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    Phosphoinositide phosphatase SHIP-1 regulates apoptosis induced by edelfosine, Fas ligation and DNA damage in mouse lymphoma cells.

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    Authors
    Alderliesten, M
    Klarenbeek, J
    van der Luit, A
    van Lummel, M
    Jones, David R
    Zerp, S
    Divecha, Nullin
    Verheij, M
    van Blitterswijk, W
    Affiliation
    Division of Cell Biology (B5), The Netherlands Cancer Institute/Antoni van Leeuwenhoek Hospital, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands.
    Issue Date
    2011-11-15
    
    Metadata
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    Abstract
    S49 mouse lymphoma cells undergo apoptosis in response to the ALP (alkyl-lysophospholipid) edelfosine (1-O-octadecyl-2-O-methyl-rac-glycero-3-phosphocholine), FasL (Fas ligand) and DNA damage. S49 cells made resistant to ALP (S49(AR)) are defective in sphingomyelin synthesis and ALP uptake, and also have acquired resistance to FasL and DNA damage. However, these cells can be re-sensitized following prolonged culturing in the absence of ALP. The resistant cells show sustained ERK (extracellular-signal-regulated kinase)/Akt activity, consistent with enhanced survival signalling. In search of a common mediator of the observed cross-resistance, we found that S49(AR) cells lacked the PtdIns(3,4,5)P(3) phosphatase SHIP-1 [SH2 (Src homology 2)-domain-containing inositol phosphatase 1], a known regulator of the Akt survival pathway. Re-sensitization of the S49(AR) cells restored SHIP-1 expression as well as phosphoinositide and sphingomyelin levels. Knockdown of SHIP-1 mimicked the S49(AR) phenotype in terms of apoptosis cross-resistance, sphingomyelin deficiency and altered phosphoinositide levels. Collectively, the results of the present study suggest that SHIP-1 collaborates with sphingomyelin synthase to regulate lymphoma cell death irrespective of the nature of the apoptotic stimulus.
    Citation
    Phosphoinositide phosphatase SHIP-1 regulates apoptosis induced by edelfosine, Fas ligation and DNA damage in mouse lymphoma cells. 2011, 440 (1):127-35 Biochem J
    Journal
    The Biochemical Journal
    URI
    http://hdl.handle.net/10541/213552
    DOI
    10.1042/BJ20110125
    PubMed ID
    21793801
    Type
    Article
    Language
    en
    ISSN
    1470-8728
    ae974a485f413a2113503eed53cd6c53
    10.1042/BJ20110125
    Scopus Count
    Collections
    All Paterson Institute for Cancer Research

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