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J. Biol. Chem., Vol. 278, Issue 4, 2669-2676, January 24, 2003
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From the Research and Education Center for Genetic Information,
Nara Institute of Science and Technology, 8916-5 Takayama, Ikoma,
Nara 630-0101, Japan
Several endoplasmic reticulum (ER)-resident
luminal proteins have a characteristic ER retrieval signal, KDEL, or
its variants at their C terminus. Our previous work searching EST
databases for proteins containing the C-terminal KDEL motif predicted
some novel murine proteins, one of which designated JPDI
(J-domain-containing protein
disulfide isomerase-like protein) is
characterized in this study. The primary structure of JPDI is unique,
because in addition to a J-domain motif adjacent to the N-terminal
translocation signal sequence, four thioredoxin-like motifs were found
in a single polypeptide. As examined by Northern blotting, the
expression of JPDI was essentially ubiquitous in tissues and almost
independent of ER stress. A computational prediction that JPDI is an
ER-resident luminal protein was experimentally supported by
immunofluorescent staining of epitope-tagged JPDI-expressing cells
together with glycosylation and protease protection studies of this
protein. JPDI probably acts as a DnaJ-like partner of BiP, because a
recombinant protein carrying the J-domain of JPDI associated with BiP
in an ATP-dependent manner and enhanced its ATPase
activity. We speculate that for the folding of some proteins in the ER,
chaperoning by BiP and formation of proper disulfide bonds may
synchronously occur in a JPDI-dependent manner.
JPDI, a Novel Endoplasmic Reticulum-resident Protein Containing
Both a BiP-interacting J-domain and Thioredoxin-like Motifs*
*
This work was supported in part by grants-in-aid for
Scientific Research (to K. K. and A. T.), Encouragement of Young
Scientists (Y. K.), and Scientific Research on Priority Areas (K. K.)
from the Ministry of Education, Culture, Sports, Science and Technology of Japan and by grants from Novartis Foundation and Yamada Science Foundation.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: Research and Education
Center for Genetic Information, Nara Institute of Science and
Technology, 8916-5 Takayama, Ikoma, Nara 630-0101, Japan. Tel.:
81-743-72-5640; Fax: 81-743-72-5649; E-mail:
kkouno@bs.aist-nara.ac.jp.
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