| http://purl.uniprot.org/citations/18172310 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/18172310 | http://www.w3.org/2000/01/rdf-schema#comment | "PAX5 is a transcription factor essential for B-cell development. Recently, it has been found as a frequent target of aberrancies in childhood acute lymphoblastic leukemia (ALL; 30% of B cell ALL cases), showing monoallelic loss, point mutations, or chromosomal translocations. The role of these aberrancies is still poorly understood. We previously cloned the PAX5/TEL fusion gene in a patient affected by B-cell precursor ALL with a t(9;12) translocation. This is the first report investigating the molecular and functional roles of PAX5/TEL protein in vitro from murine wild-type pre-BI cells. We showed that PAX5/TEL protein acts as an aberrant transcription factor with repressor function, recruiting mSin3A, down-regulating B220, CD19, BLNK, MB-1, FLT3, and mu heavy chain expression, thus suggesting a block on B-cell differentiation. In a PAX5-deficient context, the presence of PAX5/TEL did not replace PAX5 functions. PAX5/TEL protein enhances cell migration towards CXCL12, with the overexpression of CXCR4. Moreover, the presence of the fusion gene overcomes interleukin-7 withdrawal and interferes with transforming growth factor-beta1 pathway, inducing resistance and conferring cells an advantage in proliferation and survival. Thus, in vitro, the PAX5/TEL protein has a dominant effect on wild-type PAX5, interferes with the process of B-cell differentiation and migration, and induces resistance to apoptosis. Taken together, these phenomena likely represent key events in the process of B-cell transformation."xsd:string |
| http://purl.uniprot.org/citations/18172310 | http://purl.org/dc/terms/identifier | "doi:10.1158/0008-5472.can-07-2778"xsd:string |
| http://purl.uniprot.org/citations/18172310 | http://purl.uniprot.org/core/author | "Cazzaniga G."xsd:string |
| http://purl.uniprot.org/citations/18172310 | http://purl.uniprot.org/core/author | "Biondi A."xsd:string |
| http://purl.uniprot.org/citations/18172310 | http://purl.uniprot.org/core/author | "Fazio G."xsd:string |
| http://purl.uniprot.org/citations/18172310 | http://purl.uniprot.org/core/author | "Rolink A."xsd:string |
| http://purl.uniprot.org/citations/18172310 | http://purl.uniprot.org/core/author | "Palmi C."xsd:string |
| http://purl.uniprot.org/citations/18172310 | http://purl.uniprot.org/core/date | "2008"xsd:gYear |
| http://purl.uniprot.org/citations/18172310 | http://purl.uniprot.org/core/name | "Cancer Res"xsd:string |
| http://purl.uniprot.org/citations/18172310 | http://purl.uniprot.org/core/pages | "181-189"xsd:string |
| http://purl.uniprot.org/citations/18172310 | http://purl.uniprot.org/core/title | "PAX5/TEL acts as a transcriptional repressor causing down-modulation of CD19, enhances migration to CXCL12, and confers survival advantage in pre-BI cells."xsd:string |
| http://purl.uniprot.org/citations/18172310 | http://purl.uniprot.org/core/volume | "68"xsd:string |
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