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dc.contributor.authorYunta, M.-
dc.contributor.authorLazo, Pedro A.-
dc.date.accessioned2008-09-01T17:38:35Z-
dc.date.available2008-09-01T17:38:35Z-
dc.date.issued2003-
dc.identifier.citationOncogene 22: 1219-1224 (2003)en_US
dc.identifier.urihttp://hdl.handle.net/10261/7044-
dc.description.abstractThe CD53 antigen is a tetraspanin protein of the lymphoid–myeloid lineage, but its implication in biological effects is hardly known. Radioresistant tumor cells express very high levels of this antigen. We have studied the effect of CD53 antigen ligation on the survival response of tumor cells to serum deprivation, a wellknown stimulator of cell death that may mimic the tumor environment; for this aim IR938F and Jurkat cells, a Band T-cell lymphoma, were used. Ligation of CD53 triggers a survival response and reduces the number of cells that enter apoptosis. In CD53- stimulated cells there is a significant reduction in caspase activation, measured by caspase processing of poly ADP-ribose polymerase, as well as a reduction in the fragmentation of DNA. CD53- stimulated cells also have an increase in the level of bcl-XL and a reduction of bax protein, two components of the mitochondrial apoptotic pathway, changing their ratio by 24-fold in the direction of survival. This survival signal appears to be mediated by activation of the AKT, as detected by its phosphorylation in Ser473 upon CD53 ligation. The CD53 antigen interactions might contribute to cell survival in poorly vascularized regions of the tumor mass.en_US
dc.description.sponsorshipThis work was supported by grants from Ministerio de Ciencia y Tecnologı´a (SAF2000/0169), Junta de Castilla y Leo´ n (CSI1/ 01) and Fondo de Investigacio´ n Sanitaria (FIS-PI02-0585)en_US
dc.format.extent245964 bytes-
dc.format.mimetypeapplication/pdf-
dc.language.isoengen_US
dc.publisherNature Publishing Groupen_US
dc.rightsclosedAccessen_US
dc.subjectCD53en_US
dc.subjectapoptosisen_US
dc.titleApoptosis protection and survival signal by the CD53 antigenen_US
dc.typeartículoen_US
dc.description.peerreviewedPeer revieweden_US
Appears in Collections:(IBMCC) Artículos
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