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J. Biol. Chem., Vol. 277, Issue 41, 38197-38204, October 11, 2002
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From the Growth Factor Division, National Cancer Center Research
Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo 104-0045, Japan
MEN1, the gene responsible for
multiple endocrine neoplasia type 1, is a tumor suppressor gene that
encodes a protein called menin, of unknown function with no homology to
any known protein. Here we demonstrate that menin interacts with a
putative tumor metastasis suppressor nm23H1/nucleoside diphosphate
(NDP) kinase A in mammalian cells. Given the roles of nm23 as a
multi-functional protein, we searched for the possible function of
menin. Menin has no effect on the known activities of nm23; that is,
nucleoside diphosphate kinase, protein kinase, or GTPase-activating
protein for Ras-related GTPase Rad. However, we found that menin
hydrolyzes GTP to GDP efficiently in the presence of nm23, whereas nm23
or menin alone shows little or no detectable GTPase activity.
Furthermore, menin contains sequence motifs similar to those found in
all known GTPases or GTP-binding proteins and shows low affinity but
specific binding to GTP/GDP. These results suggest that menin is an
atypical GTPase stimulated by nm23.
Menin, the Multiple Endocrine Neoplasia Type 1 Gene Product,
Exhibits GTP-hydrolyzing Activity in the Presence of the Tumor
Metastasis Suppressor nm23*
,
*
This work was supported in part by the Program for Promotion
of Fundamental Studies in Health Sciences of the Organization for
Pharmaceutical Safety and Research of Japan.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.
Recipient of a research resident fellowship from the Foundation
for Promotion of Cancer Research of Japan.
§
To whom correspondence should be addressed. Tel.: 81-3-3542-2511;
Fax: 81-3-3542-8170; E-mail: nohkura@gan2.ncc.go.jp.
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