| http://purl.uniprot.org/citations/9604928 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/9604928 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/9604928 | http://www.w3.org/2000/01/rdf-schema#comment | "Gain-of-function mutations in the Caenorhabditis elegans gene egl-1 cause the HSN neurons to undergo programmed cell death. By contrast, a loss-of-function egl-1 mutation prevents most if not all somatic programmed cell deaths. The egl-1 gene negatively regulates the ced-9 gene, which protects against cell death and is a member of the bcl-2 family. The EGL-1 protein contains a nine amino acid region similar to the Bcl-2 homology region 3 (BH3) domain but does not contain a BH1, BH2, or BH4 domain, suggesting that EGL-1 may be a member of a family of cell death activators that includes the mammalian proteins Bik, Bid, Harakiri, and Bad. The EGL-1 and CED-9 proteins interact physically. We propose that EGL-1 activates programmed cell death by binding to and directly inhibiting the activity of CED-9, perhaps by releasing the cell death activator CED-4 from a CED-9/CED-4-containing protein complex."xsd:string |
| http://purl.uniprot.org/citations/9604928 | http://purl.org/dc/terms/identifier | "doi:10.1016/s0092-8674(00)81182-4"xsd:string |
| http://purl.uniprot.org/citations/9604928 | http://purl.org/dc/terms/identifier | "doi:10.1016/s0092-8674(00)81182-4"xsd:string |
| http://purl.uniprot.org/citations/9604928 | http://purl.uniprot.org/core/author | "Horvitz H.R."xsd:string |
| http://purl.uniprot.org/citations/9604928 | http://purl.uniprot.org/core/author | "Horvitz H.R."xsd:string |
| http://purl.uniprot.org/citations/9604928 | http://purl.uniprot.org/core/author | "Conradt B."xsd:string |
| http://purl.uniprot.org/citations/9604928 | http://purl.uniprot.org/core/author | "Conradt B."xsd:string |
| http://purl.uniprot.org/citations/9604928 | http://purl.uniprot.org/core/date | "1998"xsd:gYear |
| http://purl.uniprot.org/citations/9604928 | http://purl.uniprot.org/core/date | "1998"xsd:gYear |
| http://purl.uniprot.org/citations/9604928 | http://purl.uniprot.org/core/name | "Cell"xsd:string |
| http://purl.uniprot.org/citations/9604928 | http://purl.uniprot.org/core/name | "Cell"xsd:string |
| http://purl.uniprot.org/citations/9604928 | http://purl.uniprot.org/core/pages | "519-529"xsd:string |
| http://purl.uniprot.org/citations/9604928 | http://purl.uniprot.org/core/pages | "519-529"xsd:string |
| http://purl.uniprot.org/citations/9604928 | http://purl.uniprot.org/core/title | "The C. elegans protein EGL-1 is required for programmed cell death and interacts with the Bcl-2-like protein CED-9."xsd:string |
| http://purl.uniprot.org/citations/9604928 | http://purl.uniprot.org/core/title | "The C. elegans protein EGL-1 is required for programmed cell death and interacts with the Bcl-2-like protein CED-9."xsd:string |
| http://purl.uniprot.org/citations/9604928 | http://purl.uniprot.org/core/volume | "93"xsd:string |
| http://purl.uniprot.org/citations/9604928 | http://purl.uniprot.org/core/volume | "93"xsd:string |
| http://purl.uniprot.org/citations/9604928 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/9604928 |
| http://purl.uniprot.org/citations/9604928 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/9604928 |
| http://purl.uniprot.org/citations/9604928 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/9604928 |
| http://purl.uniprot.org/citations/9604928 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/9604928 |
| http://purl.uniprot.org/uniprot/O61667 | http://purl.uniprot.org/core/citation | http://purl.uniprot.org/citations/9604928 |
| http://purl.uniprot.org/uniprot/P41958 | http://purl.uniprot.org/core/citation | http://purl.uniprot.org/citations/9604928 |