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dc.contributor.authorGutierrez-Berzal, Javier-
dc.contributor.authorCastellano, Esther-
dc.contributor.authorMartín-Encabo, Susana-
dc.contributor.authorGutiérrez-Cianca, N.-
dc.contributor.authorHernández, Jesús M.-
dc.contributor.authorSantos de Dios, Eugenio-
dc.contributor.authorGuerrero Arroyo, María del Carmen-
dc.identifierdoi: 10.1016/j.yexcr.2005.12.007-
dc.identifierissn: 0014-4827-
dc.identifier.citationExperimental Cell Research 312(6): 938-948 (2006)-
dc.description.abstractA novel C3G isoform, designated p87C3G, lacking the most amino terminal region of the cognate protein has been found to be overexpressed in two CML cell lines, K562 and Boff 210, both expressing Bcr-Abl p210. p87C3G expression is also highly augmented in patients diagnosed with chronic myeloid leukemia (CML) Ph+, in comparison with healthy individuals, and returns to basal levels after treatment with STI571. p87C3G coimmunoprecipitates with both CrkL and Bcr-Abl in CML cell lines and coimmunoprecipitation between p87C3G and Bcr-Abl was also detected in primary cells from CML patients. These interactions have been confirmed by in vitro pull down experiments. The interaction between p87C3G and Bcr-Abl involves the SH3-binding domain of p87C3G and the SH3 domain of Abl and depends mostly on the first polyproline region of p87C3G. Furthermore, we also demonstrated that p87C3G is phosphorylated in vitro by a Bcr-Abl-dependent mechanism. These results indicate that p87C3G overexpression is linked to CML phenotype and that p87C3G may exert productive functional interactions with Bcr-Abl signaling components suggesting the implication of this C3G isoform in the pathogenesis of chronic myeloid leukemia. © 2005 Elsevier Inc. All rights reserved.-
dc.description.sponsorshipThis work was supported by grants SA17/02 and SA013/02 from Junta de Castilla y León, SAF2003-04177 and GEN2003- 20239-C06-02 from the Spanish Ministry of Education, FISFEDER PI021570 and FIS-FEDER PI030651 from the Spanish Ministry of Health. J.G., E.C. and S.M.-E. are predoctoral fellows supported by the Spanish Ministry of Education. J.M.H. was supported by a Biomedicine Research Grant from Sacyl, Junta de Castilla y Leon, Spain. C.G. was supported by the Ramón y Cajal Program from the Spanish Ministry of Education.-
dc.titleCharacterization of p87C3G, a novel, truncated C3G isoform that is overexpressed in chronic myeloid leukemia and interacts with Bcr-Abl-
dc.description.versionPeer Reviewed-
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