Publications by authors named "Miki Tanabe"

Article Synopsis
  • The study investigates the localization and development of myeloid cells in transgenic frogs, specifically focusing on myeloperoxidase-positive cells in the liver cortex during late tadpole stages.
  • Findings show that myelopoiesis in the liver cortex starts at stage 50 and peaks by stage 56, with transplantation experiments revealing these cells originated from the dorso-lateral plate in the neurula embryo.
  • Analysis of cells isolated from the liver indicates that myeloid cells dominate the blood cell population in larval liver, and following metamorphosis, there is an expansion of both myeloid and erythroid colonies, confirming the liver cortex as a key site for granulopoiesis.
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CPI-17 is a phosphorylation-dependent inhibitor of smooth muscle myosin light chain. Using yeast two-hybrid system, we have identified the receptor for activated C kinase 1 (RACK1) as a novel interaction partner of CPI-17. The direct interaction and co-localization of CPI-17 with RACK1 were confirmed by immunoprecipitation and confocal microscopy analysis, respectively.

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Rationale: Augmented bronchial smooth muscle (BSM) contraction is one of the causes of bronchial hyperresponsiveness. The protein RhoA and its downstream pathways have now been proposed as a new target for asthma therapy. MicroRNAs (miRNAs) play important roles in normal and diseased cell functions, and a contribution of miR-133 to RhoA expression has been suggested in cardiomyocytes.

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Interleukin-13 (IL-13) is one of the central mediators for development of airway hyperresponsiveness in asthma. The signal transducer and activation of transcription 6 (STAT6) is one of the major signal transducers activated by IL-13, and a possible involvement of IL-13/STAT6 pathway in the augmented bronchial smooth muscle (BSM) contraction has been suggested. In the present study, the effect of a novel STAT6 inhibitor, AS1517499, on the development of antigen-induced BSM hyperresponsiveness was investigated.

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