| pubmed-article:12408844 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12408844 | lifeskim:mentions | umls-concept:C0033684 | lld:lifeskim |
| pubmed-article:12408844 | lifeskim:mentions | umls-concept:C0018270 | lld:lifeskim |
| pubmed-article:12408844 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:12408844 | lifeskim:mentions | umls-concept:C0205087 | lld:lifeskim |
| pubmed-article:12408844 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:12408844 | pubmed:dateCreated | 2002-10-31 | lld:pubmed |
| pubmed-article:12408844 | pubmed:abstractText | In a genetic screen for genes that control synapse development, we have identified spinster (spin), which encodes a multipass transmembrane protein. spin mutant synapses reveal a 200% increase in bouton number and a deficit in presynaptic release. We demonstrate that spin is expressed in both nerve and muscle and is required both pre- and postsynaptically for normal synaptic growth. We have localized Spin to a late endosomal compartment and present evidence for altered endosomal/lysosomal function in spin. We also present evidence that synaptic overgrowth in spin is caused by enhanced/misregulated TGF-beta signaling. TGF-beta receptor mutants show dose-dependent suppression of synaptic overgrowth in spin. Furthermore, mutations in Dad, an inhibitory Smad, cause synapse overgrowth. We present a model for synaptic growth control with implications for the etiology of lysosomal storage and neurodegenerative disease. | lld:pubmed |
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| pubmed-article:12408844 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:12408844 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:12408844 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12408844 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:12408844 | pubmed:issn | 0896-6273 | lld:pubmed |
| pubmed-article:12408844 | pubmed:author | pubmed-author:SweeneySean... | lld:pubmed |
| pubmed-article:12408844 | pubmed:author | pubmed-author:DavisGraeme... | lld:pubmed |
| pubmed-article:12408844 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12408844 | pubmed:day | 24 | lld:pubmed |
| pubmed-article:12408844 | pubmed:volume | 36 | lld:pubmed |
| pubmed-article:12408844 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12408844 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12408844 | pubmed:pagination | 403-16 | lld:pubmed |
| pubmed-article:12408844 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:12408844 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:12408844 | pubmed:articleTitle | Unrestricted synaptic growth in spinster-a late endosomal protein implicated in TGF-beta-mediated synaptic growth regulation. | lld:pubmed |
| pubmed-article:12408844 | pubmed:affiliation | Department of Biochemistry, 513 Parnassus Avenue, HSE 901, University of California, San Francisco, San Francisco, CA 94143, USA. | lld:pubmed |
| pubmed-article:12408844 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12408844 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:12408844 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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