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Originally published In Press as doi:10.1074/jbc.M203149200 on May 7, 2002
J. Biol. Chem., Vol. 277, Issue 27, 24835-24841, July 5, 2002
The Selective Regulation of
V 1 Integrin Expression Is Based on the
Hierarchical Formation of V-containing Heterodimers*
Pekka
Koistinen § and
Jyrki
Heino ¶
From the MediCity Research Laboratory and the
Department of Medical Biochemistry, § Turku Graduate School
of Biomedical Sciences, University of Turku, FIN-20520 Turku and
the ¶ Department of Biology, University of Jyväskylä,
FIN-40351 Jyväskylä, Finland
The integrin 1 subunit can
form a heterodimer with 12 different subunits. According to the
present model, the expression level of any  complex is regulated
by the availability of the specific subunit, whereas
1 subunit is constantly present in a large excess. The
expression of several heterodimers containing the V
subunit seems to be regulated by an identical mechanism. The fact that
many cells express V 1 heterodimer, and
that this fibronectin/vitronectin receptor may be selectively
regulated, compromises the present model of the regulation of
1 and V integrins. We have tried to solve
this problem by assuming that distinct  heterodimers are formed
with different tendency. To test the hypothesis, we analyzed WM-266-4
melanoma cells transfected with a cDNA construct coding for an
intracellular single-chain anti- V integrin antibody. We
could see 70-80% reduction in the cell surface expression of
V subunit. However, the only one of the V
integrins reduced on the cell surface was
V 1. This suggests that the cell surface
expression level of V 1 is dependent on
the number of V subunits available after the formation
of other V-containing heterodimers. Thus, there seems to
be a hierarchy in the complex formation between V and
its different -partners. These observations explain how
V 1 can be specifically regulated without
concomitant changes in the expression of other V or
1 integrins.
*
This work was supported by grants from the Academy of
Finland, the Finnish Cancer Association, and the Sigrid Jusélius
Foundation (Finland), and by a fellowship (to P. K.) from the
Foundation for the Finnish Cancer Institute.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.
To whom correspondence should be addressed: Dept. of
Biological and Environmental Science, University of
Jyväskylä, P. O. Box 35, FIN-40351 Jyväskylä,
Finland. Tel.: 358-14-2602240; Fax: 358-14-2602271; E-mail:
jyrki.heino@utu.fi.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.

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Copyright © 2002 by the American Society for Biochemistry and Molecular Biology.
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