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Originally published In Press as doi:10.1074/jbc.M011209200 on March 26, 2001
J. Biol. Chem., Vol. 276, Issue 23, 20340-20345, June 8, 2001
Control of Cystic Fibrosis Transmembrane Conductance
Regulator Expression by BAP31*
Georg
Lambert §,
Bernd
Becker¶§,
Rainer
Schreiber ,
Anissa
Boucherot ,
Michael
Reth**, and
Karl
Kunzelmann 
From the Physiologisches Institut, Universität
Zürich Irchel, CH-8057 Zürich, Switzerland, the
¶ Uni-Klinik Regensburg, Department of Dermatology, 93052 Regensburg, Germany, the Department of Physiology & Pharmacology, University of Queensland, St. Lucia, QLD 4072, Brisbane,
Australia, and the ** Department of Molecular Immunology, Biology III,
University of Freiburg, and Max-Planck-Institut für
Immunobiologie, Freiburg, Germany
Expression of the cystic fibrosis
transmembrane conductance regulator (CFTR) is stringently
controlled by molecular chaperones participating in formation of the
quality control system. It has been shown that about 75% of all CFTR
protein and close to 100% of the
[ Phe508] CFTR variant are rapidly degraded
before leaving the endoplasmic reticulum (ER). B cell antigen
receptor-associated proteins (BAPs) are ubiquitously expressed
integral membrane proteins that may control association with the
cytoskeleton, vesicular transport, or retrograde transport from the
cis Golgi to the ER. The present study delivers evidence
for cytosolic co-localization of both BAP31 and CFTR and for the
control of expression of recombinant CFTR in Chinese hamster ovary
(CHO) cells and Xenopus oocytes by BAP31. Antisense
inhibition of BAP31 in various cell types increased expression of both
wild-type CFTR and [ Phe508]CFTR and enabled
cAMP-activated Cl currents in
[ Phe508]CFTR-expressing CHO cells. Coexpression of
CFTR together with BAP31 attenuated cAMP-activated Cl
currents in Xenopus oocytes. These data therefore
suggest association of BAP31 with CFTR that may control maturation or
trafficking of CFTR and thus expression in the plasma membrane.
*
This work was supported by DFG Ku756/4-1, Mukoviszidose
e.V., ARC 00/ARCS243, Cystic Fibrosis Australia, and DFG SFB 388.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.
§
These authors contributed equally to the present work.

To whom correspondence should be addressed. Tel.: 61 07 3365 4104; Fax: 61 07 3365 1766; E-mail: kunzelmann@plpk.uq.edu.au.
Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.

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Copyright © 2001 by the American Society for Biochemistry and Molecular Biology.
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