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Dive into the research topics where Shozo Irino is active.

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Featured researches published by Shozo Irino.


Stem Cells | 1996

THROMBOPOIETIN MODULATES PLATELET ACTIVATION IN VITRO THROUGH PROTEIN-TYROSINE PHOSPHORYLATION

Yoshitsugu Kubota; Takeshi Arai; Terukazu Tanaka; Genji Yamaoka; Hiroyuki Kiuchi; Tatsushi Kajikawa; Koichi Kawanishi; Hiroaki Ohnishi; Masahiro Yamaguchi; Jiro Takahara; Shozo Irino

To determine the roles of thrombopoietin (TPO) in platelet function in vitro, we examined the effects of TPO on platelet aggregation. Although several proteins in platelets were tyrosine‐phosphorylated by TPO treatment, TPO alone was unable to induce platelet aggregation. However, the secondary wave of platelet aggregation induced by adenosine diphosphate (ADP) was enhanced by TPO in a dose‐dependent manner. TPO in conjunction with ADP augmented tyrosine phosphorylation of platelet proteins, including tyrosine‐phosphorylated proteins induced by TPO alone. Genistein inhibited protein‐tyrosine phosphorylation in platelets induced by TPO with ADP and suppressed TPOenhanced platelet aggregation. Moreover, tyrosine phosphorylation of MAP‐kinases induced by TPO alone and TPO with ADP was consistent with TPO‐enhanced platelet aggregation. These findings in the present study suggest that signal transduction involved in TPO‐enhanced platelet aggregation is mediated in part by tyrosine‐phosphorylated proteins, including MAP‐kinases, in platelets through TPO‐stimulated c‐Mpl, TPO receptor.


Leukemia | 1997

Antisense src expression inhibits tyrosine phosphorylation of Shc and its association with Grb2 and Sos which leads to MAP kinase activation in U937 human leukemia cells

Masahiro Yamaguchi; Terukazu Tanaka; Masato Waki; Akira Kitanaka; Hiroshi Kamano; Yoshitsugu Kubota; Hiroaki Ohnishi; Jiro Takahara; Shozo Irino

We constructed a recombinant plasmid which expresses antisense src RNA after dexamethasone (Dexa) treatment, and transfected it into U937 human monoblastic leukemia cells (U937-ASRC). Induction of antisense src RNA expression diminished the amounts of c-Src and its protein tyrosine kinase (PTK) activity in U937-ASRC cells. The declines in c-Src and its PTK activity subsequently reduced the proliferation of U937-ASRC cells. To elucidate the growth signal transduction pathway downstream of c-Src, tyrosine phosphorylation of Shc was examined in U937-ASRC cells treated with Dexa. The decline in c-Src by induction of antisense src RNA expression decreased the level of tyrosine phosphorylation of Shc. Immunoprecipitated c-Src directly phosphorylated immunoprecipitated Shc on tyrosine residues in vitro. The amounts of Grb2 and Sos co-immunoprecipitated with Shc were decreased after Dexa treatment. However, the amount of Sos co-immunoprecipitated with Grb2 was apparently not affected by Dexa treatment. These results indicate that Grb2 and Sos constitutively associate with each other in U937 cells. Furthermore, the level of phosphorylation on tyrosine (204) essential for MAP kinase activation was decreased after Dexa treatment. Taken together with all these findings, it is suggested that c-Src directly phosphorylates Shc on tyrosine residues, which in turn binds to Grb2 constitutively associated with Sos to form a Shc-Grb2-Sos complex, and that the complex formation is coupled with MAP kinase activation mediated by Ras activation in U937 cells.


Journal of Neuroendocrinology | 1990

Effects of somatostatin on the growth hormone-releasing factor-induced growth hormone secretion in rats with electrical and chemical inhibitions of endogenous growth hormone-releasing factor and somatostatin.

Makoto Sato; Jiro Takahara; Michio Niimi; Shozo Irino

The episodic pattern of growth hormone (GH) secretion of the male rat was simulated in rats exhibiting impaired GH‐releasing factor (GRF) and Somatostatin (SRIF) secretion, by administering various combinations of human GRF‐(1–44)NH2 (hGRF) and SRIF. Electrical lesions of the arcuate nucleus resulted in a marked decrease in the amplitude of GH secretory bursts, while the administration of cysteamine (200 mg/kg) did not change the GH secretory profile in rats with arcuate nucleus lesions. Immunohistochemical examinations revealed a marked decrease of GRF and SRIF immunoreactivity in the median eminence of the cysteamine‐treated rats with arcuate nucleus lesions. The intravenous injection of 5 μg of hGRF every 3 h caused equivalent surges of GH in the cysteamine‐treated rats with arcuate nucleus lesions. The additional infusion of 4 μg/h of SRIF during the trough periods of GH secretion did not affect the amplitude of the GH surges. Hourly injection of 5 μg of hGRF caused transient desensitization to hGRF. Interestingly, the additional infusion of 4 μg/h of SRIF every 3 h enhanced the amplitude of the GH bursts induced by the fourth and the seventh hGRF injections. However, the more frequent injection of 5 μg of hGRF every 30 min caused constant desensitization to hGRF with time, and the additional infusion of 4 μg/h of SRIF every 3 h did not change the attenuated responses to hGRF. These results indicated that the simultaneous administration of hourly GRF and continuous SRIF with brief pauses was most effective for producing high GH peaks. This simulation model suggests that SRIF may play an important role not only in the production of GH troughs, but also in the maintenance of GH surges with distinct peaks in the male rat.


Leukemia Research | 1991

Usefulness of a small scale indirect 125I-labelled protein a binding assay for detection of monoclonal antibodies against hematopoietic cell surface antigens

Yoshitsugu Kubota; Terukazu Tanaka; Kyoko Iida-Tanaka; Shozo Irino

We describe a small-scale solid-phase indirect 125iodine protein A binding assay (IPA) and discuss its usefulness for detection of hematopoietic cell surface antigens and for screening hybridoma clones producing monoclonal antibodies (McAbs) against K562 cell surface antigens correlated with differentiation induced by 12-O-tetradecanoyl phorbol-13-acetate (TPA). This assay was performed in polystyrene Terasaki microtest plates instead of 96-well microtiter plates, using hematopoietic cells attached to the wells by air drying. This method facilitates washing procedures and reduces the radioactive waste. The specificity of this IPA method is as high as those of RIAs and ELISAs generally used. Titration curves of a McAb, My7, specific for CD13 on HL60 and TPA-treated HL60 (HL60-TPA) cells, were linear between the 10(-1) and 10(-4) dilutions. A difference in the CD13 expression between HL60 and HL60-TPA cells could be detected by both IPA and flow cytometry using My7 at 10(-1)-10(-3) dilutions. At the 10(-3) dilution, however, CD13 expressed on HL60 cells was detected by the IPA method but not by flow cytometry. These results show that the sensitivity of IPA is superior to that of flow cytometry. By screening hybridoma clones with this IPA method, we succeeded in producing three interesting and useful McAbs (21H73, 37G7 and 49C12) against K562 cell surface antigens whose expression was altered after the differentiation induced by TPA. We also demonstrated that the IPA method is suitable for cell surface marker analysis of leukemia cells freshly isolated from patients.


Journal of the Japan Society of the Reticuloendothelial System | 1988

An autopsy case of Gaucher's disease (adult type).

Hiroaki Ohnishi; Masami Nagai; Shozo Irino; Hitoshi Miki; Ichiro Yamadori; Tomoko Morikawa

An autopsy case of Gauchers disease (adult type) was reported. A 39-years-old man was admitted to our hospital because of dyspnea. Splenomegaly was documented when he was 3-years-old. Physical examination revealed generalized edema, kyphoscoliosis and giant splenomegaly. Any abnormal neurological findings could not detected. Bone marrow aspiration biopsy revealed several clusters of Gaucher cells with “wrinkled tissue paper” like cytoplasm and round eccentric nucleus. The acid phosphatase activity in the serum increased to 38.5u/l, whereas the angiotensin converting enzyme activity was normal, perhaps because of steroid therapy. Inspite of intensive treatement, he died of respiratory failure.Autopsy findings revealed that Gaucher cells had proliferated in spleen, liver, bone marrow and lungs. Histochemically, these cells were positive stainini for acid phosphatase, PAS, Naphthol-AS-D-chloroacetate and negative for lysozyme. Electron microscopically, characteristic spindle-shaped and membrane-delimitted inclusion bodies were observed within the cytoplasm of the cells.Biochemically, the amount of glucocerebroside extracted from autopsy liver and spleen was greatly increased and the activity of glucocerebrosidase in his cultured skin fibroblasts were markedly low comparing with normal volunteers, confirming that the defect of this enzyme was the cause of this disorder.In Japan there were only eight cases of this disease (adult type) reported.


Journal of Immunology | 1994

Characterization of unique human TCR V beta specificities for a family of streptococcal superantigens represented by rheumatogenic serotypes of M protein.

Rika Watanabe-Ohnishi; Jacob Aelion; Leighton LeGros; Mark Tomai; Evgeni V. Sokurenko; Duane Newton; Jiro Takahara; Shozo Irino; Sahar M. Rashed; Malak Kotb


Leukemia | 1994

Effect of ubenimex on the proliferation and differentiation of U937 human histiocytic lymphoma cells.

Murata M; Yoshitsugu Kubota; Terukazu Tanaka; Iida-Tanaka K; Jiro Takahara; Shozo Irino


Endocrinology | 1988

Physiological Role of Growth Hormone (GH)-Releasing Factor and Somatostatin in the Dynamics of GH Secretion in Adult Male Rat

Makoto Sato; Jiro Takahara; Yuzuru Fujioka; Michio Niimi; Shozo Irino


Leukemia | 1993

Reverse transcription-polymerase chain reaction for PML-RAR alpha fusion transcripts in acute promyelocytic leukemia and its application to minimal residual leukemia detection.

Ikeda K; Sasaki K; Taizo Tasaka; Nagai M; Kawanishi K; Jiro Takahara; Shozo Irino


AIDS Research and Human Retroviruses | 1993

Isolation of a cDNA Clone Encoding DNA-Binding Protein (TAXREB107) That Binds Specifically to Domain C of the tax-Responsive Enhancer Element in the Long Terminal Repeat of Human T-Cell Leukemia Virus Type I

Toshiro Morita; Takako Sato; Hiroshi Nyunoya; Atsumi Tsujimoto; Jiro Takahara; Shozo Irino; Kunitada Shimotohno

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Taizo Tasaka

Kawasaki Medical School

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