研究者詳細 - 岡野　栄之

論文 - 岡野　栄之

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Argos induces programmed cell death in the developing Drosophila eye by inhibition of the Ras pathway

Sawamoto Kazunobu, Taguchi Akiko, Hirota Yuki, Yamada Chiharu, Jin Ming Hao, Okano Hideyuki

Cell Death and Differentiation 5 （ 4 ） 262 - 270 1998年04月

ISSN 1350-9047

We studied the role of Ras signaling in the regulation of cell death during Drosophila eye development. Overexpression of Argos, a diffusible inhibitor of the EGF receptor and Ras signaling, caused excessive cell death in developing eyes at pupal stages. The Argos-induced cell death was suppressed by coexpression of the anti-apoptotic genes p35, diap1, or diap2 in the eye as well as by the Df(3L)H99 chromosomal deletion that lacks three apoptosis-inducing genes, reaper, head involution defective (hid) and grim. Transient misexpression of the activated Ras1 protein (Ras1(V12)) later in pupal development suppressed the Argos-induced cell death. Thus, Argos-induced cell death seemed to have resulted from the suppression of the anti-apoptotic function of Ras. Conversely, cell death induced by overexpression of Hid was suppressed by gain-of-function mutations of the genes coding for MEK and ERK. These results support the idea that Ras signaling functions in two distinct processes during eye development, first triggering the recruitment of cells and later negatively regulating cell death.

Localization of 5-HT2A receptor in rat cerebral cortex and olfactory system revealed by immunohistochemistry using two antibodies raised in rabbit and chicken

Hamada Shun, Senzaki Kouji, Hamaguchi-Hamada Kayoko, Tabuchi Katsuhiko, Yamamoto Hideko, Yamamoto Toshifumi, Yoshikawa Shingo, Okano Hideyuki, Okado Nobuo

Brain Research Molecular Brain Research 54 （ 2 ） 199 - 211 1998年03月

ISSN 0169-328X

Serotonin 2A receptor (5-HT2A receptor) is widely distributed in the central nervous system, and has been suggested to be involved in a variety of behavioral conditions and neuropsychiatric disorders. Two polyclonal antibodies were raised against the N-terminus peptide of rat 5-HT2A receptor in chickens (5-HT2A-N) and a glutathione S-transferase fusion protein that contained the C-terminus of the mouse 5-HT2A receptor in rabbits (5-HT2A-C). Affinity-purified 5-HT2A-N and -C antibodies reacted strongly with a single band of 77-78 kDa in postsynaptic density proteins prepared from the rat cortex. The distribution pattern of immunoreactive structures in the rat brain was virtually the same for the two antibodies. The highest levels of immunoreactivity were observed in the olfactory bulb, neocortex, claustrum, piriform cortex, mamillary bodies, pontine nuclei, red nucleus and cranial motor nuclei. In the olfactory bulb, mitral cells were intensely labeled. In the neocortex, many immunoreactive neurons were found in layers II-VI. In layer IV of the neocortex, strong neuropil labeling was observed. In a double-labeling study using chicken 5-HT2A-N and rabbit anti-glial fibrillary acidic protein (GFAP) antibody, a considerable number of GFAP positive cells also showed 5-HT2A immunoreactivity. By using an immunoelectron microscopic technique, 5-HT2A receptor immunoreaction was shown to be localized just beneath the postsynaptic membrane thickening of asymmetric synapses.

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Inositol 1,4,5-trisphosphate receptor mediates ventralising signals in Xenopus embryos

Kume Shoen, Muto Akira, Okano Hideyuki, Mikoshiba Katsuhiko

Zygote 6 （ 1 SUPPL. ） 1998年

ISSN 0967-1994

Caenorhabditis elegans anti-apoptotic gene ced-9 prevents ced-3-induced cell death in Drosophila cells

Hisahara Shin, Kanuka Hirotaka, Shoji Shin Ichi, Yoshikawa Shingo, Okano Hideyuki, Miura Masayuki

Journal of Cell Science 111 （ 6 ） 667 - 673 1998年

ISSN 0021-9533

ced-9, a member of the bcl-2 gene family in Caenorhabditis elegans plays a central roles in preventing cell death in worms. Overexpression of human bcl-2 can partially prevent cell death in C. elegans. However, it remains to be elucidated whether ced-9 can regulate cell death when expressed in other organisms. We demonstrated that the CED-9 protein is co-localized with BCL-2 in COS cells and Drosophila Schneider's L2 (SL2) cells, suggesting that the site of CED-9 action is located to specific cytoplasmic compartments. Overexpression of ced-9 only poorly protected cells from the death induced by ced-3 in HeLa cells, but ced-9 significantly reduced the cell death induced by ced-3 in Drosophila SL2 cells. Furthermore, apoptosis of SL2 cells that was induced by a Drosophila cell-death gene, reaper, was shown to be partially prevented by ced-9, bcl-2 and bcl-xL. These results suggest that the signaling pathway that is required for the anti-apoptotic function of bcl-2 family members, including ced-9, is conserved in Drosophila cells. In addition, SL2 cells provide a unique systems for dissecting the main machinery of cell death.

Control of the cell death pathway by Dapaf-1, a Drosophila Apaf-1/CED-4-related caspase activator

Kanuka Hirotaka, Sawamoto Kazunobu, Inohara Naohiro, Matsuno Kenji, Okano Hideyuki, Miura Masayuki

Molecular Cell 4 （ 5 ） 757 - 769 1999年11月

ISSN 1097-2765

We identified a Drosophila Apaf-1/CED-4 homolog gene, dapaf-1. Alternative splicing results in two dapaf-1 mRNA species, which encode distinct forms of caspase activator, Dapaf-1L (Apaf-1 type) and Dapaf-1S (CED-4 type). Distinct caspases were activated by these Dapaf-1 isoforms. Loss of Dapaf-1 function resulted in defective cytochrome c-dependent caspase activities and reduced apoptosis in embryo and in larval brain. Dapaf-1 activities were also involved in cell death induced by ectopic expression of reaper in the compound eye. These data suggest that Dapaf-1/cytochrome c-dependent cell death-inducing machinery is present in Drosophila, and the requirement of Dapaf-1/Apaf-1 in neural cell death is conserved through evolution.

Cloning and characterization of Dfak56, a homolog of focal adhesion kinase, in Drosophila melanogaster

Fujimoto Jiro, Sawamoto Kazunobu, Okabe Masataka, Takagi Yasumitsu, Tezuka Tohru, Yoshikawa Shingo, Ryo Haruko, Okano Hideyuki, Yamamoto Tadashi

Journal of Biological Chemistry 274 （ 41 ） 29196 - 29201 1999年10月

ISSN 0021-9258

The focal adhesion kinase (FAK) protein-tyrosine kinase plays important roles in cell adhesion in vertebrates. Using polymerase chain reaction-based cloning strategy, we cloned a Drosophila gene that is homologous to the vertebrate FAK family of protein-tyrosine kinases. We designated this gene Dfak56 and characterized its gene product. The overall protein structure and deduced amino acid sequence of Dfak56 show significant similarity to those of FAK and PYK2. Dfak56 has in vitro autophosphorylation activity at tyrosine residues. Expression of the Dfak56 mRNA and the protein was observed in the central nervous system and the muscle-epidermis attachment site in the embryo, where Drosophila position-specific integrins are localized. The results suggest that like FAK in vertebrates, Dfak56 functions downstream of integrins. Dfak56 was tyrosine-phosphorylated upon integrin-dependent attachment of the cell to the extracellular matrix. We conclude that the Dfak56 tyrosine kinase is involved in integrin-mediated cell adhesion signaling and thus is a functional homolog of vertebrate FAK.

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Musashi and Seven in absentia downregulate Tramtrack through distinct mechanisms in Drosophila eye development

Hirota Yuki, Okabe Masataka, Imai Takao, Kurusu Mitsuhiko, Yamamoto Atsuyo, Miyao Sachiyo, Nakamura Makoto, Sawamoto Kazunobu, Okano Hideyuki

Mechanisms of Development 87 （ 1-2 ） 93 - 101 1999年09月

ISSN 0925-4773

We have examined the roles played by the Drosophila neural RNA-binding protein Musashi (MSI) in eye development. MSI expression was observed in the nuclei of all photoreceptor cells (R1-R8). Although a msi loss-of-function mutation resulted in only weak abnormalities in photoreceptor differentiation, we found that the msi eye phenotype was significantly enhanced in a seven in absentia (sina) background. sina is known to be involved in the degradation of the Tramtrack (TTK) protein, leading to the specification of the R7 fate. We demonstrated that MSI also functions to regulate TTK expression. The sina msi mutants showed significantly high ectopic expression of TTK69 and failure in the determination of the R1, R6, and R7 fates. Other photoreceptor cells also failed to differentiate with abnormalities occurring late in the differentiation process. These results suggest that MSI and SINA function redundantly to downregulate TTK in developing photoreceptor cells. Copyright (C) 1999 Elsevier Science Ireland Ltd.

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Mammalian ELAV-like neuronal RNA-binding proteins HuB and HuC promote neuronal development in both the central and the peripheral nervous systems

Akamatsu Wado, Okano Hirotaka J., Osumi Noriko, Inoue Takayoshi, Nakamura Shun, Sakakibara Shin Ichi, Miura Masayuki, Matsuo Nobutake, Darnell Robert B., Okano Hideyuki

Proceedings of the National Academy of Sciences of the United States of America 96 （ 17 ） 9885 - 9890 1999年08月

ISSN 0027-8424

Hu proteins are mammalian embryonic lethal abnormal visual system (ELAV)-like neuronal RNA-binding proteins that contain three RNA recognition motifs. Although Drosophila ELAV is required for the correct differentiation and survival of neurons, the roles played by the Hu genes in the mammalian nervous system remain largely unknown. To explore the in vivo functions of mouse Hu proteins, we overexpressed them in rat pheochromocytoma PC12 cells, where they induced neuronal phenotype in the absence of nerve growth factor. We have characterized the functions of various forms of mHuB and mHuC bearing point mutations or deletions. Mutants of mHuC that had amino acid exchanges in the RNP1 domain of the first or second RNA recognition motifs (RRMs) lost biologic activity as well as RNA-binding activity. In addition, the mutants containing only the third RRM failed to induce the neuronal phenotype in PC12 cells and inhibited the biologic activity of cotransfected wild-type mHuB and mHuC, thus acting as a dominant-negative form. However, these mutants could not suppress the nerve growth factor-induced differentiation of PC12 cells. Further, we misexpressed wild-type and dominant-negative Hu in E9.5 mouse embryos, by using electroporation into the neural tube at the level of the rhombencephalon, mHuB and mHuC induced the ectopic expression of neuronal markers, whereas the dominant-negative forms of mHuB and mHuC suppressed the differentiation of central nervous system motor neurons. From these results, we suggest that Hu proteins are required for neuronal differentiation in the mammalian nervous system.

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The Drosophila Ral GTPase regulates developmental cell shape changes through the Jun NH₂-terminal kinase pathway

Sawamoto Kazunobu, Winge Per, Koyama Shinya, Hirota Yuki, Yamada Chiharu, Miyao Sachiyo, Yoshikawa Shingo, Jin Ming Hao, Kikuchi Akira, Okano Hideyuki

Journal of Cell Biology 146 （ 2 ） 361 - 372 1999年07月

ISSN 0021-9525

The Ral GTPase is activated by RalGDS, which is one of the effector proteins for Ras. Previous studies have suggested that Ral might function to regulate the cytoskeleton; however, its in vivo function is unknown. We have identified a Drosophila homologue of Ral that is widely expressed during embryogenesis and imaginal disc development. Two mutant Drosophila Ral (DRal) proteins, DRal(G20V) and DRal(S25N), were generated and analyzed for nucleotide binding and GTPase activity. The biochemical analyses demonstrated that DRal(G20V) and DRal(S25N) act as constitutively active and dominant negative mutants, respectively. Overexpression of the wild-type DRal did not cause any visible phenotype, whereas DRal(G20V) and DRal(S25N) mutants caused defects in the development of various tissues including the cuticular surface, which is covered by parallel arrays of polarized structures such as hairs and sensory bristles. The dominant negative DRal protein caused defects in the development of hairs and bristles. These phenotypes were genetically suppressed by loss of function mutations of hemipterous and basket, encoding Drosophila Jun NH₂-terminal kinase kinase (JNKK) and Jun NH₂-terminal kinase (JNK), respectively. Expression of the constitutively active DRal protein caused defects in the process of dorsal closure during embryogenesis and inhibited the phosphorylation of JNK in cultured S2 cells. These results indicate that DRal regulates developmental cell shape changes through the JNK pathway.

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Caspase activity is required for nephrogenesis in the developing mouse metanephros

Araki Takashi, Saruta Takao, Okano Hideyuki, Miura Masayuki

Experimental Cell Research 248 （ 2 ） 423 - 429 1999年05月

ISSN 0014-4827

Programmed cell death is a mechanism through which organisms get rid of unwanted cells and is thought to be an important process in organogenesis. Although large-scale cell death is observed in the developing kidney, the precise roles of cell death in kidney organogenesis remain to be elucidated. To address this question, we prevented cell death in metanephric explants by applying caspase inhibitors. Administration of caspase inhibitors (Z-D- CH₂DCB and Ac-DEVD-CHO) effectively prevented the cell death that is normally observed in nondifferentiating mesenchymal cells. Both ureteric bud branching and nephrogenesis were prevented by caspase inhibition. Our results suggest that caspases are crucial in kidney organogenesis and cell death in the nondifferentiating mesenchyme.

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Structure, backbone dynamics and interactions with RNA of the C-terminal RNA-binding domain of a mouse neural RNA-binding protein, Musashi1

Nagata Takashi, Kanno Reisuke, Kurihara Yasuyuki, Uesugi Seiichi, Imai Takao, Sakakibara Shin ichi, Okano Hideyuki, Katahira Masato

Journal of Molecular Biology 287 （ 2 ） 315 - 330 1999年03月

ISSN 0022-2836

Musashi1 is an RNA-binding protein abundantly expressed in the developing mouse central nervous system. Its restricted expression in neural precursor cells suggests that it is involved in the regulation of asymmetric cell division. Musashi1 contains two ribonucleoprotein (RNP)-type RNA-binding domains (RBDs), RBD1 and RBD2. Our previous studies showed that RBD1 alone binds to RNA, while the binding of RBD2 is not detected under the same conditions. Joining of RBD2 to RBD1, however, increases the affinity to greater than that of RBD1 alone, indicating that RBD2 contributes to RNA-binding. We have determined the three-dimensional solution structure of the C-terminal RBD (RBD2) of Musashi1 by NMR. It folds into a compact up structure comprising a four-stranded antiparallel β-sheet packed against two α-helices, which is characteristic of RNP-type RBDs. Special structural features of RBD2 include a β-bulge in β2 and a shallow twist of the β-sheet. The smaller ¹H-¹⁵N nuclear Overhauser enhancement values for the residues of loop 3 between β2 and β3 suggest that this loop is flexible in the time-scale of nano- to picosecond order. The smaller ¹⁵N T₂ values for the residues around the border between α2 and the following loop (loop 5) suggest this region undergoes conformational exchange in the milli- to microsecond time-scale. Chemical shift perturbation analysis indicated that RBD2 binds to an RNA oligomer obtained by in vitro selection under the conditions for NMR measurements, and thus the nature of the weak RNA-binding of RBD2 was successfully characterized by NMR, which is otherwise difficult to assess. Mainly the residues of the surface composed of the four-stranded β-sheet, loops and C-terminal region are involved in the interaction. The appearance of side-chain NH proton resonances of arginine residues of loop 3 and imino proton resonances of RNA bases upon complex formation suggests the formation of intermolecular hydrogen bonds. The structural arrangement of the rings of the conserved aromatic residues of β2 and β3 is suitable for stacking interaction with RNA bases, known to be one of the major protein-RNA interactions, but a survey of the perturbation data suggested that the stacking interaction is not ideally achieved in the complex, which may be related to the weaker RNA-binding of RBD2.

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Ectopic expression of constitutively activated Ral GTPase inhibits cell shape changes during Drosophila eye development

Sawamoto Kazunobu, Yamada Chiharu, Kishida Shosei, Hirota Yuki, Taguchi Akiko, Kikuchi Akira, Okano Hideyuki

Oncogene 18 （ 11 ） 1967 - 1974 1999年03月

ISSN 0950-9232

The small GTP-binding protein Ral is activated by RalGDS, one of the effector molecules for Ras. Active Ral binds to a GTPase activating protein for CDC42 and Rac. Although previous studies suggest a role for Ral in the regulation of CDC42 and Rac, which are involved in arranging the cytoskeleton, its in in vivo function is largely unknown. To examine the effect of overexpressing Ral on development, transgenic Drosophila were generated that overexpress wild-type or mutated Ral during eye development. While wild-type Ral caused no developmental defects, expression of a constitutively activated protein resulted in a rough eye phenotype. Activated Rat did not affect cell fate determination in the larval eye discs but caused severe disruption of the ommatidial organization later in pupal development. Phalloidin staining showed that activated Ral perturbed the cytoskeletal structure and cell shape changes during pupal development. This phenotype is similar to that caused by RhoA overexpression. In addition, the phenotype was synergistically enhanced by the coexpression of RhoA. These results suggest that Ral functions to control the cytoskeletal structure required for cell shape changes during Drosophila development.

Stimulation of myelin basic protein gene transcription by fyn tyrosine kinase for myelination

Umemori Hisashi, Kadowaki Yasunori, Hirosawa Kazushige, Yoshida Yutaka, Hironaka Katsunori, Okano Hideyuki, Yamamoto Tadashi

Journal of Neuroscience 19 （ 4 ） 1393 - 1397 1999年02月

ISSN 0270-6474

Myelin is synthesized about the time of birth. The Src-family tyrosine kinase Fyn is involved in the initial events of myelination. Fyn is present in myelin-forming cells and is activated through stimulation of celt surface receptors such as large myelin-associated glycoprotein (L-MAG). Here we show that Fyn stimulates transcription of the myelin basic protein (MBP) gene for myelination. MBP is a major component of the myelin membrane. In 4-week-old Fyn-deficient mice, MBP is significantly reduced, and electron microscopic analysis showed that myelination is delayed, compared with wild-type mice. The Fyn-deficient mice had thinner, more irregular myelin than the wild- type. We found that Fyn stimulates the promoter activity of the MBP gene by approximately sevenfold. The region responsible for the transactivation by Fyn is located between nucleotides -675 and -647 with respect to the transcription start site. Proteins binding to this region were found by gel shift study, and the binding activity correlates with Fyn activity during myelination. These results suggest that transactivation of the MBP gene by Fyn is important for myelination.

Proapoptotic activity of Caenorhabditis elegans CED-4 protein in Drosophila

Kanuka Hirotaka, Hisahara Shin, Sawamoto Kazunobu, Shoji Shin Ichi, Okano Hideyuki, Miura Masayuki

Proceedings of the National Academy of Sciences of the United States of America 96 （ 1 ） 145 - 150 1999年01月

ISSN 0027-8424

CED-4 protein plays an important role in the induction of programmed cell death in Caenorhabditis elegans through the activation of caspases. However, the precise mechanisms by which it activates caspases remain unknown. To investigate the conservation of CED-4 function in evolution, transgenic Drosophila lines that express CED-4 in the compound eye were generated. Ectopic expression of CED-4 in the eyes induced massive apoptotic cell death through caspase activation. An ATP-binding site (P-loop) mutation in CED-4 (K165R) causes a loss of function in its ability to activate Drosophila caspase, and an ATPase inhibitor blocks the CED-4-dependent caspase activity in Drosophila S2 cells. Immunoprecipitation analysis showed that both CED-4 and CED-4 (K165R) bind directly to Drosophila caspase drICE, and the overexpression of CED-4 (K165R) inhibits CED-4-, ecdysone-, or cycloheximide-dependent caspase activation in S2 cells. Furthermore, CED-4 (K165R) partially prevented cell death induced by CED-4 in Drosophila compound eyes. Thus, CED-4 function is evolutionarily conserved in Drosophila, and the molecular mechanisms by which CED-4 activates caspases might require ATP binding and direct interaction with the caspases.

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A genetic approach to visualization neurotechnique of multisynaptic neural pathways using plant lectin transgene

Yoshihara Yoshihiro, Mizuno Takeo, Nakahira Masakiyo, Kawasaki Miwa, Watanabe Yasuyoshi, Kagamiyama Hiroyuki, Jishage Kou ichi, Ueda Otoya, Suzuki Hiroshi, Tabuchi Katsuhiko, Sawamoto Kazunobu, Okano Hideyuki, Noda Tetsuo, Mori Kensaku

Neuron 22 （ 1 ） 33 - 41 1999年01月

ISSN 0896-6273

The wiring patterns among various types of neurons via specific synaptic connections are the basis of functional logic employed by the brain for information processing. This study introduces a powerful method of analyzing the neuronal connectivity patterns by delivering a tracer selectively to specific types of neurons while simultaneously transsynaptically labeling their target neurons. We developed a novel genetic approach introducing cDNA for a plant lectin, wheat germ agglutinin (WGA), as a transgene under the control of specific promoter elements. Using this method, we demonstrate three examples of visualization of specific transsynaptic neural pathways: the mouse cerebellar efferent pathways, the mouse olfactory pathways, and the Drosophila visual pathways. This strategy should greatly facilitate studies on the anatomical and functional organization of the developing and mature nervous system.

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WRM-1 activates the LIT-1 protein kinase to transduce anterior/posterior polarity signals in C. elegans

Rocheleau C. E., Yasuda J., Tae Ho Shin Ho Shin, Lin R., Sawa H., Okano H., Priess J. R., Davis R. J., Mello C. C.

Cell 97 （ 6 ） 717 - 726 1999年

ISSN 0092-8674

During C. elegans development, Wnt/WG signaling is required for differences in cell fate between sister cells born from anterior/posterior divisions. A β-catenin-related gene, wrm-1, and the lit-1 gene are effectors of this signaling pathway and appear to downregulate the activity of POP-1, a TCF/LEF-related protein, in posterior daughter cells. We show here that lit- 1 encodes a serine/threonine protein kinase homolog related to the Drosophila tissue polarity protein Nemo. We demonstrate that the WRM-1 protein binds to LIT-1 in vivo and that WRM-1 can activate the LIT-1 protein kinase when coexpressed in vertebrate tissue culture cells. This activation leads to phosphorylation of POP-1 and to apparent changes in its subcellular localization. Our findings provide evidence for novel regulatory avenues for an evolutionarily conserved Wnt/WG signaling pathway.

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Involvement of caspases in cytotoxic cytokine-mediated oligodendrocyte cell death

Miura M., Hisahara S., Takano R., Shoji S., Okano H.

Protoplasma 206 （ 4 ） 219 - 223 1999年

ISSN 0033-183X

Oligodendrocytes are myelin-forming cells in the mammalian central nervous system. About 50% of oligodendrocytes undergo cell death in normal development. In addition, massive oligodendrocyte cell death has been observed in multiple sclerosis. Tumor necrosis factor (TNF) is thought to be one of the mediators responsible for the damage of oligodendrocytes in multiple sclerosis. The addition of TNF-α to primary cultures of oligodendrocytes significantly decreased the number of live cells in 72 h. DNA fragmentation was detected in TNF-treated oligodendrocytes at 36h by TUNEL assay. Chemical inhibitors Ac-YVAD-CHO (a specific inhibitor of caspase-1[ICE]-like proteases) as well as Ac-DEVD-CHO (a specific inhibitor of caspase-3[CPP32]-like proteases) enhanced the survival of oligodendrocytes treated with TNF-α, indicating that caspase-1- and the caspase-3-mediated cell-death pathways are activated in TNF-induced oligodendrocyte cell death. Caspase-11 is involved in activation of caspase-1. Oligodendrocytes from CASP-11-deficient mice are partially resistant to TNF-induced oligodendrocyte cell death. Our results suggest that the inhibition of caspases may be a novel approach to treat multiple sclerosis.

Learning and memory

Okano Hideyuki, Hirano Tomoo, Balaban Evan

Proceedings of the National Academy of Sciences of the United States of America 97 （ 23 ） 12403 - 12404 2000年11月

ISSN 0027-8424

Memory is one of the most fundamental mental processes. Neuroscientists study this process by using extremely diverse strategies. Two different approaches aimed at understanding learning and memory were introduced in this symposium. The first focuses on the roles played by synaptic plasticity, especially in long-term depression in the cerebellum in motor learning, and its regulatory mechanism. The second approach uses an elegant chick-quail transplantation system on defined brain regions to study how neural populations interact in development to form behaviorally important neural circuits and to elucidate neurobiological correlates of perceptual and motor predispositions.

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神経細胞の再生

柴田護，岡野栄之

日本老年医学会雑誌 37 （ 10 ） 763-770 2000年10月

研究論文（学術雑誌）, 共著

Caspases determine the vulnerability of oligodendrocytes in the ischemic brain

Shibata Mamoru, Hisahara Shin, Hara Hideaki, Yamawaki Takemori, Fukuuchi Yasuo, Yuan Junying, Okano Hideyuki, Miura Masayuki

Journal of Clinical Investigation 106 （ 5 ） 643-653 2000年09月

研究論文（学術雑誌）, 共著

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岡野 栄之

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