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  • Open Access

    REVIEW

    Anti-nutritional characteristics and mechanism of soybean agglutinin

    LI PAN1, JIAWEI LIU1, MOHAMMED HAMDY FAROUK2,*, GUIXIN QIN1,*, NAN BAO1, YUAN ZHAO1, HUI SUN1

    BIOCELL, Vol.45, No.3, pp. 451-459, 2021, DOI:10.32604/biocell.2021.014289 - 03 March 2021

    Abstract Soybean agglutinin (SBA) is an important anti-nutritional factor in soybean. SBA can induce animal growth inhibition, cause pathological changes of intestinal tissue, and decrease in the immune system functioning. Recently, a great deal of research has been done on the effects of SBA on cell morphology, division, apoptosis, autophagy, as well as the correlated signal transduction pathway. This review mainly covers the chemical and biological characteristics of SBA, describes the multifaceted aspects of SBA anti-nutritional functions, and highlights the possible cellular and molecular mechanism of anti-nutritional effects of SBA. This review has important implications for More >

  • Open Access

    ARTICLE

    Different dynamics of IL-15R activation following IL-15 cis- or trans-presentation

    Harmonie Perdreau1,2, Erwan Mortier1,2, Grégory Bouchaud1,2, Véronique Solé1,2, Yvan Boublik3, Ariane Plet1,2,*, Yannick Jacques1,2,*

    European Cytokine Network, Vol.21, No.4, pp. 297-307, 2010, DOI:10.1684/ecn.2010.0207

    Abstract Interleukin (IL)-15 is a cytokine critical for the homeostasis and the function of NK cells, NK-Tcells, and memory CD8+ T cells. IL-15 signals are delivered through the IL-15Rβ and the commonγ (γc) receptorchains. The third receptor chain, IL-15Rα, confers specificity and high affinity for the cytokine. While IL-15 canactivate with high affinity the trimeric receptor expressed by a target cell (cis-presentation), IL-15Rα is alsoknown to trans-present IL-15 with high affinity to target cells expressing the IL-15Rβ/γc complex. In order tocompare the IL-15 cis- and trans-presentation processes, and using a T cell line expressing both IL-15Rα/β/γc andIL-15Rβ/γc, we analyzed cell… More >

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