| pubmed-article:12694406 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12694406 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:12694406 | lifeskim:mentions | umls-concept:C0521390 | lld:lifeskim |
| pubmed-article:12694406 | lifeskim:mentions | umls-concept:C0596290 | lld:lifeskim |
| pubmed-article:12694406 | lifeskim:mentions | umls-concept:C1160466 | lld:lifeskim |
| pubmed-article:12694406 | lifeskim:mentions | umls-concept:C0812245 | lld:lifeskim |
| pubmed-article:12694406 | lifeskim:mentions | umls-concept:C1417663 | lld:lifeskim |
| pubmed-article:12694406 | lifeskim:mentions | umls-concept:C0547047 | lld:lifeskim |
| pubmed-article:12694406 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:12694406 | pubmed:dateCreated | 2003-4-15 | lld:pubmed |
| pubmed-article:12694406 | pubmed:abstractText | APP-BP1, first identified as a protein that interacts with the carboxyl (C) terminus of the amyloid precursor protein (APP), is one-half of the bipartite activating enzyme for the ubiquitin-like protein NEDD8. We report here that APP-BP1 also specifically interacts with apoptosis stimulating protein of p53 ASPP2 in non-transfected cells through the functional predominant N-terminal domain ASPP2(332-483). ASPP2 inhibits the ability of APP-BP1 to rescue the ts41 cell cycle mutation and inhibits APP-BP1 induced apoptosis in primary neurons. ASPP2 reduces the ability of NEDD8 to conjugate to Cullin-1, inhibits APP-BP1-dependent ts41 cell proliferation, and blocks the ability of APP-BP1 to cause apoptosis and to cause DNA synthesis in neurons. We also show that ASPP2 activates nuclear factor-kappaB (NF-kappaB) transcriptional activity, which seems to be inhibited by the neddylation pathway since the dominant negative NEDD8 activating enzyme causes enhanced NF-kappaB activity. Our data provide the first in vivo evidence that ASPP2 is a negative regulator of the neddylation pathway through specific interaction with APP-BP1 and suggest that dysfunction of the APP-BP1 interaction with APP may be one cause of Alzheimer's disease. | lld:pubmed |
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| pubmed-article:12694406 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:12694406 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:12694406 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12694406 | pubmed:month | May | lld:pubmed |
| pubmed-article:12694406 | pubmed:issn | 0022-3042 | lld:pubmed |
| pubmed-article:12694406 | pubmed:author | pubmed-author:ChenYuzhiY | lld:pubmed |
| pubmed-article:12694406 | pubmed:author | pubmed-author:NeveRachael... | lld:pubmed |
| pubmed-article:12694406 | pubmed:author | pubmed-author:NaumovskiLoui... | lld:pubmed |
| pubmed-article:12694406 | pubmed:author | pubmed-author:LiuWenyunW | lld:pubmed |
| pubmed-article:12694406 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12694406 | pubmed:volume | 85 | lld:pubmed |
| pubmed-article:12694406 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12694406 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12694406 | pubmed:pagination | 801-9 | lld:pubmed |
| pubmed-article:12694406 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:12694406 | pubmed:year | 2003 | lld:pubmed |
| pubmed-article:12694406 | pubmed:articleTitle | ASPP2 inhibits APP-BP1-mediated NEDD8 conjugation to cullin-1 and decreases APP-BP1-induced cell proliferation and neuronal apoptosis. | lld:pubmed |
| pubmed-article:12694406 | pubmed:affiliation | Department of Psychiatry, Harvard Medical School, McLean Hospital, Belmont, Massachusetts, USA. ychen@helix.mgh.harvard.edu | lld:pubmed |
| pubmed-article:12694406 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12694406 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:12694406 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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