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http://purl.uniprot.org/citations/14751929http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/14751929http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/14751929http://www.w3.org/2000/01/rdf-schema#comment"Ahi-1/AHI-1 (Abelson helper integration site-1) encodes a family of protein isoforms containing one Src homology 3 (SH3) domain and multiple tryptophan-aspartic acid 40 (WD40)-repeat domains. The function of these proteins is unknown, but involvement in leukemogenesis has been suggested by the high frequency of Ahi-1 mutations seen in certain virus-induced murine leukemias. Here we show that in both mice and humans, Ahi-1/AHI-1 expression is highest in the most primitive hematopoietic cells with specific patterns of down-regulation in different lineages. Cells from patients with chronic myeloid leukemia (CML; n = 28) show elevated AHI-1 transcripts in all disease phases and, in chronic phase, in the leukemic cells at all stages of differentiation, including quiescent (G(0)) CD34(+) cells as well as terminally differentiating cells. In the most primitive lin(-)CD34(+)CD38(-) CML cells, transcripts for the 2 shorter isoforms of AHI-1 are also increased. Although 15 of 16 human lymphoid and myeloid leukemic cell lines showed aberrant control of AHI-1 expression, this was not seen in blasts obtained directly from patients with acute Philadelphia chromosome-negative (Ph(-)) leukemia (n = 15). Taken together, our results suggest that down-regulation of AHI-1 expression is an important conserved step in primitive normal hematopoietic cell differentiation and that perturbations in AHI-1 expression may contribute to the development of specific types of human leukemia."xsd:string
http://purl.uniprot.org/citations/14751929http://purl.org/dc/terms/identifier"doi:10.1182/blood-2003-11-4026"xsd:string
http://purl.uniprot.org/citations/14751929http://purl.org/dc/terms/identifier"doi:10.1182/blood-2003-11-4026"xsd:string
http://purl.uniprot.org/citations/14751929http://purl.uniprot.org/core/author"Jiang X."xsd:string
http://purl.uniprot.org/citations/14751929http://purl.uniprot.org/core/author"Jiang X."xsd:string
http://purl.uniprot.org/citations/14751929http://purl.uniprot.org/core/author"Kennedy S."xsd:string
http://purl.uniprot.org/citations/14751929http://purl.uniprot.org/core/author"Kennedy S."xsd:string
http://purl.uniprot.org/citations/14751929http://purl.uniprot.org/core/author"Zhao Y."xsd:string
http://purl.uniprot.org/citations/14751929http://purl.uniprot.org/core/author"Zhao Y."xsd:string
http://purl.uniprot.org/citations/14751929http://purl.uniprot.org/core/author"Chan W.-Y."xsd:string
http://purl.uniprot.org/citations/14751929http://purl.uniprot.org/core/author"Chan W.-Y."xsd:string
http://purl.uniprot.org/citations/14751929http://purl.uniprot.org/core/author"Eaves A."xsd:string
http://purl.uniprot.org/citations/14751929http://purl.uniprot.org/core/author"Eaves A."xsd:string
http://purl.uniprot.org/citations/14751929http://purl.uniprot.org/core/author"Eaves C."xsd:string
http://purl.uniprot.org/citations/14751929http://purl.uniprot.org/core/author"Eaves C."xsd:string
http://purl.uniprot.org/citations/14751929http://purl.uniprot.org/core/author"Nicolini F."xsd:string
http://purl.uniprot.org/citations/14751929http://purl.uniprot.org/core/author"Nicolini F."xsd:string
http://purl.uniprot.org/citations/14751929http://purl.uniprot.org/core/author"Pang E."xsd:string
http://purl.uniprot.org/citations/14751929http://purl.uniprot.org/core/author"Pang E."xsd:string
http://purl.uniprot.org/citations/14751929http://purl.uniprot.org/core/author"Vercauteren S."xsd:string
http://purl.uniprot.org/citations/14751929http://purl.uniprot.org/core/author"Vercauteren S."xsd:string
http://purl.uniprot.org/citations/14751929http://purl.uniprot.org/core/date"2004"xsd:gYear
http://purl.uniprot.org/citations/14751929http://purl.uniprot.org/core/date"2004"xsd:gYear