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(Received for publication, December 22, 1995, and in revised form, March 12, 1996)
From the The genetic elements and regulatory mechanisms
responsible for human interleukin 9 (IL-9) gene expression in a human T
cell leukemia virus type I-transformed human T cell line, C5MJ2, were
investigated. We demonstrated that IL-9 gene expression is controlled,
at least in part, by transcriptional activation. Transient expression
of the luciferase reporter gene linked to serially deleted sequences of
the 5
Volume 271, Number 26,
Issue of June 28, 1996
pp. 15815-15822
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.
§
,
,§¶
Walther Oncology Center,
§ Department of Medicine (Hematology/Oncology), and
¶ Department of Biochemistry/Molecular Biology, Indiana
University School of Medicine, Indianapolis, Indiana 46202 and the
Biological Carcinogenis and Development Program, SAIC/Frederick,
NCI-Frederick Cancer Research and Development Center,
Frederick, Maryland 21702-1201
-flanking region of the IL-9 gene has revealed several positive
and negative regulatory elements involved in the basal and inducible
expression of the IL-9 gene in C5MJ2 cells. An AP-1 site at 
146 to
140 was shown to be involved in the expression of the IL-9 gene. A
proximal region between 46 and 80 was identified as the minimum
sequence for the basal and inducible expression of the IL-9 gene in
C5MJ2 cells. Within this region, an NF-
B site at 59 to 50 and
its adjacent 20-base pair upstream sequence were demonstrated to play a
critical role for the IL-9 promoter activity. DNA-protein binding
studies indicated that NF-B, c-Jun, and potentially novel proteins
(around 35 kDa) can bind to this important sequence. Mutations at
different sites within this proximal promoter region abolished the
promoter activity as well as the DNA binding. Taken together, these
results suggest that the cooperation of different transcription factors
is essential for IL-9 gene expression in T cells.
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