| pubmed-article:8643476 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8643476 | lifeskim:mentions | umls-concept:C0033684 | lld:lifeskim |
| pubmed-article:8643476 | lifeskim:mentions | umls-concept:C0039065 | lld:lifeskim |
| pubmed-article:8643476 | lifeskim:mentions | umls-concept:C0085255 | lld:lifeskim |
| pubmed-article:8643476 | lifeskim:mentions | umls-concept:C0598964 | lld:lifeskim |
| pubmed-article:8643476 | lifeskim:mentions | umls-concept:C0205164 | lld:lifeskim |
| pubmed-article:8643476 | lifeskim:mentions | umls-concept:C0205224 | lld:lifeskim |
| pubmed-article:8643476 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:8643476 | pubmed:dateCreated | 1996-7-18 | lld:pubmed |
| pubmed-article:8643476 | pubmed:abstractText | Synaptophysin (syp I) is a synaptic vesicle membrane protein that constitutes approximately 7% of the total vesicle protein. Multiple lines of evidence implicate syp I in a number of nerve terminal functions. To test these, we have disrupted the murine Syp I gene. Mutant mice lacking syp I were viable and fertile. No changes in the structure and protein composition of the mutant brains were observed except for a decrease in synaptobrevin/VAMP II. Synaptic transmission was normal with no detectable changes in synaptic plasticity or the probability of release. Our data demonstrate that one of the major synaptic vesicle membrane proteins is not essential for synaptic transmission, suggesting that its function is either redundant or that it has a more subtle function not apparent in the assays used. | lld:pubmed |
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| pubmed-article:8643476 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8643476 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8643476 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:8643476 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8643476 | pubmed:month | May | lld:pubmed |
| pubmed-article:8643476 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:8643476 | pubmed:author | pubmed-author:SiegelbaumS... | lld:pubmed |
| pubmed-article:8643476 | pubmed:author | pubmed-author:HammerR ERE | lld:pubmed |
| pubmed-article:8643476 | pubmed:author | pubmed-author:SüdhofT CTC | lld:pubmed |
| pubmed-article:8643476 | pubmed:author | pubmed-author:McMahonH THT | lld:pubmed |
| pubmed-article:8643476 | pubmed:author | pubmed-author:JanzRR | lld:pubmed |
| pubmed-article:8643476 | pubmed:author | pubmed-author:BolshakovV... | lld:pubmed |
| pubmed-article:8643476 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8643476 | pubmed:day | 14 | lld:pubmed |
| pubmed-article:8643476 | pubmed:volume | 93 | lld:pubmed |
| pubmed-article:8643476 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8643476 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8643476 | pubmed:pagination | 4760-4 | lld:pubmed |
| pubmed-article:8643476 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:8643476 | pubmed:year | 1996 | lld:pubmed |
| pubmed-article:8643476 | pubmed:articleTitle | Synaptophysin, a major synaptic vesicle protein, is not essential for neurotransmitter release. | lld:pubmed |
| pubmed-article:8643476 | pubmed:affiliation | Howard Hughes Medical Institute, The University of Texas Southwestern Medical School, Dallas 75235, USA. | lld:pubmed |
| pubmed-article:8643476 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8643476 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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