Junko Oki
National Institute of Advanced Industrial Science and Technology
Network
Latest external collaboration on country level. Dive into details by clicking on the dots.
Publication
Featured researches published by Junko Oki.
Molecular Endocrinology | 2008
Masashi Suzuki; Yuriko Uehara; Kaori Motomura-Matsuzaka; Junko Oki; Yoshinori Koyama; Miho Kimura; Masahiro Asada; Akiko Komi-Kuramochi; Syuichi Oka; Toru Imamura
Fibroblast growth factor (FGF) 21, a structural relative of FGF23 that regulates phosphate homeostasis, is a regulator of insulin-independent glucose transport in adipocytes and plays a role in the regulation of body weight. It also regulates ketogenesis and adaptive responses to starvation. We report that in a reconstituted receptor activation assay system using BaF3 cells, which do not endogenously express any type of FGF receptor (FGFR) or heparan sulfate proteoglycan, FGF21 alone does not activate FGFRs and that betaKlotho is required for FGF21 to activate two specific FGFR subtypes: FGFR1c and FGFR3c. Coexpression of betaKlotho and FGFR1c on BaF3 cells enabled FGF21, but not FGF23, to activate receptor signaling. Conversely, coexpression of FGFR1c and Klotho, a protein related to betaKlotho, enabled FGF23 but not FGF21 to activate receptor signaling, indicating that expression of betaKlotho/Klotho confers target cell specificity on FGF21/FGF23. In all of these cases, heparin enhanced the activation but was not essential. In 3T3-L1 adipocytes, up-regulation of glucose transporter (GLUT) expression by FGF21 was associated with expression of betaKlotho, which was absent in undifferentiated 3T3-L1 fibroblasts. It is thus suggested that betaKlotho expression is a crucial determinant of the FGF21 specificity of the target cells upon which it acts in an endocrine fashion.
Journal of Investigative Dermatology | 2012
Miho Kimura-Ueki; Yuko Oda; Junko Oki; Akiko Komi-Kuramochi; Emi Honda; Masahiro Asada; Masashi Suzuki; Toru Imamura
Hair follicles repeatedly cycle through growth (anagen), regression (catagen), and resting (telogen) phases. Although the signaling molecules involved in the anagen and anagen-catagen transition have been studied extensively, the signaling that controls telogen is only partly understood. Here we show that fibroblast growth factor (Fgf)18 is expressed in a hair stem cell niche throughout telogen, and that it regulates the hair cycle through the non-growth phases. When the Fgf18 gene is conditionally knocked out in keratin 5-positive epithelial cells in mice, telogen becomes very short, giving rise to a strikingly rapid succession of hair cycles. In wild-type mice, hair follicle growth during anagen is strongly suppressed by local delivery of FGF18 protein. Our results demonstrate that epithelial FGF18 signaling and its reduction in the milieu of hair stem cells are crucial for the maintenance of resting and growth phase, respectively.
Biochimica et Biophysica Acta | 2008
Kaori Motomura; Akiko Hagiwara; Akiko Komi-Kuramochi; Yoshiro Hanyu; Emi Honda; Masashi Suzuki; Miho Kimura; Junko Oki; Masahiro Asada; Nagako Sakaguchi; Fumiaki Nakayama; Makoto Akashi; Toru Imamura
Structural instability of wild-type fibroblast growth factor (FGF)-1 and its dependence on exogenous heparin for optimal activity diminishes its potential utility as a therapeutic agent. Here we evaluated FGFC, an FGF1:FGF2 chimeric protein, for its receptor affinity, absolute heparin-dependence, stability and potential clinical applicability. Using BaF3 transfectants overexpressing each FGF receptor (FGFR) subtype, we found that, like FGF1, FGFC activates all of the FGFR subtypes (i.e., FGFR1c, FGFR1b, FGFR2c, FGFR2b, FGFR3c, FGFR3b and FGFR4) in the presence of heparin. Moreover, FGFC activates FGFRs even in the absence of heparin. FGFC stimulated keratinocytes proliferation much more strongly than FGF2, as would be expected from its ability to activate FGFR2b. FGFC showed greater structural stability, biological activity and resistance to trypsinization, and less loss in solution than FGF1 or FGF2. When FGFC was intraperitoneally administered to BALB/c mice prior to whole body gamma-irradiation, survival of small intestine crypts was significantly enhanced, as compared to control mice. These results suggest that FGFC could be useful in a variety of clinical applications, including promotion of wound healing and protection against radiation-induced damage.
Growth Factors Journal | 1999
Takehito Uruno; Junko Oki; Kazuo Ozawa; Kazuko Miyakawa; Hikaru Ueno; Toru Imamura
We studied the role of fibroblast growth factor (FGF)-1 in the physiology of myoblast differentiation. We found that, while endogenous FGF-1 in L6-10 rat myoblasts did not suppress the progress of differentiation, the addition of FGF-1 to the culture medium suppressed it. Moreover, L6-10 cells stably transfected with full length FGF-1 undergo enhanced differentiation. The latter was well correlated with myogenin expression and myotube formation. Constitutive expression of a mutant FGF-1 (FGF-1U) that lacked a nuclear localization signal, promoted the differentiation of the myoblasts even more strongly. Furthermore, the expression of FGF-1U in an inducible expression system enhanced myogenin expression promptly. In L6-10 transfectants expressing a dominant-negative mutant of FGF receptor, stable transfection of FGF-1 promoted differentiation as it did in parent cells. Studies with FGF receptors and MAP kinase suggest that both are involved in the effect of FGF-1 when it is supplemented to culture medium but not during the effect of endogenous FGF-1 synthesized in cells. We conclude that intracellular (endogenous) and extracellular (exogenous) FGF-1 have differential effects on the regulation of myogenic differentiation of L6-10 cells.
Glycoconjugate Journal | 2001
Atsuko Yoneda; Masahiro Asada; Saori Yamamoto; Junko Oki; Yuko Oda; Keiko Ota; Yoko Ogi; Sachi Fujishima; Toru Imamura
Controlled protein remodeling with O-linked glycans has been limited by our incomplete understanding of the process of glycosylation. Here we describe a secretable fibroblast growth factor (FGF) with multiple mucin-type O-glycans produced by introducing a minimum pentapeptide glycosylation unit in a decarepeat format at its N- or C-terminus. Expressed in Chinese hamster ovary cells, chemical and biochemical analyses of the resultant proteins (Nm10-FGF and Cm10-FGF, respectively) demonstrated that all O-glycosylation units were glycosylated and the dominant structure was sialylated Gal[β1–3]GalNAc. This indicates that minimum O-glycosylation unit in multirepeat format serves as a remarkably efficient acceptor in CHO cells. The Nm10-FGF and Cm10-FGF proteins maintained the mitogenic activity to vascular endothelial cells. In addition, intact Cm10-FGF and its desialylated form interacted with several lectins in the same way as mucin-type glycoproteins. The intact Cm10-FGF with multiple sialylated O-glycans exhibited a longer lifetime in circulating blood, whereas the Cm10-FGF with desialylated O-glycans exhibited a shorter lifetime than the deglycosylated form of Cm10-FGF. Our approach would thus appear to be highly effective for engineering neoglycoproteins, the characteristics of which are determined by their multiple mucin-type O-glycans.
Journal of Endocrinology | 2005
Akiko Komi-Kuramochi; Mitsuko Kawano; Yuko Oda; Masahiro Asada; Masashi Suzuki; Junko Oki; Toru Imamura
Journal of Investigative Dermatology | 2005
Mitsuko Kawano; Akiko Komi-Kuramochi; Masahiro Asada; Masashi Suzuki; Junko Oki; Ju Jiang; Toru Imamura
Archive | 2008
Masashi Suzuki; Toru Imamura; Yuriko Uehara; Kaori Motomura; Junko Oki; Syuichi Oka; Masahiro Asada; Akiko Kuramochi; Miho Kimura
International Journal of Radiation Oncology Biology Physics | 2010
Fumiaki Nakayama; Akiko Hagiwara; Sachiko Umeda; Masahiro Asada; Megumi Goto; Junko Oki; Masashi Suzuki; Toru Imamura; Makoto Akashi
Journal of Investigative Dermatology | 2004
Mitsuko Kawano; Satoshi Suzuki; Masashi Suzuki; Junko Oki; Toru Imamura
Collaboration
Dive into the Junko Oki's collaboration.
National Institute of Advanced Industrial Science and Technology
View shared research outputsNational Institute of Advanced Industrial Science and Technology
View shared research outputsNational Institute of Advanced Industrial Science and Technology
View shared research outputsNational Institute of Advanced Industrial Science and Technology
View shared research outputsNational Institute of Advanced Industrial Science and Technology
View shared research outputsNational Institute of Advanced Industrial Science and Technology
View shared research outputsNational Institute of Advanced Industrial Science and Technology
View shared research outputs