UNSPECIFIED (2000) CD40 ligand, Bcl-2, and Bcl-x(L) spare group I Burkitt lymphoma cells from CD77-directed killing via Verotoxin-1 B chain but fail to protect against the holotoxin. CELL DEATH AND DIFFERENTIATION, 7 (9). pp. 785-794. ISSN 1350-9047

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Abstract

Owing to its lineage and differentiation stage-restricted expression, CD77 has been mooted as a therapeutic target in Burkitt lymphoma (BL). The recognition that the globotriaosyl moiety of this neutral glycosphingolipid is a receptor for Escherichia coli derived Verotoxin-1 (Shiga-Like Toxin-1) offers a potential delivery system for the attack, Here we show that CD77-expressing Group I BL cells which are normally susceptible to activation-induced death on binding Verotoxin-1 B chain are protected in the presence of CD40 ligand, Ectopic expression of either bcl-2 or bcl-x(L) also afforded resistance to the actions of the B chain. In total contrast, neither of the survival genes nor a CD40 signal - even when acting in concert - protected against killing mediated by the holotoxin. These findings indicate that while therapeutic modalities for CD77-expressing B cell tumors (which include follicular lymphoma) based on the use of Verotoxin-1 B chain might be compromised by the activation of endogenous or exogenous survival pathways, those exploiting the holotoxin should be left unscathed.

Item Type:	Journal Article
Subjects:	Q Science > QD Chemistry Q Science > QH Natural history > QH301 Biology
Journal or Publication Title:	CELL DEATH AND DIFFERENTIATION
Publisher:	NATURE PUBLISHING GROUP
ISSN:	1350-9047
Date:	September 2000
Volume:	7
Number:	9
Number of Pages:	10
Page Range:	pp. 785-794
Publication Status:	Published
URI:	http://wrap.warwick.ac.uk/id/eprint/13027

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