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http://purl.uniprot.org/citations/22039307http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/22039307http://www.w3.org/2000/01/rdf-schema#comment"Treatment of hematopoietic malignancies often requires allogeneic bone marrow transplantation, and the subsequent graft-versus-leukemia response is crucial for the elimination of malignant cells. Cytotoxic T lymphocytes and NK cells responsible for the immunoelimination express Fas ligand and strongly rely on the induction of Fas receptor-mediated apoptosis for their action. Although cancer cells are removed successfully by graft-versus-leukemia reactions in myeloid malignancies, their efficiency is low in T cell leukemias. This may be partially because of the ability of malignant T cells to escape apoptosis. Our work shows that Eph family receptor EphB3 is consistently expressed by malignant T lymphocytes, most frequently in combination with EphB6, and that stimulation with their common ligands, ephrin-B1 and ephrin-B2, strongly suppresses Fas-induced apoptosis in these cells. This effect is associated with Akt activation and with the inhibition of the Fas receptor-initiated caspase proteolytic cascade. Akt proved to be crucial for the prosurvival response, because inhibition of Akt, but not of other molecules central to T cell biology, including Src kinases, MEK1 and MEK2, blocked the antiapoptotic effect. Overall, this demonstrates a new role for EphB receptors in the protection of malignant T cells from Fas-induced apoptosis through Akt engagement and prevention of caspase activation. Because Fas-triggered apoptosis is actively involved in the graft-versus-leukemia response and cytotoxic T cells express ephrin-Bs, our observations suggest that EphB receptors are likely to support immunoevasivenes of T cell malignancies and may represent promising targets for therapies, aiming to enhance immunoelimination of cancerous T cells."xsd:string
http://purl.uniprot.org/citations/22039307http://purl.org/dc/terms/identifier"doi:10.4049/jimmunol.1003482"xsd:string
http://purl.uniprot.org/citations/22039307http://purl.uniprot.org/core/author"Xiang J."xsd:string
http://purl.uniprot.org/citations/22039307http://purl.uniprot.org/core/author"Dean J."xsd:string
http://purl.uniprot.org/citations/22039307http://purl.uniprot.org/core/author"Narendran A."xsd:string
http://purl.uniprot.org/citations/22039307http://purl.uniprot.org/core/author"Weng A."xsd:string
http://purl.uniprot.org/citations/22039307http://purl.uniprot.org/core/author"Freywald A."xsd:string
http://purl.uniprot.org/citations/22039307http://purl.uniprot.org/core/author"Napper S."xsd:string
http://purl.uniprot.org/citations/22039307http://purl.uniprot.org/core/author"Freywald T."xsd:string
http://purl.uniprot.org/citations/22039307http://purl.uniprot.org/core/author"Truitt L."xsd:string
http://purl.uniprot.org/citations/22039307http://purl.uniprot.org/core/author"Arsenault R."xsd:string
http://purl.uniprot.org/citations/22039307http://purl.uniprot.org/core/author"Allonby O."xsd:string
http://purl.uniprot.org/citations/22039307http://purl.uniprot.org/core/author"Maddigan A."xsd:string
http://purl.uniprot.org/citations/22039307http://purl.uniprot.org/core/date"2011"xsd:gYear
http://purl.uniprot.org/citations/22039307http://purl.uniprot.org/core/name"J Immunol"xsd:string
http://purl.uniprot.org/citations/22039307http://purl.uniprot.org/core/pages"5983-5994"xsd:string
http://purl.uniprot.org/citations/22039307http://purl.uniprot.org/core/title"EphB receptors trigger Akt activation and suppress Fas receptor-induced apoptosis in malignant T lymphocytes."xsd:string
http://purl.uniprot.org/citations/22039307http://purl.uniprot.org/core/volume"187"xsd:string
http://purl.uniprot.org/citations/22039307http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/22039307
http://purl.uniprot.org/citations/22039307http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/22039307
http://purl.uniprot.org/uniprot/#_A0A0G2JNC5-mappedCitation-22039307http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22039307
http://purl.uniprot.org/uniprot/#_O15197-mappedCitation-22039307http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22039307
http://purl.uniprot.org/uniprot/#_F8WCM8-mappedCitation-22039307http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22039307
http://purl.uniprot.org/uniprot/#_J3KQU5-mappedCitation-22039307http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22039307