Journal article

Deletion of cIAP1 and cIAP2 in murine B lymphocytes constitutively activates cell survival pathways and inactivates the germinal center response

Sandra Gardam, Vivian M Turner, Holly Anderton, Sandhya Limaye, Antony Basten, Frank Koentgen, David L Vaux, John Silke, Robert Brink

BLOOD | AMER SOC HEMATOLOGY | Published : 2011

Abstract

B cells require signals delivered through B-cell activating factor of the TNF family receptor (BAFF-R) and CD40 to survive and produce antibody responses in vivo. In vitro data indicate that these signals are controlled by the homologous RING finger proteins cIAP1 and cIAP2, in collaboration with TRAF2 and TRAF3. There is also mounting evidence that all 4 of these signaling molecules can act as tumor suppressors in human B-lineage malignancies. However, it has not been possible to identify the roles of cIAP1 and cIAP2 in controlling B-cell physiology because of the absence of an appropriate in vivo model. Here we describe a unique genetically modified mouse in which the linked cIap1 and cIap..

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Grants

Awarded by National Health and Medical Research Council of Australia


Funding Acknowledgements

This work was supported by the National Health and Medical Research Council of Australia (program grant 427620, A. B., R. B.; project grants 433013, 541901, and 541902, J.S.; and project grants 384404 and 433063, D. L. V.) as well as a Leukemia & Lymphoma Society Center (D. L. V.). S. G. was supported by a National Health and Medical Research Council Postgraduate Research Scholarship. V. M. T. was supported by an Australian Postgraduate Research Award and Cancer Institute of NSW Award. J.S. and R. B. were supported by National Health and Medical Research Council Senior Research Fellowships.