|
|
|
|
|
|
|
||
J. Exp. Med.,
Volume 187, Number 7, April 6, 1998 973-984
By
From the * Department of Oncology, Bristol-Myers Squibb Pharmaceutical Research Institute,
Princeton, New Jersey 08543-4000; the The c-rel protooncogene encodes a member of the Rel/nuclear factor (NF)- Department of Microbiology, Bristol-Myers Squibb
Pharmaceutical Research Institute,Wallingford, Connecticut 06492; and the § Department of
Pathology, Uniformed Services, University of Health Sciences, Bethesda, Maryland 20814
B family of transcriptional factors. To assess the role of the transcriptional activation domain of c-Rel in vivo, we generated mice expressing a truncated c-Rel (
c-Rel) that lacks the COOH-terminal region, but retains a functional Rel homology domain. Mice with an homozygous mutation in
the c-rel region encoding the COOH terminus of c-Rel (c-rel
CT/CT) display marked defects
in proliferative and immune functions. c-relCT/CT animals present histopathological alterations
of hemopoietic tissues, such as an enlarged spleen due to lymphoid hyperplasia, extramedullary
hematopoiesis, and bone marrow hypoplasia. In older c-relCT/CT mice, lymphoid hyperplasia
was also detected in lymph nodes, liver, lung, and stomach. These animals present a more severe phenotype than mice lacking the entire c-Rel protein. Thus, in c-relCT/CT mice, the lack
of c-Rel activity is less efficiently compensated by other NF-B proteins.
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
| TABLE OF CONTENTS |
|
