| http://purl.uniprot.org/citations/23207522 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/23207522 | http://www.w3.org/2000/01/rdf-schema#comment | "We have previously identified a tyrosine kinase-independent, guanine nucleotide exchange factor (GEF) activity, which is contained within the region of p210 no expansion BCR/ABL that distinguishes it from p190 BCR/ABL. In the current study, we have compared the transforming activity of p190 BCR/ABL, p210 BCR/ABL and a mutant that lacks GEF activity (p210 BCR/ABL(S509A)). In cell-based, ex vivo, and murine bone marrow transplantation (BMT) assays the transforming activity of p210 BCR/ABL(S509A) mimics p190 BCR/ABL, and is distinct from p210 BCR/ABL. Thus, in the BMT assay, the p190 BCR/ABL- and p210 BCR/ABL(S509A)-transplanted mice exhibit a more rapid onset of disease than mice transplanted with p210 BCR/ABL. The reduced disease latency is associated with erythroid hyperplasia in the absence of anemia, and expansion of the megakaryocyte-erythrocyte progenitor (MEP), common myeloid progenitor (CMP) and granulocyte-macrophage progenitor (GMP) populations, producing a phenotype that is similar to acute myeloid leukemia (AML-M6). The disease phenotype is readily transplantable into secondary recipients. This is consistent with ex vivo clonogenicity assays, where p210 BCR/ABL preferentially supports the growth of colony forming unit (CFU)-granulocyte-macrophage (GM), whereas p190 BCR/ABL and the mutant preferentially support the growth of burst forming unit-erythroid (BFU-E). These results suggest that the GEF activity that distinguishes p210 BCR/ABL from p190 BCR/ABL actively regulates disease progression."xsd:string |
| http://purl.uniprot.org/citations/23207522 | http://purl.org/dc/terms/identifier | "doi:10.1038/leu.2012.351"xsd:string |
| http://purl.uniprot.org/citations/23207522 | http://purl.uniprot.org/core/author | "Chen R."xsd:string |
| http://purl.uniprot.org/citations/23207522 | http://purl.uniprot.org/core/author | "Hu T."xsd:string |
| http://purl.uniprot.org/citations/23207522 | http://purl.uniprot.org/core/author | "Williams D.A."xsd:string |
| http://purl.uniprot.org/citations/23207522 | http://purl.uniprot.org/core/author | "Whitehead I.P."xsd:string |
| http://purl.uniprot.org/citations/23207522 | http://purl.uniprot.org/core/author | "Fitzpatrick E.R."xsd:string |
| http://purl.uniprot.org/citations/23207522 | http://purl.uniprot.org/core/author | "Tala I."xsd:string |
| http://purl.uniprot.org/citations/23207522 | http://purl.uniprot.org/core/date | "2013"xsd:gYear |
| http://purl.uniprot.org/citations/23207522 | http://purl.uniprot.org/core/name | "Leukemia"xsd:string |
| http://purl.uniprot.org/citations/23207522 | http://purl.uniprot.org/core/pages | "1080-1089"xsd:string |
| http://purl.uniprot.org/citations/23207522 | http://purl.uniprot.org/core/title | "Contributions of the RhoGEF activity of p210 BCR/ABL to disease progression."xsd:string |
| http://purl.uniprot.org/citations/23207522 | http://purl.uniprot.org/core/volume | "27"xsd:string |
| http://purl.uniprot.org/citations/23207522 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/23207522 |
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