start-ver=1.4 cd-journal=joma no-vol=69 cd-vols= no-issue=3 article-no= start-page=145 end-page=153 dt-received= dt-revised= dt-accepted= dt-pub-year=2015 dt-pub=201506 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Eosinophil Cationic Protein Shows Survival Effect on H9c2 Cardiac Myoblast Cells with Enhanced Phosphorylation of ERK and Akt/GSK-3β under Oxidative Stress en-subtitle= kn-subtitle= en-abstract= kn-abstract=Eosinophil cationic protein (ECP) is well known as a cationic protein contained in the basic granules of activated eosinophils. Recent studies have reported that ECP exhibits novel activities on various types of cells, including rat neonatal cardiomyocytes. Here we evaluated the effects of ECP on rat cardiac myoblast H9c2 cells. Our results showed that ECP enhanced the survival of the cells, in part by promoting the ERK and Akt/GSK-3β signaling pathways. ECP attenuated the cytotoxic effects of H2O2 on H9c2 cells as well as the production of reactive oxygen species, the number of apoptotic cells and caspase 3/7 activity in the cells. In conclusion, ECP activated the ERK and Akt/GSK-3β pathways, resulting in anti-oxidative effects on H9c2 cells that attenuated apoptosis. en-copyright= kn-copyright= en-aut-name=IshiiHiroko en-aut-sei=Ishii en-aut-mei=Hiroko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=KamikawaShigeshi en-aut-sei=Kamikawa en-aut-mei=Shigeshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 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=3 ORCID= en-aut-name=MizutaniAkifumi en-aut-sei=Mizutani en-aut-mei=Akifumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=AbeKoji en-aut-sei=Abe en-aut-mei=Koji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=SenoMasaharu en-aut-sei=Seno en-aut-mei=Masaharu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 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=7 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=8 ORCID= affil-num=1 en-affil= kn-affil=Departments of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine affil-num=2 en-affil= kn-affil=Departments of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine affil-num=3 en-affil= kn-affil=Departments of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine affil-num=4 en-affil= kn-affil=Department of Chemistry and Biotechnology, Graduate School of Natural Science and Technology, Okayama University affil-num=5 en-affil= kn-affil=Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, affil-num=6 en-affil= kn-affil=Department of Chemistry and Biotechnology, Graduate School of Natural Science and Technology, Okayama University affil-num=7 en-affil= kn-affil=Departments of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine affil-num=8 en-affil= kn-affil=Departments of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine en-keyword=ECP kn-keyword=ECP en-keyword=reactive oxygen species kn-keyword=reactive oxygen species en-keyword=Akt kn-keyword=Akt en-keyword=ERK kn-keyword=ERK 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=124 cd-vols= no-issue=1 article-no= start-page=1 end-page=4 dt-received= dt-revised= dt-accepted= dt-pub-year=2012 dt-pub=20120401 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Perinodal ECM―its role in diffusion barrier formation and conduction velocity in the CNS kn-title=ランビエ絞輪周囲のECMによるdiffusion barrier形成と跳躍伝導における役割 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=BekkuYoko en-aut-sei=Bekku en-aut-mei=Yoko kn-aut-name=別宮洋子 kn-aut-sei=別宮 kn-aut-mei=洋子 aut-affil-num=1 ORCID= en-aut-name=NinomiyaYoshifumi en-aut-sei=Ninomiya en-aut-mei=Yoshifumi kn-aut-name=二宮善文 kn-aut-sei=二宮 kn-aut-mei=善文 aut-affil-num=2 ORCID= en-aut-name=OohashiToshitaka en-aut-sei=Oohashi en-aut-mei=Toshitaka kn-aut-name=大橋俊孝 kn-aut-sei=大橋 kn-aut-mei=俊孝 aut-affil-num=3 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 分子医化学 affil-num=2 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 分子医化学 affil-num=3 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 分子医化学 en-keyword=proteoglycan kn-keyword=proteoglycan en-keyword=node of Ranvier kn-keyword=node of Ranvier en-keyword=action potential kn-keyword=action potential en-keyword=extracellular space kn-keyword=extracellular space en-keyword=diffusion barrier kn-keyword=diffusion barrier END start-ver=1.4 cd-journal=joma no-vol=30 cd-vols= no-issue=4 article-no= start-page=258 end-page=266 dt-received= dt-revised= dt-accepted= dt-pub-year=2011 dt-pub=201105 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Drosophila type XV/XVIII collagen, Mp, is involved in Wingless distribution en-subtitle= kn-subtitle= en-abstract= kn-abstract=Multiplexin (Mp) is the Drosophila orthologue of vertebrate collagens XV and XVIII. Like them, Mp is widely distributed in the basement membranes of the developing embryos, including those of neuroblasts in the central and peripheral nervous systems, visceral muscles of the gut, and contractile cardioblasts. Here we report the identification of mutant larvae bearing piggyBac transposon insertions that exhibit decrease Mp production associated with abdominal cuticular and wing margin defects, malformation of sensory organs and impaired sensitivity to physical stimuli. Additional findings include the abnormal ultrastructure of fatbody associated with abnormal collagen IV deposition, and reduced Wingless deposition. Collectively, these findings are consistent with the notion that Mp is required for the proper formation and/or maintenance of basement membrane, and that Mp may be involved in establishing the Wingless signaling gradients in the Drosophila embryo. en-copyright= kn-copyright= en-aut-name=MomotaRyusuke en-aut-sei=Momota en-aut-mei=Ryusuke kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=NaitoIchiro en-aut-sei=Naito en-aut-mei=Ichiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 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=3 ORCID= en-aut-name=OhtsukaAiji en-aut-sei=Ohtsuka en-aut-mei=Aiji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= affil-num=1 en-affil= kn-affil=Department of Human Morphology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Human Morphology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=3 en-affil= kn-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=4 en-affil= kn-affil=Department of Human Morphology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences en-keyword=Extracellular matrix kn-keyword=Extracellular matrix en-keyword=Basement membrane kn-keyword=Basement membrane en-keyword=Collagen kn-keyword=Collagen en-keyword=Proteoglycan kn-keyword=Proteoglycan en-keyword=Chondroitin sulfate kn-keyword=Chondroitin sulfate en-keyword=Wingless/Wnt kn-keyword=Wingless/Wnt END start-ver=1.4 cd-journal=joma no-vol=41 cd-vols= no-issue=3 article-no= start-page=134 end-page=139 dt-received= dt-revised= dt-accepted= dt-pub-year=2008 dt-pub=200802 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Association of elevated plasma B-type natriuretic peptide levels with paroxysmal atrial fibrillation in patients with nonobstructive hypertrophic cardiomyopathy en-subtitle= kn-subtitle= en-abstract= kn-abstract=

Objectives: To investigate the relationship between the plasma B-type natriuretic peptide (BNP) level and the occurrence of atrial fibrillation (AF) in nonobstructive hypertrophic cardiomyopathy (HCM) patients.
Methods: Patients (n=97) were classified into chronic AF (CAF; n=14), paroxysmal AF (PAF; n=18) and normal sinus rhythm (NSR; n=65) groups. The plasma BNP values were analyzed with logarithmic transformation.
Results: The PAF group showed significantly higher plasma BNP levels than the NSR group [mean (range; -1 SD and +1 SD); 248.3 (143.5, 429.5) vs. 78.2 (27.9, 218.8 ng/L), p<0.0001]. The CAF group also showed significantly higher plasma BNP levels than the NSR group [291.1 (161.4, 524.8 ng/L), p<0.0001]. Multivariate analysis with other clinical factors selected association of PAF as one of the factors that increased the plasma BNP level.
Conclusions: The present study indicated that plasma BNP level is clinically useful for identification of nonobstructive HCM patients who have a risk of PAF.

en-copyright= kn-copyright= en-aut-name=MatsuuraHiroko en-aut-sei=Matsuura en-aut-mei=Hiroko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=MurakamiTakashi en-aut-sei=Murakami en-aut-mei=Takashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=HinaKazuyoshi en-aut-sei=Hina en-aut-mei=Kazuyoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=YamamotoKeizo en-aut-sei=Yamamoto en-aut-mei=Keizo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=KawamuraHiroshi en-aut-sei=Kawamura en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=SogoTaiji en-aut-sei=Sogo en-aut-mei=Taiji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=ShinohataRyoko en-aut-sei=Shinohata en-aut-mei=Ryoko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=UsuiShinichi en-aut-sei=Usui en-aut-mei=Shinichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 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=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= affil-num=1 en-affil= kn-affil=Department of Medicine and Medical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Cardiology, Cardiovascular Center, Sakakibara Hospital affil-num=3 en-affil= kn-affil=Department of Cardiology, Cardiovascular Center, Sakakibara Hospital affil-num=4 en-affil= kn-affil=Department of Cardiology, Cardiovascular Center, Sakakibara Hospital affil-num=5 en-affil= kn-affil=Department of Cardiology, Cardiovascular Center, Sakakibara Hospital affil-num=6 en-affil= kn-affil=Department of Cardiovascular Medicine, Takamatsu Red Cross Hospital affil-num=7 en-affil= kn-affil=Department of Medical Technology, Okayama University Graduate School of Health Sciences affil-num=8 en-affil= kn-affil=Department of Medical Technology, Okayama University Graduate School of Health Sciences affil-num=9 en-affil= kn-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=10 en-affil= kn-affil=Department of Medical Technology, Okayama University Graduate School of Health Sciences en-keyword=clinical study kn-keyword=clinical study en-keyword=cardiomyopathy kn-keyword=cardiomyopathy en-keyword=tachyarrhythmia kn-keyword=tachyarrhythmia en-keyword=enzyme immunoassay kn-keyword=enzyme immunoassay en-keyword=peptide kn-keyword=peptide en-keyword=sensitivity and specificity kn-keyword=sensitivity and specificity END start-ver=1.4 cd-journal=joma no-vol=131 cd-vols= no-issue=7 article-no= start-page=1619 end-page=1628 dt-received= dt-revised= dt-accepted= dt-pub-year=2004 dt-pub=200404 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Collagen IV is essential for basement membrane stability but dispensable for initiation of its assembly during early development en-subtitle= kn-subtitle= en-abstract= kn-abstract=Basement membranes are specialized extracellular matrices consisting of tissue-specific organizations of multiple matrix molecules and serve as structural barriers as well as substrates for cellular interactions. The network of collagen IV is thought to define the scaffold integrating other components such as, laminins, nidogens or perlecan, into highly organized supramolecular architectures. To analyze the functional roles of the major collagen IV isoform α1(IV 2α2(IV) for basement membrane assembly and embryonic development, we generated a null allele of the Col4a1/2 locus in mice, thereby ablating both α-chains. Unexpectedly, embryos developed up to E9.5 at the expected Mendelian ratio and showed a variable degree of growth retardation. Basement membrane proteins were deposited and assembled at expected sites in mutant embryos, indicating that this isoform is dispensable for matrix deposition and assembly during early development. However, lethality occurred between E10.5-E11.5, because of structural deficiencies in the basement membranes and finally by failure of the integrity of Reichert's membrane. These data demonstrate for the first time that collagen IV is fundamental for the maintenance of integrity and function of basement membranes under conditions of increasing mechanical demands, but dispensable for deposition and initial assembly of components. Taken together with other basement membrane protein knockouts, these data suggest that laminin is sufficient for basement membrane-like matrices during early development, but at later stages the specific composition of components including collagen IV defines integrity, stability and functionality. en-copyright= kn-copyright= en-aut-name=P?schlErnst en-aut-sei=P?schl en-aut-mei=Ernst kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=Schl?tzer-SchrehardtUrsula en-aut-sei=Schl?tzer-Schrehardt en-aut-mei=Ursula kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=BrachvogelBent en-aut-sei=Brachvogel en-aut-mei=Bent kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=SaitoKenji en-aut-sei=Saito en-aut-mei=Kenji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 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=5 ORCID= en-aut-name=MayerUlrike en-aut-sei=Mayer en-aut-mei=Ulrike kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= affil-num=1 en-affil= kn-affil=Department of Experimental Medicine I, University Erlangen-N?rnberg affil-num=2 en-affil= kn-affil=Department of Ophthalmology, University Erlangen-N?rnberg affil-num=3 en-affil= kn-affil=Department of Experimental Medicine I, University Erlangen-N?rnberg affil-num=4 en-affil= kn-affil=Department of Molecular Biology and Biochemistry, Okayama University Medical School affil-num=5 en-affil= kn-affil=Department of Molecular Biology and Biochemistry, Okayama University Medical School affil-num=6 en-affil= kn-affil=Wellcome Trust Centre for Cell-Matrix Research, School of Biological Sciences, University of Manchester en-keyword=Collagen IV kn-keyword=Collagen IV en-keyword=Col4a1 kn-keyword=Col4a1 en-keyword=Col4a2 kn-keyword=Col4a2 en-keyword=Knockout kn-keyword=Knockout en-keyword=Basement kn-keyword=Basement en-keyword=membrane kn-keyword=membrane en-keyword=Development kn-keyword=Development END start-ver=1.4 cd-journal=joma no-vol=111 cd-vols= no-issue=14 article-no= start-page=1929 end-page=1940 dt-received= dt-revised= dt-accepted= dt-pub-year=1998 dt-pub=19987 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Initiation of skin basement membrane formation at the epidermo-dermal interface involves assembly of laminins through binding to cell membrane receptors en-subtitle= kn-subtitle= en-abstract= kn-abstract=

To study the mechanism of basement membrane formation, we determined by immunochemistry temporal and spatial expression of laminin-5 (Ln-5), laminin-1 (Ln-1) and their integrin receptors during early skin morphogenesis. A 3-dimensional skin culture was used that allows the study of the sequential molecular events of basement membrane formation at the epidermodermal interface. During early anchorage of keratinocytes to the extracellular matrix there is expression of Ln-5, BP-230 antigen and α3, β1 integrin subunits. During epidermal stratification and prior to the formation of the lamina densa there is assembly of Ln-5, Ln-1, collagen IV and nidogen accompanied by keratinocyte basal clustering of α2, α3, α6, β1, and β4 integrin subunits. The assembly pattern of Ln-1 and Ln-5 can be disturbed with functional antibodies against the β1 (AIIB2) and α6 (GoH3) integrin subunits. Ln-1 assembly can also be disturbed with antibodies against its E8 domain and by competitive inhibition with a synthetic peptide (AG-73) derived from its G-4 domain. Quantitative RT-PCR showed that the dermis contributes about 80% of the laminin γ1 chain mRNA while 20% is produced by the epidermis which emphasizes its dual tissue origin and the major contribution of the mesenchyma in laminin production. The laminin γ2 chain mRNA, present in Ln-5, was mostly of epidermal origin. This study presents evidence that during the initiation of basement membrane formation, laminins bind to keratinocyte plasma membrane receptors and thus may serve as nucleation sites for further polymerization of these compounds by a self-assembly process.

en-copyright= kn-copyright= en-aut-name=FleischmajerRaul en-aut-sei=Fleischmajer en-aut-mei=Raul kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=UtaniAtsushi en-aut-sei=Utani en-aut-mei=Atsushi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=Douglas MacDonald IIE. en-aut-sei=Douglas MacDonald II en-aut-mei=E. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=PerlishJerome S en-aut-sei=Perlish en-aut-mei=Jerome S kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=PanTe-Cheng en-aut-sei=Pan en-aut-mei=Te-Cheng kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=ChuMon-Li en-aut-sei=Chu en-aut-mei=Mon-Li kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=NomizuMotoyoshi en-aut-sei=Nomizu en-aut-mei=Motoyoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 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=8 ORCID= en-aut-name=YamadaYoshihiko en-aut-sei=Yamada en-aut-mei=Yoshihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= affil-num=1 en-affil= kn-affil=Mount Sinai School of Medicine, New York affil-num=2 en-affil= kn-affil=National Institute of Dental Research, National Institutes of Health affil-num=3 en-affil= kn-affil=Mount Sinai School of Medicine, New York affil-num=4 en-affil= kn-affil=Mount Sinai School of Medicine, New York affil-num=5 en-affil= kn-affil=Thomas Jefferson University affil-num=6 en-affil= kn-affil=Thomas Jefferson University affil-num=7 en-affil= kn-affil=National Institute of Dental Research, National Institutes of Health affil-num=8 en-affil= kn-affil=Okayama University affil-num=9 en-affil= kn-affil=National Institute of Dental Research, National Institutes of Health en-keyword=Basement membrane kn-keyword=Basement membrane en-keyword=Laminin kn-keyword=Laminin en-keyword=Integrin kn-keyword=Integrin END start-ver=1.4 cd-journal=joma no-vol=52 cd-vols= no-issue=5 article-no= start-page=1451 end-page=1460 dt-received= dt-revised= dt-accepted= dt-pub-year=2005 dt-pub=20055 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=ADAMTS-9 is synergistically induced by interleukin-1 and tumor necrosis factor in OUMS-27 chondrosarcoma cells and in human chondrocytes en-subtitle= kn-subtitle= en-abstract= kn-abstract=

Objective
To compare induction of the aggrecanases (ADAMTS-1, ADAMTS-4, ADAMTS-5, ADAMTS-8, ADAMTS-9, and ADAMTS-15) by interleukin-1 (IL-1) and tumor necrosis factor (TNF) in chondrocyte-like OUMS-27 cells and human chondrocytes, and to determine the mechanism of induction of the most responsive aggrecanase gene.

Methods
OUMS-27 cells were stimulated for different periods of time and with various concentrations of IL-1 and/or TNF. Human chondrocytes obtained from osteoarthritic joints and human skin fibroblasts were also stimulated with IL-1 and/or TNF. Total RNA was extracted, reverse transcribed, and analyzed by quantitative real-time polymerase chain reaction and Northern blotting. ADAMTS-9 protein was examined by Western blotting, and the role of the MAPK signaling pathway for ADAMTS9 induction in IL-1-stimulated OUMS-27 cells was investigated.

Results IL-1 increased messenger RNA (mRNA) levels of ADAMTS4, ADAMTS5, and ADAMTS9 but not ADAMTS1 and ADAMTS8. The fold increase for ADAMTS9 mRNA was greater than that for mRNA of the other aggrecanase genes. The increase of ADAMTS9 mRNA by IL-1 stimulation was greater in chondrocytes than in fibroblasts. The combination of IL-1 and TNF had a synergistic effect, resulting in a considerable elevation in the level of ADAMTS9 mRNA. ADAMTS-9 protein was also induced in IL-1-stimulated OUMS-27 cells. The MAPK inhibitors SB203580 and PD98059 decreased ADAMTS9 up-regulation in OUMS-27 cells.

Conclusion
ADAMTS9 is an IL-1- and TNF-inducible gene that appears to be more responsive to these proinflammatory cytokines than are other aggrecanase genes. Furthermore, these cytokines had a synergistic effect on ADAMTS9. Together with the known ability of ADAMTS-9 to proteolytically degrade aggrecan and its potential to cleave other cartilage molecules, the data suggest that ADAMTS-9 may have a pathologic role in arthritis.

en-copyright= kn-copyright= en-aut-name=DemircanKadir en-aut-sei=Demircan en-aut-mei=Kadir kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 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=2 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=3 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=4 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=5 ORCID= en-aut-name=YonezawaTomoko en-aut-sei=Yonezawa en-aut-mei=Tomoko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=ApteSuneel S. en-aut-sei=Apte en-aut-mei=Suneel S. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 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=8 ORCID= affil-num=1 en-affil= kn-affil=Okayama University Graduate School of Medicine and Dentistry affil-num=2 en-affil= kn-affil=Okayama University Graduate School of Medicine and Dentistry affil-num=3 en-affil= kn-affil=Okayama University Graduate School of Medicine and Dentistry affil-num=4 en-affil= kn-affil=Okayama University Graduate School of Medicine and Dentistry affil-num=5 en-affil= kn-affil=Okayama University Graduate School of Medicine and Dentistry affil-num=6 en-affil= kn-affil=Okayama University Graduate School of Medicine and Dentistry affil-num=7 en-affil= kn-affil=Lerner Research Institute, Cleveland Clinic Foundation affil-num=8 en-affil= kn-affil=Okayama University Graduate School of Medicine and Dentistry en-keyword=ADAMTS kn-keyword=ADAMTS en-keyword=aggrecanase kn-keyword=aggrecanase en-keyword=arthritis kn-keyword=arthritis en-keyword=chondrocyte kn-keyword=chondrocyte en-keyword=metalloproteinases kn-keyword=metalloproteinases en-keyword=IL-1 kn-keyword=IL-1 END start-ver=1.4 cd-journal=joma no-vol=54 cd-vols= no-issue=3 article-no= start-page=103 end-page=109 dt-received= dt-revised= dt-accepted= dt-pub-year=2000 dt-pub=200006 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Heat shock protein 72 expression in the right ventricle of patients undergoing congenital cardiac surgery. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

While heat shock protein (HSP) 72 is known as a stress protein, there have been no reports of HSP 72 expression in patients who have undergone surgery for congenital heart disease. Fourteen patients (7 males and 7 females) who had undergone surgery for congenital heart disease were studied. The ages of the patients ranged from 2 months to 43 years old (mean 6.5 +/- 10.8 years old; median 3.0 years old). The diagnoses were Tetralogy of Fallot in seven, pulmonary atresia with ventricular septal defect (VSD) in three, complex anomalies in three, and VSD in one patient. Histological study and HSP analysis using Western blots and immunostaining with anti-HSP 72 monoclonal antibody were performed for right ventricular muscle samples resected during the surgery. The histological findings showed hypertrophic changes of ventricular cardiomyocytes in all samples studied. Western blots detected HSP 72 expression of various degrees in all specimens. Immunostaining using monoclonal antibody against HSP 72 showed that the protein was present in the nuclei and cytoplasm of cardiomyocytes. In conclusion, although it is difficult to determine the cause of the "stress" that triggers HSP 72 expression in cardiomyocytes, low O2 saturation and pressure overload might act as a "stress", and the only common factor that induced HSP 72 in every sample was hypertrophy.

en-copyright= kn-copyright= en-aut-name=NakamuraKoki en-aut-sei=Nakamura en-aut-mei=Koki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=IrieHiroyuki en-aut-sei=Irie en-aut-mei=Hiroyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=FujisawaEmi en-aut-sei=Fujisawa en-aut-mei=Emi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=YoshiokaHidekatsu en-aut-sei=Yoshioka en-aut-mei=Hidekatsu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 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=5 ORCID= en-aut-name=SakumaIsao en-aut-sei=Sakuma en-aut-mei=Isao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=SanoShunji en-aut-sei=Sano en-aut-mei=Shunji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=Okayama University affil-num=5 en-affil= kn-affil=Okayama University affil-num=6 en-affil= kn-affil=Okayama University affil-num=7 en-affil= kn-affil=Okayama University en-keyword=heat shock protein 72 (HSP 72) kn-keyword=heat shock protein 72 (HSP 72) en-keyword=human kn-keyword=human en-keyword=heart kn-keyword=heart en-keyword=congentional cardiac surgery kn-keyword=congentional cardiac surgery en-keyword=hypertrophy kn-keyword=hypertrophy END start-ver=1.4 cd-journal=joma no-vol=63 cd-vols= no-issue=2 article-no= start-page=79 end-page=85 dt-received= dt-revised= dt-accepted= dt-pub-year=2009 dt-pub=200904 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=The 3'-untranslated region of ADAMTS1 regulates its mRNA stability en-subtitle= kn-subtitle= en-abstract= kn-abstract=

ADAMTS1 (a disintegrin and metalloproteinase with thrombospondin motifs 1) is an inflammatory-induced gene. We have previously reported that ADAMTS1 was strongly but transiently expressed in the infarcted heart. In this study, we investigated whether a 3'-untranslated region (UTR) affects the mRNA stability of this gene. When stimulated with tissue necrosis factor (TNF)-alpha, the expression level of ADAMTS1 mRNA rapidly increased, but the induction of ADAMTS1 mRNA peaked at 6h after stimulation, after which the expression levels of ADAMTS1 mRNA decreased. The 3'-UTR ADAMTS1 mRNA contains multiple adenine and uridine-rich elements, suggesting that the 3'-UTR may regulate gene stability. The addition of actinomycin D, an RNA synthesis inhibitor, demonstrated the decay of induced ADAMTS1 mRNA by TNF-alpha. Furthermore, a region containing multiple AUUUA motifs within the ADAMTS1 3'-UTR destabilized transfected Enhanced Green Fluorescence Protein (EGFP) mRNA expression. These results demonstrated that the ADAMTS1 3'-UTR may regulate the expression of ADAMTS1 mRNA.

en-copyright= kn-copyright= 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=1 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=2 ORCID= en-aut-name=YaykasliKursat Oguz en-aut-sei=Yaykasli en-aut-mei=Kursat Oguz kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 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=4 ORCID= en-aut-name=DemircanKadir en-aut-sei=Demircan en-aut-mei=Kadir kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=ShinohataRyoko en-aut-sei=Shinohata en-aut-mei=Ryoko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=YonezawaTomoko en-aut-sei=Yonezawa en-aut-mei=Tomoko 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=KusachiShozo en-aut-sei=Kusachi en-aut-mei=Shozo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 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=10 ORCID= affil-num=1 en-affil= kn-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=3 en-affil= kn-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=4 en-affil= kn-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=5 en-affil= kn-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=6 en-affil= kn-affil=Department of Medical Technology, Graduate School of Health Sciences, Okayama University affil-num=7 en-affil= kn-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=8 en-affil= kn-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=9 en-affil= kn-affil=Department of Medical Technology, Graduate School of Health Sciences, Okayama University affil-num=10 en-affil= kn-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences en-keyword=ADAMTS1 kn-keyword=ADAMTS1 en-keyword=gene regulation kn-keyword=gene regulation en-keyword=metalloproteinase kn-keyword=metalloproteinase END start-ver=1.4 cd-journal=joma no-vol=56 cd-vols= no-issue=1 article-no= start-page=25 end-page=29 dt-received= dt-revised= dt-accepted= dt-pub-year=2002 dt-pub=200202 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Human BRAL1 and BCAN genes that belong to the link-module superfamily are tandemly arranged on chromosome 1q21-23. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

We herein determined by fluorescence in situ hybridization the chromosomal localization of 2 human genes, BRAL1 and BCAN, both of which belong to the link-module superfamily, i.e. to the same band of chromosome 1q21-23. Further analysis of the genomic organization of BRAL1 and BCAN revealed that the BRAL1 gene was located 20-kb upstream of the BCAN start site. We isolated a polymorphic dinucleotide (CA) repeat sequence from a genomic clone containing the BCAN gene. High heterozygosity (0.79) makes this polymorphism a useful marker in the study of genetic disorders. Knowledge of the structure of the genes and the marker provides essential information for further analysis of the gene locus at chromosome 1q21-23.

en-copyright= kn-copyright= en-aut-name=NomotoHiroyuki en-aut-sei=Nomoto en-aut-mei=Hiroyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 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=2 ORCID= en-aut-name=HirakawaSatoshi en-aut-sei=Hirakawa en-aut-mei=Satoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=UekiYasuyoshi en-aut-sei=Ueki en-aut-mei=Yasuyoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=OhtsukiHiroshi en-aut-sei=Ohtsuki en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 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=6 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=Okayama University affil-num=5 en-affil= kn-affil=Okayama University affil-num=6 en-affil= kn-affil=Okayama University en-keyword=BRAL1 kn-keyword=BRAL1 en-keyword=BCAN kn-keyword=BCAN en-keyword=FISH kn-keyword=FISH en-keyword=schizophrenia kn-keyword=schizophrenia en-keyword=polymorphic marker kn-keyword=polymorphic marker END start-ver=1.4 cd-journal=joma no-vol=50 cd-vols= no-issue=3 article-no= start-page=145 end-page=150 dt-received= dt-revised= dt-accepted= dt-pub-year=1996 dt-pub=199606 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Regulation of Interleukin-2 Receptor y Chain mRNA Expression in Human Monocytic Cell Line THP-1 en-subtitle= kn-subtitle= en-abstract= kn-abstract=

Circulating hepatitis C virus (HCV) particles can be fractionated by means of differential flotation centrifugation. It is reported that in the bottom fraction HCV is in the form immune complexes, whereas in the top, it is free of antibodies. We evaluated the significance of circulating complex and free HCV in chronic hepatitis C, and assessed the relationship in terms of the response to interferon (IFN) therapy. We examined sera before, just after, and 1 year after administering IFN to 18 patients with chronic hepatitis C, 10 of whom responded (group CR), and 8 did not (group NR). The amounts of virus were similar between both groups before therapy. After differential flotation centrifugation with 1.063 g/ml of NaCl, the top and bottom fractions were assayed for HCV RNA. Before therapy, HCV RNA was detected in the top fraction in 1 of 10 in group CR, and in 6 of 8 in group NR (P < 0.05, chi-square test). HCV RNA was positive in the bottom fraction of all samples. In a follow-up study of group NR, HCV RNA was detected in the top fraction in 3 of 8 just after IFN therapy, and in 7 of 8 after 1 year. This study suggests that the presence of HCV in the top fraction can predict a poor response to IFN therapy.

en-copyright= kn-copyright= en-aut-name=YanaiHiroyuki en-aut-sei=Yanai en-aut-mei=Hiroyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=YoshinoTadashi en-aut-sei=Yoshino en-aut-mei=Tadashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=TakahashiKiyoshi en-aut-sei=Takahashi en-aut-mei=Kiyoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 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=4 ORCID= en-aut-name=AkagiTadaatsu en-aut-sei=Akagi en-aut-mei=Tadaatsu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=Okayama University affil-num=5 en-affil= kn-affil=Okayama University en-keyword=IL-2R ??chain kn-keyword=IL-2R ??chain en-keyword=phorbol ester kn-keyword=phorbol ester en-keyword=monocyte kn-keyword=monocyte en-keyword=differentiation kn-keyword=differentiation en-keyword=protein kinase kn-keyword=protein kinase END start-ver=1.4 cd-journal=joma no-vol=14 cd-vols= no-issue= article-no= start-page=7 end-page=11 dt-received= dt-revised= dt-accepted= dt-pub-year=1997 dt-pub=199710 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=コラーゲン遺伝子改変と動物の疾患モデル en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=NinomiyaYoshifumi en-aut-sei=Ninomiya en-aut-mei=Yoshifumi kn-aut-name=二宮喜文 kn-aut-sei=二宮 kn-aut-mei=喜文 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部分子医化学 END