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http://purl.uniprot.org/citations/12135666http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/12135666http://www.w3.org/2000/01/rdf-schema#comment"

Objective

BCR-ABL is a unique oncoprotein of which sole expression can cause cancer. A number of signaling molecules were shown to be activated by BCR-ABL. One of the important molecules that contributes to BCR-ABL-mediated cell proliferation is signal transducer and activator of transcription (STAT) 5. To elucidate the mechanism of BCR-ABL-mediated leukemogenesis, a role of pim-1, one of the important target genes of STAT5, was investigated.

Materials and methods

A temperature-sensitive mutant of p210(BCR-ABL) was introduced in interleukin-3-dependent murine hematopoietic cell line Ba/F3 cells, and downstream signaling after activation of BCR-ABL was investigated. Effects of the expression of a dominant-negative (dn) Pim-1 and a dn STAT5A in BCR-ABL-driven cell proliferation also were studied in Ba/F3 cells.

Results

We found that pim-1 was markedly up-regulated following activation of BCR-ABL tyrosine kinase with activation of STAT5. Overexpression of pim-1 alone induced cytokine-independent cell growth of Ba/F3 cells in a dose-dependent manner. However, expression of the dn Pim-1 did not affect growth of Ba/F3 cells transformed by BCR-ABL, whereas that of the dn STAT5A did suppress it.

Conclusion

Pim-1 is one of the redundant molecules that contributes to induction of autonomous cell growth and is dispensable for leukemogenesis by BCR-ABL."xsd:string
http://purl.uniprot.org/citations/12135666http://purl.org/dc/terms/identifier"doi:10.1016/s0301-472x(02)00808-1"xsd:string
http://purl.uniprot.org/citations/12135666http://purl.uniprot.org/core/author"Kitamura T."xsd:string
http://purl.uniprot.org/citations/12135666http://purl.uniprot.org/core/author"Nosaka T."xsd:string
http://purl.uniprot.org/citations/12135666http://purl.uniprot.org/core/date"2002"xsd:gYear
http://purl.uniprot.org/citations/12135666http://purl.uniprot.org/core/name"Exp Hematol"xsd:string
http://purl.uniprot.org/citations/12135666http://purl.uniprot.org/core/pages"697-702"xsd:string
http://purl.uniprot.org/citations/12135666http://purl.uniprot.org/core/title"Pim-1 expression is sufficient to induce cytokine independence in murine hematopoietic cells, but is dispensable for BCR-ABL-mediated transformation."xsd:string
http://purl.uniprot.org/citations/12135666http://purl.uniprot.org/core/volume"30"xsd:string
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