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http://purl.uniprot.org/citations/15122313http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/15122313http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/15122313http://www.w3.org/2000/01/rdf-schema#comment"Enforced expression of the antiapoptotic Bcl-2 family protein Mcl-1 promotes lymphomagenesis in the mouse; however, the functional role of Mcl-1 in human B-cell lymphoma remains unclear. We demonstrate that Mcl-1 is widely expressed in malignant B-cells, and high-level expression of Mcl-1 is required for B-lymphoma cell survival, since transfection of Mcl-1-specific antisense oligodeoxynucleotides was sufficient to promote apoptosis in Akata6 lymphoma cells. Mcl-1 was efficiently cleaved by caspases at evolutionarily conserved aspartic acid residues in vitro, and during cisplatin-induced apoptosis in B-lymphoma cell lines and spontaneous apoptosis of primary malignant B-cells. Overexpression of the Mcl-1 cleavage product that accumulated during apoptosis was sufficient to kill cells. Therefore, Mcl-1 is an essential survival molecule for B-lymphoma cells and is cleaved by caspases to a death-promoting molecule during apoptosis. In contrast to Mcl-1, Bcl-2 and Bcl-XL were relatively resistant to caspase cleavage in vitro and in intact cells. Interfering with Mcl-1 function appears to be an effective means of inducing apoptosis in Mcl-1-positive B-cell lymphoma, and the unique sensitivity of Mcl-1 to caspase-mediated cleavage suggests an attractive strategy for converting it to a proapoptotic molecule."xsd:string
http://purl.uniprot.org/citations/15122313http://purl.org/dc/terms/identifier"doi:10.1038/sj.onc.1207648"xsd:string
http://purl.uniprot.org/citations/15122313http://purl.org/dc/terms/identifier"doi:10.1038/sj.onc.1207648"xsd:string
http://purl.uniprot.org/citations/15122313http://purl.uniprot.org/core/author"Packham G."xsd:string
http://purl.uniprot.org/citations/15122313http://purl.uniprot.org/core/author"Packham G."xsd:string
http://purl.uniprot.org/citations/15122313http://purl.uniprot.org/core/author"Marcusson E.G."xsd:string
http://purl.uniprot.org/citations/15122313http://purl.uniprot.org/core/author"Marcusson E.G."xsd:string
http://purl.uniprot.org/citations/15122313http://purl.uniprot.org/core/author"Zhang K.Y.J."xsd:string
http://purl.uniprot.org/citations/15122313http://purl.uniprot.org/core/author"Zhang K.Y.J."xsd:string
http://purl.uniprot.org/citations/15122313http://purl.uniprot.org/core/author"O'Neill J.W."xsd:string
http://purl.uniprot.org/citations/15122313http://purl.uniprot.org/core/author"O'Neill J.W."xsd:string
http://purl.uniprot.org/citations/15122313http://purl.uniprot.org/core/author"Brimmell M."xsd:string
http://purl.uniprot.org/citations/15122313http://purl.uniprot.org/core/author"Brimmell M."xsd:string
http://purl.uniprot.org/citations/15122313http://purl.uniprot.org/core/author"Craig R.W."xsd:string
http://purl.uniprot.org/citations/15122313http://purl.uniprot.org/core/author"Craig R.W."xsd:string
http://purl.uniprot.org/citations/15122313http://purl.uniprot.org/core/author"Dallman C.L."xsd:string
http://purl.uniprot.org/citations/15122313http://purl.uniprot.org/core/author"Dallman C.L."xsd:string
http://purl.uniprot.org/citations/15122313http://purl.uniprot.org/core/author"Habens F."xsd:string
http://purl.uniprot.org/citations/15122313http://purl.uniprot.org/core/author"Habens F."xsd:string
http://purl.uniprot.org/citations/15122313http://purl.uniprot.org/core/author"Johnson P.W.M."xsd:string
http://purl.uniprot.org/citations/15122313http://purl.uniprot.org/core/author"Johnson P.W.M."xsd:string
http://purl.uniprot.org/citations/15122313http://purl.uniprot.org/core/author"Michels J."xsd:string
http://purl.uniprot.org/citations/15122313http://purl.uniprot.org/core/author"Michels J."xsd:string