pubmed-article:15650752 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:15650752 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
pubmed-article:15650752 | lifeskim:mentions | umls-concept:C1330957 | lld:lifeskim |
pubmed-article:15650752 | lifeskim:mentions | umls-concept:C0010656 | lld:lifeskim |
pubmed-article:15650752 | lifeskim:mentions | umls-concept:C0441655 | lld:lifeskim |
pubmed-article:15650752 | lifeskim:mentions | umls-concept:C1334889 | lld:lifeskim |
pubmed-article:15650752 | lifeskim:mentions | umls-concept:C0596311 | lld:lifeskim |
pubmed-article:15650752 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:15650752 | pubmed:dateCreated | 2005-2-15 | lld:pubmed |
pubmed-article:15650752 | pubmed:abstractText | Excessive signaling via the Notch1 receptor inhibits apoptosis in T lymphocytes. Since several antiapoptotic proteins are cleaved by caspases during cell death, we investigated whether Notch1 was a caspase substrate. Results demonstrate that the intracellular domain of Notch1 (NICD) is cleaved into six fragments during apoptosis in Jurkat cells or peripheral T lymphocytes. Notch1 cleavage is prevented by the caspase inhibitors DEVD-fmk and VEID-fmk or by Bcl-2 expression. Caspase-3 and caspase-6 cleave the NICD into six fragments using sites located within the NF-kappaB binding domain, the ankyrin repeats and the transactivation domain. Notch1 cleavage correlates with the loss of HES-1 expression in apoptotic T cells. Notch1 fragments cannot inhibit activation-induced cell death in a T-cell hybridoma, confirming the abrogation of Notch1 antiapoptotic activity by caspases. The ability of the NICD but not the fragments to antagonize Nur77 activity supports a role for this factor in Notch1 antiapoptotic function. | lld:pubmed |
pubmed-article:15650752 | pubmed:language | eng | lld:pubmed |
pubmed-article:15650752 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15650752 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:15650752 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15650752 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15650752 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15650752 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:15650752 | pubmed:month | Mar | lld:pubmed |
pubmed-article:15650752 | pubmed:issn | 1350-9047 | lld:pubmed |
pubmed-article:15650752 | pubmed:author | pubmed-author:ChenMM | lld:pubmed |
pubmed-article:15650752 | pubmed:author | pubmed-author:BouchardAA | lld:pubmed |
pubmed-article:15650752 | pubmed:author | pubmed-author:LazureCC | lld:pubmed |
pubmed-article:15650752 | pubmed:author | pubmed-author:BourbonnièreM... | lld:pubmed |
pubmed-article:15650752 | pubmed:author | pubmed-author:CohenL YLY | lld:pubmed |
pubmed-article:15650752 | pubmed:author | pubmed-author:SabbaghLL | lld:pubmed |
pubmed-article:15650752 | pubmed:author | pubmed-author:JeannequinPP | lld:pubmed |
pubmed-article:15650752 | pubmed:author | pubmed-author:SékalyR-PRP | lld:pubmed |
pubmed-article:15650752 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:15650752 | pubmed:volume | 12 | lld:pubmed |
pubmed-article:15650752 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:15650752 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:15650752 | pubmed:pagination | 243-54 | lld:pubmed |
pubmed-article:15650752 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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pubmed-article:15650752 | pubmed:year | 2005 | lld:pubmed |
pubmed-article:15650752 | pubmed:articleTitle | Notch1 antiapoptotic activity is abrogated by caspase cleavage in dying T lymphocytes. | lld:pubmed |
pubmed-article:15650752 | pubmed:affiliation | Laboratoire d'Immunologie, CR-CHUM, campus St-Luc, Pavillon Edouard-Asselin, 264 Bd. René Lévesque E., Montréal, Québec, Canada H2X 1P1. luchino.cohen@umontreal.ca | lld:pubmed |
pubmed-article:15650752 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:15650752 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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