| http://purl.uniprot.org/citations/10082135 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/10082135 | http://www.w3.org/2000/01/rdf-schema#comment | "Fanconi anemia (FA) is a genetic syndrome predisposing to hematopoietic failure. Little is known about the pathophysiology of FA, except that tumor necrosis factor-alpha (TNF-alpha) is overexpressed in patients. FA group C (Fac) gene knockout mice have been developed in order to model the human disease, but the mice do not spontaneously exhibit aplasia. To investigate secondary influences on hematopoiesis in the Fac-null mice, we studied the sensitivity of hematopoietic progenitor cells (HPC) to death receptor triggering by TNF-alpha and Fas receptor (CD95) ligation. Previously we had found that overexpression of a human FAC transgene protects hematopoietic progenitors from Fas-mediated apoptosis (Wang et al., 1998, Cancer Res 58:3538-3541). In the present experiments with Fac-null mice, growth of erythroid burst-forming units (BFU-E) was significantly inhibited by TNF-alpha and CD95 ligation. Flow cytometric analysis revealed that CD95 was induced more readily in the Fac-null CD34+ cell fraction. Apoptosis induced by TNF-alpha alone or with CD95 ligation also occurred more frequently in null mouse HPC. We then bred null mice against transgenic mice overexpressing TNF-alpha (at serum levels in the range of 100 pg/ml). Resultant Fac-null mice that overexpressed TNF-alpha not only yielded decreased numbers of BFU-E but also expressed higher levels of CD95 in the CD34+ fraction. We conclude that mutation in the Fac protein induces heightened sensitivity to TNF-alpha and Fas receptor ligation, results that may explain the mechanism of anemia in FA-C patients."xsd:string |
| http://purl.uniprot.org/citations/10082135 | http://purl.org/dc/terms/identifier | "doi:10.1002/(sici)1097-4652(199904)179:1<79::aid-jcp10>3.0.co;2-o"xsd:string |
| http://purl.uniprot.org/citations/10082135 | http://purl.uniprot.org/core/author | "Otsuki T."xsd:string |
| http://purl.uniprot.org/citations/10082135 | http://purl.uniprot.org/core/author | "Wang J."xsd:string |
| http://purl.uniprot.org/citations/10082135 | http://purl.uniprot.org/core/author | "Grompe M."xsd:string |
| http://purl.uniprot.org/citations/10082135 | http://purl.uniprot.org/core/author | "Liu J.M."xsd:string |
| http://purl.uniprot.org/citations/10082135 | http://purl.uniprot.org/core/author | "Bloom M."xsd:string |
| http://purl.uniprot.org/citations/10082135 | http://purl.uniprot.org/core/author | "Nagakura S."xsd:string |
| http://purl.uniprot.org/citations/10082135 | http://purl.uniprot.org/core/date | "1999"xsd:gYear |
| http://purl.uniprot.org/citations/10082135 | http://purl.uniprot.org/core/name | "J Cell Physiol"xsd:string |
| http://purl.uniprot.org/citations/10082135 | http://purl.uniprot.org/core/pages | "79-86"xsd:string |
| http://purl.uniprot.org/citations/10082135 | http://purl.uniprot.org/core/title | "Tumor necrosis factor-alpha and CD95 ligation suppress erythropoiesis in Fanconi anemia C gene knockout mice."xsd:string |
| http://purl.uniprot.org/citations/10082135 | http://purl.uniprot.org/core/volume | "179"xsd:string |
| http://purl.uniprot.org/citations/10082135 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/10082135 |
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