| http://purl.uniprot.org/citations/29414782 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/29414782 | http://www.w3.org/2000/01/rdf-schema#comment | "Apoptosis is mediated through the extrinsic or intrinsic pathway. Key regulators of the intrinsic apoptotic pathway are the family of B cell lymphoma 2 (Bcl-2) proteins. The activity of the prototypical Bcl-2 protein is usually considered antiapoptotic. However, under some conditions, Bcl-2 associates with the orphan nuclear hormone receptors Nur77 and Nor-1, converting Bcl-2 into a proapoptotic molecule. Expression of Nur77 and Nor-1 is induced by a variety of signals, including those leading to apoptosis. Translocation of Nur77/Nor-1 to mitochondria results in their association with Bcl-2, exposing the Bcl-2 homology (BH) 3 domain and causing apoptosis. However, the molecular details of this interaction are incompletely understood. Here, through extensive Bcl-2 mutagenesis and functional assays, we identified residues within Bcl-2 that are essential for its interaction with Nur77/Nor-1. Although an initial report has suggested that an unstructured loop region between the Bcl-2 BH4 and BH3 domains is required for Bcl-2's interaction with Nur77/Nor-1, we found that it is dispensable for this interaction. Instead, we found important interacting residues at the BH4 domain and crucial interacting residues between the BH1 and BH2 domains. Bcl-2 alanine mutants at this region could no longer interact with Nur77/Nor-1 and could not initiate Nur77/Bcl-2-mediated cell death. However, they still retained their anti-apoptotic capability in two different death assays. These results establish crucial residues in Bcl-2 required for Nur77/Nor-1-mediated apoptosis and point to potential new strategies for manipulating Bcl-2 function."xsd:string |
| http://purl.uniprot.org/citations/29414782 | http://purl.org/dc/terms/identifier | "doi:10.1074/jbc.ra117.001101"xsd:string |
| http://purl.uniprot.org/citations/29414782 | http://purl.uniprot.org/core/author | "Wang X."xsd:string |
| http://purl.uniprot.org/citations/29414782 | http://purl.uniprot.org/core/author | "Das P."xsd:string |
| http://purl.uniprot.org/citations/29414782 | http://purl.uniprot.org/core/author | "Winoto A."xsd:string |
| http://purl.uniprot.org/citations/29414782 | http://purl.uniprot.org/core/author | "Banta K.L."xsd:string |
| http://purl.uniprot.org/citations/29414782 | http://purl.uniprot.org/core/date | "2018"xsd:gYear |
| http://purl.uniprot.org/citations/29414782 | http://purl.uniprot.org/core/name | "J Biol Chem"xsd:string |
| http://purl.uniprot.org/citations/29414782 | http://purl.uniprot.org/core/pages | "4724-4734"xsd:string |
| http://purl.uniprot.org/citations/29414782 | http://purl.uniprot.org/core/title | "B cell lymphoma 2 (Bcl-2) residues essential for Bcl-2's apoptosis-inducing interaction with Nur77/Nor-1 orphan steroid receptors."xsd:string |
| http://purl.uniprot.org/citations/29414782 | http://purl.uniprot.org/core/volume | "293"xsd:string |
| http://purl.uniprot.org/citations/29414782 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/29414782 |
| http://purl.uniprot.org/citations/29414782 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/29414782 |
| http://purl.uniprot.org/uniprot/#_P10417-mappedCitation-29414782 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/29414782 |
| http://purl.uniprot.org/uniprot/#_A0A1Q1MKH5-mappedCitation-29414782 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/29414782 |
| http://purl.uniprot.org/uniprot/#_A0A1Q1MKI1-mappedCitation-29414782 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/29414782 |
| http://purl.uniprot.org/uniprot/#_A0A6F8X1J9-mappedCitation-29414782 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/29414782 |
| http://purl.uniprot.org/uniprot/#_A2VCP5-mappedCitation-29414782 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/29414782 |
| http://purl.uniprot.org/uniprot/#_A2VCP6-mappedCitation-29414782 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/29414782 |
| http://purl.uniprot.org/uniprot/#_Q8BQK4-mappedCitation-29414782 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/29414782 |
| http://purl.uniprot.org/uniprot/#_Q9QZB6-mappedCitation-29414782 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/29414782 |
| http://purl.uniprot.org/uniprot/#_P12813-mappedCitation-29414782 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/29414782 |
| http://purl.uniprot.org/uniprot/#_Q545Q1-mappedCitation-29414782 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/29414782 |
| http://purl.uniprot.org/uniprot/#_Q6NTH7-mappedCitation-29414782 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/29414782 |