The Human gC1qR/p32 Gene, C1qBP
GENOMIC ORGANIZATION AND PROMOTER ANALYSIS*
Angela J.
Tye
,
Berhane
Ghebrehiwet§,
Ning
Guo¶,
Kedarnath
N.
Sastry¶,
Billy K. C.
Chow
,
Ellinor I. B.
Peerschke
, and
Boon-Leong
Lim***
Department of Zoology, University of Hong Kong,
Pokfulam, Hong Kong, China, § Department of Medicine,
State University of New York, Stony Brook, New York, 11794-8161, ¶ Department of Pathology, Weill College of Medicine, Cornell
University, New York, New York 10021, and
Department of
Pathology and Laboratory Medicine, Boston University School of
Medicine, Boston, Massachusetts 02118
gC1qR is an ubiquitously expressed cell
protein that interacts with the globular heads of C1q (gC1q) and many
other ligands. In this study, the 7.8-kilobase pair (kb) human
gC1qR/p32 (C1qBP) gene was cloned and found to consist of 6 exons and 5 introns. Analysis of a 1.3-kb DNA fragment at the
5'-flanking region of this gene revealed the presence of multiple TATA,
CCAAT, and Sp1 binding sites. Luciferase reporter assays performed in
different human cell lines demonstrated that the reporter gene was
ubiquitously driven by this 1.3-kb fragment. Subsequent 5' and 3'
deletion of this fragment confined promoter elements to within 400 base pairs (bp) upstream of the translational start site. Because the removal of the 8-bp consensus TATATATA at
399 to
406 and
CCAAT at
410 to
414 did not significantly affect the transcription efficiency of the promoter, GC-rich sequences between this TATA box and
the translation start site may be very important for the promoter
activity of the C1qBP gene. One of seven GC-rich sequences in this region binds specifically to PANC-1 nuclear extracts, and the
transcription factor Sp1 was shown to bind to this GC-rich sequence by
the supershift assay. Primer extension analysis mapped three major
transcription start regions. The farthest transcription start site is
49 bp upstream of the ATG translation initiation codon and is in close
proximity of the specific SP1 binding site.
*
This work was supported in part by Grants
RGC HKU198/95 from the Hong Kong Research Grant Council (to
B-L. L.) and RPG-95068-04-CIM from the American Cancer Society (to
B. G.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section
1734 solely to indicate this fact.