methionine substitution and colocalizes with BDNF in secretory granules in neurons. A truncated form of sortilin causes BDNF missorting to the constitutive secretory pathway without affecting neurotrophin-4 (NT-4) secretion. In addition, sortilin small interfering RNA introduced into primary neurons also led to BDNF missorting from the regulated to the constitutive secretory pathway. Together, these data suggest a mechanism to understand the defect associated with variant BDNF and provide a framework, based on divergent presynaptic regulation of sorting to secretory pathways, to explain how two ligands for tropomyosin-related kinase B, BDNF and NT-4, can mediate diverse biological responses. | lld:pubmed |
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| pubmed-article:15987945 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15987945 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15987945 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:15987945 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15987945 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:15987945 | pubmed:issn | 1529-2401 | lld:pubmed |
| pubmed-article:15987945 | pubmed:author | pubmed-author:LeeFrancis... | lld:pubmed |
| pubmed-article:15987945 | pubmed:author | pubmed-author:HerreraDaniel... | lld:pubmed |
| pubmed-article:15987945 | pubmed:author | pubmed-author:TengHenryH | lld:pubmed |
| pubmed-article:15987945 | pubmed:author | pubmed-author:NykjaerAnders... | lld:pubmed |
| pubmed-article:15987945 | pubmed:author | pubmed-author:HempsteadBarb... | lld:pubmed |
| pubmed-article:15987945 | pubmed:author | pubmed-author:IeraciAlessan... | lld:pubmed |
| pubmed-article:15987945 | pubmed:author | pubmed-author:ChenZhe-YuZY | lld:pubmed |
| pubmed-article:15987945 | pubmed:author | pubmed-author:MengChui-Xian... | lld:pubmed |
| pubmed-article:15987945 | pubmed:author | pubmed-author:DallHenningH | lld:pubmed |
| pubmed-article:15987945 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:15987945 | pubmed:day | 29 | lld:pubmed |
| pubmed-article:15987945 | pubmed:volume | 25 | lld:pubmed |
| pubmed-article:15987945 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15987945 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15987945 | pubmed:pagination | 6156-66 | lld:pubmed |
| pubmed-article:15987945 | pubmed:dateRevised | 2011-9-26 | lld:pubmed |
| pubmed-article:15987945 | pubmed:meshHeading | pubmed-meshheading:15987945... | lld:pubmed |
| pubmed-article:15987945 | pubmed:meshHeading | pubmed-meshheading:15987945... | lld:pubmed |
| pubmed-article:15987945 | pubmed:meshHeading | pubmed-meshheading:15987945... | lld:pubmed |
