pubmed-article:9342387 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:9342387 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
pubmed-article:9342387 | lifeskim:mentions | umls-concept:C0061355 | lld:lifeskim |
pubmed-article:9342387 | lifeskim:mentions | umls-concept:C0872078 | lld:lifeskim |
pubmed-article:9342387 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
pubmed-article:9342387 | lifeskim:mentions | umls-concept:C0162610 | lld:lifeskim |
pubmed-article:9342387 | lifeskim:mentions | umls-concept:C1313915 | lld:lifeskim |
pubmed-article:9342387 | lifeskim:mentions | umls-concept:C0425087 | lld:lifeskim |
pubmed-article:9342387 | pubmed:issue | 22 | lld:pubmed |
pubmed-article:9342387 | pubmed:dateCreated | 1997-12-4 | lld:pubmed |
pubmed-article:9342387 | pubmed:databankReference | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9342387 | pubmed:abstractText | Mutant presenilins have been found to cause Alzheimer disease. Here, we describe the identification and characterization of HOP-1, a Caenorhabditis elegans presenilin that displays much more lower sequence identity with human presenilins than does the other C. elegans presenilin, SEL-12. Despite considerable divergence, HOP-1 appears to be a bona fide presenilin, because HOP-1 can rescue the egg-laying defect caused by mutations in sel-12 when hop-1 is expressed under the control of sel-12 regulatory sequences. HOP-1 also has the essential topological characteristics of the other presenilins. Reducing hop-1 activity in a sel-12 mutant background causes synthetic lethality and terminal phenotypes associated with reducing the function of the C. elegans lin-12 and glp-1 genes. These observations suggest that hop-1 is functionally redundant with sel-12 and underscore the intimate connection between presenilin activity and LIN-12/Notch activity inferred from genetic studies in C. elegans and mammals. | lld:pubmed |
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pubmed-article:9342387 | pubmed:language | eng | lld:pubmed |
pubmed-article:9342387 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9342387 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:9342387 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:9342387 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:9342387 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:9342387 | pubmed:month | Oct | lld:pubmed |
pubmed-article:9342387 | pubmed:issn | 0027-8424 | lld:pubmed |
pubmed-article:9342387 | pubmed:author | pubmed-author:LULL | lld:pubmed |
pubmed-article:9342387 | pubmed:author | pubmed-author:GreenwaldII | lld:pubmed |
pubmed-article:9342387 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:9342387 | pubmed:day | 28 | lld:pubmed |
pubmed-article:9342387 | pubmed:volume | 94 | lld:pubmed |
pubmed-article:9342387 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:9342387 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:9342387 | pubmed:pagination | 12204-9 | lld:pubmed |
pubmed-article:9342387 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:9342387 | pubmed:year | 1997 | lld:pubmed |
pubmed-article:9342387 | pubmed:articleTitle | HOP-1, a Caenorhabditis elegans presenilin, appears to be functionally redundant with SEL-12 presenilin and to facilitate LIN-12 and GLP-1 signaling. | lld:pubmed |
pubmed-article:9342387 | pubmed:affiliation | Integrated Program in Cellular, Molecular and Biophysical Studies, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA. | lld:pubmed |
pubmed-article:9342387 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:9342387 | pubmed:publicationType | Comparative Study | lld:pubmed |
pubmed-article:9342387 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:9342387 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
entrez-gene:172017 | entrezgene:pubmed | pubmed-article:9342387 | lld:entrezgene |
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