| http://purl.uniprot.org/citations/24046015 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/24046015 | http://www.w3.org/2000/01/rdf-schema#comment | "Hematopoietic stem and progenitor cells with inactivated Fanconi anemia (FA) genes, FANCA and FANCC, are hypersensitive to inflammatory cytokines. One of these, tumor necrosis factor α (TNF-α), is also overproduced by FA mononuclear phagocytes in response to certain Toll-like receptor (TLR) agonists, creating an autoinhibitory loop that may contribute to the pathogenesis of progressive bone marrow (BM) failure and selection of TNF-α-resistant leukemic stem cell clones. In macrophages, the TNF-α overproduction phenotype depends on p38 mitogen-activated protein kinase (MAPK), an enzyme also known to induce expression of other inflammatory cytokines, including interleukin 1β (IL-1β). Reasoning that IL-1β might be involved in a like autoinhibitory loop, we determined that (1) TLR activation of FANCA- and FANCC-deficient macrophages induced overproduction of both TNF-α and IL-1β in a p38-dependent manner; (2) exposure of Fancc-deficient BM progenitors to IL-1β potently suppressed the expansion of multipotent progenitor cells in vitro; and (3) although TNF-α overexpression in FA cells is controlled posttranscriptionally by the p38 substrate MAPKAPK-2, p38-dependent overproduction of IL-1β is controlled transcriptionally. We suggest that multiple inflammatory cytokines overproduced by FANCA- and FANCC-deficient mononuclear phagocytes may contribute to the progressive BM failure that characterizes FA, and that to achieve suppression of this proinflammatory state, p38 is a more promising molecular therapeutic target than either IL-1β or TNF-α alone."xsd:string |
| http://purl.uniprot.org/citations/24046015 | http://purl.org/dc/terms/identifier | "doi:10.1182/blood-2013-02-484816"xsd:string |
| http://purl.uniprot.org/citations/24046015 | http://purl.uniprot.org/core/author | "Yates J.E."xsd:string |
| http://purl.uniprot.org/citations/24046015 | http://purl.uniprot.org/core/author | "Bagby G.C."xsd:string |
| http://purl.uniprot.org/citations/24046015 | http://purl.uniprot.org/core/author | "Keeble W."xsd:string |
| http://purl.uniprot.org/citations/24046015 | http://purl.uniprot.org/core/author | "Garbati M.R."xsd:string |
| http://purl.uniprot.org/citations/24046015 | http://purl.uniprot.org/core/author | "Rathbun R.K."xsd:string |
| http://purl.uniprot.org/citations/24046015 | http://purl.uniprot.org/core/author | "Hays L.E."xsd:string |
| http://purl.uniprot.org/citations/24046015 | http://purl.uniprot.org/core/date | "2013"xsd:gYear |
| http://purl.uniprot.org/citations/24046015 | http://purl.uniprot.org/core/name | "Blood"xsd:string |
| http://purl.uniprot.org/citations/24046015 | http://purl.uniprot.org/core/pages | "3197-3205"xsd:string |
| http://purl.uniprot.org/citations/24046015 | http://purl.uniprot.org/core/title | "FANCA and FANCC modulate TLR and p38 MAPK-dependent expression of IL-1beta in macrophages."xsd:string |
| http://purl.uniprot.org/citations/24046015 | http://purl.uniprot.org/core/volume | "122"xsd:string |
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