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J. Biol. Chem., Vol. 276, Issue 45, 42213-42218, November 9, 2001
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§,
, and
From the The bone morphogenic proteins (BMPs) play a key
role in skeletal development and patterning. Using the technique of
differential display polymerase chain reaction (ddPCR), we have
identified a novel gene whose expression is increased during
BMP-2-induced differentiation of the prechondroblastic cell line,
MLB13MYC clone 17, to an osteoblastic phenotype. The
6.5-kilobase mRNA recognized by this ddPCR product is
increased 10-fold by BMP-2 treatment of the MLB13MYC clone 17 cells.
The mRNA recognized by this ddPCR product is also increased as
MC3T3-E1 cells recapitulate the program of osteoblast differentiation
during prolonged culture. The full-length transcript corresponding to
this ddPCR product was cloned from a MLB13MYC clone 17 cell cDNA
library. Analysis of the deduced amino acid sequence demonstrated that
this gene encodes a novel 126-kDa putative serine/threonine protein
kinase containing a nuclear localization signal. The kinase domain,
expressed in Escherichia coli, is capable of
autophosphorylation as well as phosphorylation of myelin basic protein.
The gene was, therefore, named BIKe
(BMP-2-Inducible Kinase). The BIKe nuclear localization signal
is able to direct green fluorescent protein to the nucleus in
transfected COS-7 cells. When stably expressed in MC3T3-E1 cells, BIKe
significantly decreases alkaline phosphatase activity and osteocalcin
mRNA levels and retards mineral deposition relative to vector
control. This novel kinase, therefore, is likely to play an
important regulatory role in attenuating the program of osteoblast differentiation.
Division of Endocrinology, Diabetes,
Metabolism and Nutrition, Mayo Clinic, Rochester, Minnesota 55905 and
¶ Endocrine Unit, Massachusetts General Hospital, Harvard Medical
School, Boston, Massachusetts 02114
The nucleotide sequence(s) reported in this paper has been submitted to the GenBankTM/EMBL Data Bank with accession number(s) AYe50249.
§ Both authors contributed equally to this work.
To whom correspondence should be sent: Endocrine Unit,
Massachusetts General Hospital, Harvard Medical School, Wellman 503, 50 Blossom St. Tel.: 617-726-3966; Fax: 617-726-7543; E-mail: demay@helix.mgh.harvard.edu.
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