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Molecular and Cellular Biology, February 2000, p. 1227-1233, Vol. 20, No. 4
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
The B-Cell-Specific src-Family Kinase Blk Is
Dispensable for B-Cell Development and Activation
Gemma
Texido,1,
I-hsin
Su,2
Ingrid
Mecklenbräuker,2
Kaoru
Saijo,2
Sami N.
Malek,3
Stephen
Desiderio,3
Klaus
Rajewsky,1 and
Alexander
Tarakhovsky2,*
Department of
Immunology1 and Laboratory of Lymphocyte
Signaling,2 Institute for Genetics,
University of Köln, D-50931 Cologne, Germany, and
Department of Molecular Biology and Genetics, Howard Hughes
Medical Institute, The Johns Hopkins University School of Medicine,
Baltimore, Maryland 212053
Received 5 August 1999/Returned for modification 15 September
1999/Accepted 12 November 1999
The B-cell lymphocyte kinase (Blk) is a src-family protein tyrosine
kinase specifically expressed in B-lineage cells of mice. The early
onset of Blk expression during B-cell development in the bone marrow
and the high expression levels of Blk in mature B cells suggest a
possible important role of Blk in B-cell physiology. To study the in
vivo function of Blk, mice homozygous for the targeted disruption of
the blk gene were generated. In homozygous mutant mice,
neither blk mRNA nor Blk protein is expressed. Despite the
absence of Blk, the development, in vitro activation, and humoral
immune responses of B cells to T-cell-dependent and -independent antigens are unaltered. These data are consistent with functional redundancy of Blk in B-cell development and immune responses.
*
Corresponding author. Mailing address: Laboratory of
Lymphocyte Signaling, Institute for Genetics, University of Köln,
Weyertal 121, D-50931 Cologne, Germany. Phone: 49-221-470 3419. Fax:
49-221-470 4970. E-mail:
sasha{at}mac.genetik.uni-koeln.de.

Present address: EMBL, D-69117 Heidelberg,
Germany.
Molecular and Cellular Biology, February 2000, p. 1227-1233, Vol. 20, No. 4
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
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