Molecular and Cellular Biology, May 2001, p. 3206-3219, Vol. 21, No. 9
0270-7306/01/$04.00+0 DOI: 10.1128/MCB.21.9.3206-3219.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Department of Cell Biology and Physiology,1 Department of Molecular Biology and Pharmacology,2 Department of Pathology and Immunology,3 Department of Genetics,4 Howard Hughes Medical Institute,5 and Department of Medicine,6 Washington University School of Medicine, St. Louis, Missouri 63110-1093
Received 22 November 2000/Returned for modification 3 January 2001/Accepted 26 January 2001
Emk is a serine/threonine protein kinase implicated in regulating
polarity, cell cycle progression, and microtubule dynamics. To
delineate the role of Emk in development and adult tissues, mice
lacking Emk were generated by targeted gene disruption.
Emk
/
mice displayed growth retardation and
immune cell dysfunction. Although B- and T-cell development were
normal, CD4+T cells lacking Emk exhibited a
marked upregulation of the memory marker CD44/pgp-1 and produced more
gamma interferon and interleukin-4 on stimulation through the T-cell
receptor in vitro. In addition, B-cell responses to T-cell-dependent
and -independent antigen challenge were altered in vivo. As
Emk
/
animals aged, they developed
splenomegaly, lymphadenopathy, membranoproliferative glomerulonephritis, and lymphocytic infiltrates in the lungs, parotid
glands and kidneys. Taken together, these results demonstrate that the
Emk protein kinase is essential for maintaining immune system
homeostasis and that loss of Emk may contribute to autoimmune disease
in mammals.
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