| http://purl.uniprot.org/citations/18596915 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/18596915 | http://www.w3.org/2000/01/rdf-schema#comment | "BackgroundThe Rel/NF-kappaB transcription factors are often activated in solid or hematological malignancies. In most cases, NF-kappaB activation is found in malignant cells and results from activation of the canonical NF-kappaB pathway, leading to RelA and/or c-Rel activation. Recently, NF-kappaB activity in inflammatory cells infiltrating solid tumors has been shown to contribute to solid tumor initiation and progression. Noncanonical NF-kappaB activation, which leads to RelB activation, has also been reported in breast carcinoma, prostate cancer, and lymphoid leukemia.Methodology/principal findingsHere we report a novel role for RelB in stromal cells that promote T-cell leukemogenesis. RelB deficiency delayed leukemia onset in the TEL-JAK2 transgenic mouse model of human T acute lymphoblastic leukemia. Bone marrow chimeric mouse experiments showed that RelB is not required in the hematopoietic compartment. In contrast, RelB plays a role in radio-resistant stromal cells to accelerate leukemia onset and increase disease severity.Conclusions/significanceThe present results are the first to uncover a role for RelB in the crosstalk between non-hematopoietic stromal cells and leukemic cells. Thus, besides its previously reported role intrinsic to specific cancer cells, the noncanonical NF-kappaB pathway may also play a pro-oncogenic role in cancer microenvironmental cells."xsd:string |
| http://purl.uniprot.org/citations/18596915 | http://purl.org/dc/terms/identifier | "doi:10.1371/journal.pone.0002555"xsd:string |
| http://purl.uniprot.org/citations/18596915 | http://purl.uniprot.org/core/author | "dos Santos N.R."xsd:string |
| http://purl.uniprot.org/citations/18596915 | http://purl.uniprot.org/core/author | "Ghysdael J."xsd:string |
| http://purl.uniprot.org/citations/18596915 | http://purl.uniprot.org/core/author | "Janin A."xsd:string |
| http://purl.uniprot.org/citations/18596915 | http://purl.uniprot.org/core/author | "Cormier F."xsd:string |
| http://purl.uniprot.org/citations/18596915 | http://purl.uniprot.org/core/author | "Weih F."xsd:string |
| http://purl.uniprot.org/citations/18596915 | http://purl.uniprot.org/core/author | "Gachet S."xsd:string |
| http://purl.uniprot.org/citations/18596915 | http://purl.uniprot.org/core/author | "Williame M."xsd:string |
| http://purl.uniprot.org/citations/18596915 | http://purl.uniprot.org/core/author | "Weih D."xsd:string |
| http://purl.uniprot.org/citations/18596915 | http://purl.uniprot.org/core/date | "2008"xsd:gYear |
| http://purl.uniprot.org/citations/18596915 | http://purl.uniprot.org/core/name | "PLoS One"xsd:string |
| http://purl.uniprot.org/citations/18596915 | http://purl.uniprot.org/core/pages | "e2555"xsd:string |
| http://purl.uniprot.org/citations/18596915 | http://purl.uniprot.org/core/title | "RelB-dependent stromal cells promote T-cell leukemogenesis."xsd:string |
| http://purl.uniprot.org/citations/18596915 | http://purl.uniprot.org/core/volume | "3"xsd:string |
| http://purl.uniprot.org/citations/18596915 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/18596915 |
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| http://purl.uniprot.org/uniprot/#_A0A0G2JGK6-mappedCitation-18596915 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/18596915 |
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| http://purl.uniprot.org/uniprot/#_F6Z9G5-mappedCitation-18596915 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/18596915 |
| http://purl.uniprot.org/uniprot/#_P01849-mappedCitation-18596915 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/18596915 |
| http://purl.uniprot.org/uniprot/#_P25799-mappedCitation-18596915 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/18596915 |