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Articles by K Masuda
Total Records ( 3 ) for K Masuda
  M Imada , K Masuda , R Satoh , Y Ito , Y Goto , T Matsuoka , S Endo , A Nakamura , H Kawamoto and T. Takai

Activated mature T cells induce various inhibitory receptors implicated in maintaining peripheral tolerance in response to the trans-acting ligands. Interestingly, paired Ig-like receptor (PIR)-B, an inhibitory MHC class I receptor on B cells and myeloid cells, could be involved in regulating early T cell development because epitope for PIR is detected on pre-thymic T/NK progenitors but not on thymocytes or mature T cells. We hypothesized that PIR-B is not only a regulator for T cell development but is also detrimental if expressed on mature T cells. Here we demonstrated, using PIR-B-deficient fetuses, that PIR-B is indeed expressed on the T cell progenitors but failed to identify its distinctive roles in the development. Forced expression of PIR-B in thymocytes and mature T cells also resulted in no abnormalities in development. However, upon antigenic or allogeneic stimulation, peripheral T cells with the ectopic PIR-B showed reduced Th type 1 responses due to the suppression of proximal TCR signaling by constitutive binding of PIR-B to MHC class I on the same cell surface. Our findings suggest that T cell expression of PIR-B with the cis-interacting MHC class I is strictly prohibited in periphery so as to secure prompt immune responses.

  K Takeo , T Kawai , K Nishida , K Masuda , S Teshima Kondo , T Tanahashi and K. Rokutan

The tra2β gene encoding an alternative splicing regulator, transformer 2-β (Tra2β), generates five alternative splice variant transcripts (tra2β15). Functionally active, full-length Tra2β is encoded by tra2β1 isoform. Expression and physiological significance of the other isoforms, particularly tra2β4, are not fully understood. Rat gastric mucosa constitutively expressed tra2β1 isoform and specifically generated tra2β4 isoform that includes premature termination codon-containing exon 2, when exposed to restraint and water immersion stress. Treatment of a gastric cancer cell line (AGS) with arsenite (100 µM) preferentially generated tra2β4 isoform and caused translocation of Tra2β from the nucleus to the cytoplasm in association with enhanced phosphorylation during the initial 4–6 h (acute phase). Following the acute phase, AGS cells continued upregulated tra2β1 mRNA expression, and higher amounts of Tra2β were reaccumulated in their nuclei. Treatment with small interference RNAs targeting up-frameshift-1 or transfection of a plasmid containing tra2β1 cDNA did not induce tra2β4 isoform expression and did not modify the arsenite-induced expression of this isoform, suggesting that neither the nonsense-mediated mRNA decay nor the autoregulatory control by excess amounts of Tra2β participated in the tra2β4 isoform generation. Knockdown of Tra2β facilitated skipping of the central variable region of the CD44 gene and suppressed cell growth. In contrast, overexpression of Tra2β stimulated combinatorial inclusion of multiple variable exons in the region and cell growth. The similar skipping and inclusion of the variable region were observed in arsenite-treated cells. Our results suggest that Tra2β may regulate cellular oxidative response by changing alternative splicing of distinct genes including CD44.

  A Kimura , T Naka , T Nakahama , I Chinen , K Masuda , K Nohara , Y Fujii Kuriyama and T. Kishimoto

Toll-like receptor (TLR) signals perform a crucial role in innate immune responses to pathogens. In this study, we found that the aryl hydrocarbon receptor (Ahr) negatively regulates inflammatory responses mediated by lipopolysaccharide (LPS) in macrophages. Ahr was induced in macrophages stimulated by LPS, but not by transforming growth factor (TGF)-β plus interleukin (IL)-6, which can induce Ahr in naive T cells. The production of IL-6 and tumor necrosis factor (TNF)- by LPS was significantly elevated in Ahr-deficient macrophages compared with that in wild-type (WT) cells. Ahr-deficient mice were more highly sensitive to LPS-induced lethal shock than WT mice. Signal transducer and activator of transcription 1 (Stat1) deficiency, as well as Ahr deficiency, augmented LPS-induced IL-6 production. We found that Ahr forms a complex with Stat1 and nuclear factor-kappa B (NF-B) in macrophages stimulated by LPS, which leads to inhibition of the promoter activity of IL-6. Ahr thus plays an essential role in the negative regulation of the LPS signaling pathway through interaction with Stat1.

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