start-ver=1.4 cd-journal=joma no-vol=6 cd-vols= no-issue=12 article-no= start-page=e05743 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2020 dt-pub=202012 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Antioxidative attributes of rice bran extracts in ameliorative effects of atherosclerosis-associated risk factors en-subtitle= kn-subtitle= en-abstract= kn-abstract=Oxidative stress, chronic inflammation, dyslipidemia, hyperglycemia, and shear stress (physical effect) are risk factors associated with the pathogenesis of atherosclerosis. Rice bran, a by-product of rice milling process, is known to house polyphenols and vitamins which exhibit potent antioxidant and anti-inflammatory properties. Through recent emerging knowledge of rice bran in health and wellness, the present study was aimed to assess the ameliorative effects of rice bran extracts (RBE) derived from Japanese colored rice varieties in modulating risk factors of atherosclerosis via in vitro and in vivo study models. Pre-treatment of lipopolysaccharide (LPS)-stimulated murine J774A.1 macrophage-like cells with RBE alleviated nitric oxide (NO) overproduction and downregulated gene expressions of pro-inflammatory modulators: tumor necrosis factor-ƒΏ (TNF-ƒΏ), interleukin (IL)-ƒΏ (IL-1ƒΏ), IL-1ƒΐ, IL-6, and inducible nitric oxide synthase (iNOS). In addition, RBE also significantly attenuated LPS-stimulated protein expressions of iNOS, TNF-ƒΏ, IL-1ƒΏ, and IL-6 in J774A.1 macrophage-like cells as compared to non-treated LPS control group. In in vivo, 12 weeks of RBE dietary supplementations significantly reduced (p < 0.05) total cholesterol, triglycerides, and pro-atherogenic oxidized LDL/ƒΐ2-glycoprotein I (oxLDL/ƒΐ2GPI) complexes at plasma levels, in high fat diet (HFD) induced low density lipoprotein receptor knockout (Ldlr?/-) mice. En face pathological assessments of murine aortas also revealed significant reductions by 38% (p < 0.05) in plaque sizes of RBE-supplemented HFD mice groups as compared to non RBE-supplemented HFD control mice group. Moreover, gene expressions of aortic (iNOS, TNF-ƒΏ, IL-1ƒΐ) and hepatic (TNF-ƒΏ, IL-1ƒΏ, IL-1ƒΐ) pro-inflammatory modulators were also downregulated in RBE-supplemented mice groups. Present study has revealed the potent health attributes and application of RBE as a dietary supplement to attenuate risks of inadvertent oxidative damage and chronic inflammation underlying the pathogenesis of atherosclerosis. Intrinsically, present preliminary findings may provide global health prospects for future dietary implementation of RBE in management of atherosclerosis. en-copyright= kn-copyright= en-aut-name=XianWen Tan en-aut-sei=Xian en-aut-mei=Wen Tan kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=KobayashiKazuko en-aut-sei=Kobayashi en-aut-mei=Kazuko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=LianhuaShen en-aut-sei=Lianhua en-aut-mei=Shen kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=InagakiJunko en-aut-sei=Inagaki en-aut-mei=Junko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=IdeMasahiro en-aut-sei=Ide en-aut-mei=Masahiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=HwangSiaw San en-aut-sei=Hwang en-aut-mei=Siaw San kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=MatsuuraEiji en-aut-sei=Matsuura en-aut-mei=Eiji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= affil-num=1 en-affil=Department of Cell Chemistry, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences kn-affil= affil-num=2 en-affil=Collaborative Research Center for OMIC, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences kn-affil= affil-num=3 en-affil=Department of Pathophysiology, Zunyi Medical University kn-affil= affil-num=4 en-affil=Department of Cell Chemistry, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences kn-affil= affil-num=5 en-affil=Department of Cell Chemistry, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences kn-affil= affil-num=6 en-affil=School of Chemical Engineering and Science, Faculty of Engineering, Computing and Science, Swinburne University of Technology Sarawak Campus kn-affil= affil-num=7 en-affil=Department of Cell Chemistry, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences kn-affil= en-keyword=Food science kn-keyword=Food science en-keyword=Food analysis kn-keyword=Food analysis en-keyword=Rice bran extract (RBE) kn-keyword=Rice bran extract (RBE) en-keyword=Functional food kn-keyword=Functional food en-keyword=Phytochemicals kn-keyword=Phytochemicals en-keyword=Atherosclerosis kn-keyword=Atherosclerosis en-keyword=Oxidative stress kn-keyword=Oxidative stress en-keyword=Inflammation kn-keyword=Inflammation en-keyword=Antioxidant kn-keyword=Antioxidant en-keyword=Anti-inflammation kn-keyword=Anti-inflammation en-keyword=Oxidized lipoprotein (oxLDL) kn-keyword=Oxidized lipoprotein (oxLDL) END start-ver=1.4 cd-journal=joma no-vol=21 cd-vols= no-issue=9 article-no= start-page=3140 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2020 dt-pub=20200429 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Induction of CEMIP in Chondrocytes by Inflammatory Cytokines: Underlying Mechanisms and Potential Involvement in Osteoarthritis en-subtitle= kn-subtitle= en-abstract= kn-abstract=In patients with osteoarthritis (OA), there is a decrease in both the concentration and molecular size of hyaluronan (HA) in the synovial fluid and cartilage. Cell migration-inducing hyaluronidase 1 (CEMIP), also known as hyaluronan (HA)-binding protein involved in HA depolymerization (HYBID), was recently reported as an HA depolymerization-related molecule expressed in the cartilage of patients with OA. However, the underlying mechanism of CEMIP regulation is not well understood. We found that CEMIP expression was transiently increased by interleukine-1 beta (IL-1 beta) stimulation in chondrocytic cells. We also observed that ERK activation and NF-kappa B nuclear translocation were involved in the induction of CEMIP by IL-1 beta. In addition, both administration of HA and mechanical strain attenuated the CEMIP induction in IL-1 beta-stimulated chondrocytes. In conclusion, we clarified the regulatory mechanism of CEMIP in chondrocytes by inflammatory cytokines and suggested the potential involvement in osteoarthritis development. en-copyright= kn-copyright= en-aut-name=OhtsukiTakashi en-aut-sei=Ohtsuki en-aut-mei=Takashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=HatipogluOmer F. en-aut-sei=Hatipoglu en-aut-mei=Omer F. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=AsanoKeiichi en-aut-sei=Asano en-aut-mei=Keiichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=InagakiJunko en-aut-sei=Inagaki en-aut-mei=Junko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=NishidaKeiichiro en-aut-sei=Nishida en-aut-mei=Keiichiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=HirohataSatoshi en-aut-sei=Hirohata en-aut-mei=Satoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= affil-num=1 en-affil=Department of Medical Technology, Graduate School of Health Sciences, Okayama University kn-affil= affil-num=2 en-affil=Department of Medical Technology, Graduate School of Health Sciences, Okayama University kn-affil= affil-num=3 en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=4 en-affil=Department of Cell Chemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=5 en-affil=Department of Orthopaediac Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=6 en-affil=Department of Medical Technology, Graduate School of Health Sciences, Okayama University kn-affil= en-keyword=cell migration-inducing hyaluronidase 1 (CEMIP) kn-keyword=cell migration-inducing hyaluronidase 1 (CEMIP) en-keyword=chondrocyte kn-keyword=chondrocyte en-keyword=hyaluronan kn-keyword=hyaluronan en-keyword=mechanical strain kn-keyword=mechanical strain en-keyword=nuclear factor kappa B (NF-kappa B) kn-keyword=nuclear factor kappa B (NF-kappa B) en-keyword=osteoarthritis kn-keyword=osteoarthritis END start-ver=1.4 cd-journal=joma no-vol=383 cd-vols= no-issue=2 article-no= start-page=111556 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2019 dt-pub=20191015 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Mechanical strain attenuates cytokine-induced ADAMTS9 expression via transient receptor potential vanilloid type 1 en-subtitle= kn-subtitle= en-abstract= kn-abstract= The synovial fluids of patients with osteoarthritis (OA) contain elevated levels of inflammatory cytokines, which induce the expression of a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) and of the matrix metalloproteinase (MMP) in chondrocytes. Mechanical strain has varying effects on organisms depending on the strength, cycle, and duration of the stressor; however, it is unclear under inflammatory stimulation how mechanical strain act on. Here, we show that mechanical strain attenuates inflammatory cytokine-induced expression of matrix-degrading enzymes. Cyclic tensile strain (CTS), as a mechanical stressor, attenuated interleukin (IL)-1ƒΐ and tumor necrosis factor (TNF)-ƒΏ-induced mRNA expression of ADAMTS4, ADAMTS9, and MMP-13 in normal chondrocytes (NHAC-kn) and in a chondrocytic cell line (OUMS-27). This effect was abolished by treating cells with mechano-gated channel inhibitors, such as gadolinium, transient receptor potential (TRP) family inhibitor, ruthenium red, and with pharmacological and small interfering RNA-mediated TRPV1 inhibition. Furthermore, nuclear factor ƒΘB (NF-ƒΘB) translocation from the cytoplasm to the nucleus resulting from cytokine stimulation was also abolished by CTS. These findings suggest that mechanosensors such as the TRPV protein are potential therapeutic targets in treating OA. en-copyright= kn-copyright= en-aut-name=OhtsukiTakashi en-aut-sei=Ohtsuki en-aut-mei=Takashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=ShinaokaAkira en-aut-sei=Shinaoka en-aut-mei=Akira kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=Kumagishi-ShinaokaKanae en-aut-sei=Kumagishi-Shinaoka en-aut-mei=Kanae kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=AsanoKeiichi en-aut-sei=Asano en-aut-mei=Keiichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=HatipogluOmer Faruk en-aut-sei=Hatipoglu en-aut-mei=Omer Faruk kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=InagakiJunko en-aut-sei=Inagaki en-aut-mei=Junko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=TakahashiKen en-aut-sei=Takahashi en-aut-mei=Ken kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=OohashiToshitaka en-aut-sei=Oohashi en-aut-mei=Toshitaka kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=NishidaKeiichiro en-aut-sei=Nishida en-aut-mei=Keiichiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=NaruseKeiji en-aut-sei=Naruse en-aut-mei=Keiji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=HirohataSatoshi en-aut-sei=Hirohata en-aut-mei=Satoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= affil-num=1 en-affil=Department of Medical Technology, Graduate School of Health Sciences, Okayama University kn-affil= affil-num=2 en-affil=Department of Human Morphology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=3 en-affil=Department of Human Morphology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=4 en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=5 en-affil=Department of Medical Technology, Graduate School of Health Sciences, Okayama University kn-affil= affil-num=6 en-affil=Department of Cell Chemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=7 en-affil=Department of Cardiovascular Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=8 en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=9 en-affil=Department of Orthopaedic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=10 en-affil=Department of Cardiovascular Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=11 en-affil=Department of Medical Technology, Graduate School of Health Sciences, Okayama University kn-affil= END start-ver=1.4 cd-journal=joma no-vol=103 cd-vols= no-issue=10 article-no= start-page=1889 end-page=1897 dt-received= dt-revised= dt-accepted= dt-pub-year=2012 dt-pub=201210 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Tumor growth inhibitory effect of ADAMTS1 is accompanied by the inhibition of tumor angiogenesis en-subtitle= kn-subtitle= en-abstract= kn-abstract=Angiogenesis plays an important role in tumor progression. Several reports have demonstrated that a disintegrin and metalloproteinase with thrombospondin motifs1 (ADAMTS1) inhibited angiogenesis via multiple mechanisms. The aim of this study was to investigate the effect of ADAMTS1 on endothelial cells in vitro and on tumor growth with regard to angiogenesis in vivo. We examined the effects of the transfection of ADAMTS1 using two constructs, full-length ADAMTS1 (full ADAMTS1) and catalytic domain-deleted ADAMTS1 (delta ADAMTS1). Transfection of both the full ADAMTS1 and delta ADAMTS1 gene constructs demonstrated the secretion of tagged-ADAMTS1 protein into the conditioned medium, so we examined the effects of ADAMTS1-containing conditioned medium on endothelial cells. Both types of conditioned media inhibited endothelial tube formation, and this effect was completely abolished after immunoprecipitation of the secreted protein from the medium. Both types of conditioned media also inhibited endothelial cell migration and proliferation. We then examined the impact of ADAMTS1 on endothelial cell apoptosis. Both conditioned media increased the number of Annexin V-positive endothelial cells and caspase-3 activity and this effect was attenuated when z-vad was added. These results indicated that ADAMTS1 induced endothelial cell apoptosis. We next examined the effects of ADAMTS1 gene transfer into tumor-bearing mice. Both full ADAMTS1 and delta ADAMTS1 significantly inhibited the subcutaneous tumor growth. Collectively, our results demonstrated that ADAMTS1 gene transfer inhibited angiogenesis in vitro and in vivo, likely as a result of the induction of endothelial cell apoptosis by ADAMTS1 that occurs independent of the protease activity. en-copyright= kn-copyright= en-aut-name=ObikaMasanari en-aut-sei=Obika en-aut-mei=Masanari kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=OgawaHiroko en-aut-sei=Ogawa en-aut-mei=Hiroko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=TakahashiKatsuyuki en-aut-sei=Takahashi en-aut-mei=Katsuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=LiJiayi en-aut-sei=Li en-aut-mei=Jiayi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=HatipogluOmer Faruk en-aut-sei=Hatipoglu en-aut-mei=Omer Faruk kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=CilekMehmet Zeynel en-aut-sei=Cilek en-aut-mei=Mehmet Zeynel kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=MiyoshiToru en-aut-sei=Miyoshi en-aut-mei=Toru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=InagakiJunko en-aut-sei=Inagaki en-aut-mei=Junko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=OhtsukiTakashi en-aut-sei=Ohtsuki en-aut-mei=Takashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=KusachiShozo en-aut-sei=Kusachi en-aut-mei=Shozo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=NinomiyaYoshifumi en-aut-sei=Ninomiya en-aut-mei=Yoshifumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=HirohataSatoshi en-aut-sei=Hirohata en-aut-mei=Satoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= affil-num=1 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Mol Biol & Biochem affil-num=2 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Mol Biol & Biochem affil-num=3 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Mol Biol & Biochem affil-num=4 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Mol Biol & Biochem affil-num=5 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Mol Biol & Biochem affil-num=6 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Mol Biol & Biochem affil-num=7 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Mol Biol & Biochem affil-num=8 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Mol Biol & Biochem affil-num=9 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Mol Biol & Biochem affil-num=10 en-affil= kn-affil=Okayama Univ, Grad Sch Hlth Sci, Dept Med Technol affil-num=11 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Mol Biol & Biochem affil-num=12 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Mol Biol & Biochem END start-ver=1.4 cd-journal=joma no-vol=100 cd-vols= no-issue= article-no= start-page=3 end-page=7 dt-received= dt-revised= dt-accepted= dt-pub-year=2011 dt-pub=20110201 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Purification and Characterization of l-Methionine Decarboxylase from Streptomyces sp. 590 kn-title=•ϊό‹ΫStreptomyces sp.590—R—ˆl-ƒƒ`ƒIƒjƒ“’E’YŽ_y‘f‚̐Έ»‚¨‚ζ‚ѐ«ŽΏŒŸ“’ en-subtitle= kn-subtitle= en-abstract= kn-abstract=L-Methionine decarboxylase [EC 4.1.1.57] catalyzes the decarboxylation of L-methionine and is a pyridoxal 5f-phosohate(PLP)-dependent enzyme. L-Methionine decarboxylase has been purified 630-fold by DEAE-Toyopearl 650M, Phenyl-Toyopearl 650M and Sephacryl S-300 column chromatographies from Streptomyces sp.590. The enzyme has a dimeric structure with identical subunits of Mr 60,000. This enzyme shows optimum activity at pH7.0 and 45‹C, and is stable between pH5.7 and pH9.0. L-Methionine decarboxylase has antitumor activity against RERF-LC-AI and HeLa cells. Ten N-terminal amino acid sequence of L-methionine decarboxylase was determined, and the sequence showed no homology with other reported proteins. en-copyright= kn-copyright= en-aut-name=MaemuraTomomi en-aut-sei=Maemura en-aut-mei=Tomomi kn-aut-name=‘O‘Ί’m”ό kn-aut-sei=‘O‘Ί kn-aut-mei=’m”ό aut-affil-num=1 ORCID= en-aut-name=UchitomiKumiko en-aut-sei=Uchitomi en-aut-mei=Kumiko kn-aut-name=“ΰ•x‹v”όŽq kn-aut-sei=“ΰ•x kn-aut-mei=‹v”όŽq aut-affil-num=2 ORCID= en-aut-name=KusakaChika en-aut-sei=Kusaka en-aut-mei=Chika kn-aut-name=“ϊ‰Ί’m kn-aut-sei=“ϊ‰Ί kn-aut-mei=’m aut-affil-num=3 ORCID= en-aut-name=InagakiJunko en-aut-sei=Inagaki en-aut-mei=Junko kn-aut-name=ˆξŠ_ƒŽq kn-aut-sei=ˆξŠ_ kn-aut-mei=ƒŽq aut-affil-num=4 ORCID= en-aut-name=TamuraTakashi en-aut-sei=Tamura en-aut-mei=Takashi kn-aut-name=“c‘Ί—² kn-aut-sei=“c‘Ί kn-aut-mei=—² aut-affil-num=5 ORCID= en-aut-name=SodaKenji en-aut-sei=Soda en-aut-mei=Kenji kn-aut-name=Ά‰E“cŒ’ŽŸ kn-aut-sei=Ά‰E“c kn-aut-mei=Œ’ŽŸ aut-affil-num=6 ORCID= en-aut-name=InagakiKenji en-aut-sei=Inagaki en-aut-mei=Kenji kn-aut-name=ˆξŠ_Œ«“ρ kn-aut-sei=ˆξŠ_ kn-aut-mei=Œ«“ρ aut-affil-num=7 ORCID= affil-num=1 en-affil= kn-affil=”_Œ|‰»ŠwƒR[ƒX affil-num=2 en-affil= kn-affil=”_Œ|‰»ŠwƒR[ƒX affil-num=3 en-affil= kn-affil=”_Œ|‰»ŠwƒR[ƒX affil-num=4 en-affil= kn-affil=‰ͺŽR‘εŠw‘εŠw‰@ˆγŽ•–ςŠw‘‡Œ€‹†‰Θ affil-num=5 en-affil= kn-affil=”_Œ|‰»ŠwƒR[ƒX affil-num=6 en-affil= kn-affil=‹ž“s‘εŠw affil-num=7 en-affil= kn-affil=”_Œ|‰»ŠwƒR[ƒX en-keyword=L-methionine decarboxylase kn-keyword=L-methionine decarboxylase en-keyword=pyridoxal 5f-phosohate kn-keyword=pyridoxal 5f-phosohate en-keyword=Streptomyces kn-keyword=Streptomyces en-keyword=decarboxylation of L-methionine kn-keyword=decarboxylation of L-methionine END start-ver=1.4 cd-journal=joma no-vol= cd-vols= no-issue= article-no= start-page= end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=1994 dt-pub=19940930 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=ƒ†[ƒOƒŒƒiŒυ‰»ŠwŒn‡U30kDa ƒ^ƒ“ƒpƒNŽΏ‚Μ—t—Ξ‘Μ‚Φ‚Μ—A‘—‚ΙŠΦ‚·‚ιŒ€‹† kn-title=STUDIES ON TRANSPORT OF THE NUCLEUS-ENCODED 30 kDa PROTEIN OF PHOTOSYSTEM ‡U INTO EUGLENA CHLOROPLASTS en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=InagakiJunko en-aut-sei=Inagaki en-aut-mei=Junko kn-aut-name=ˆξŠ_ƒŽq kn-aut-sei=ˆξŠ_ kn-aut-mei=ƒŽq aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=‰ͺŽR‘εŠw END