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Jung, J.S., Kim, D.H. and Kim, H.S. (2010) Ginsenoside Rh1 suppressesinducible nitric oxide synthase gene expression in IFN-gamma-stimulated microglia via modulation of JAK/STAT and ERK signaling pathways. Biochemical and Biophysical Research Communications, 397, 323-328. doi:10.1016/j.bbrc.2010.05.117

has been cited by the following article:

• TITLE: The talented interferon-gamma

  AUTHORS: Fan-Ching Lin, Howard A. Young

  KEYWORDS: IFN-γ; Inflammation; Autoimmune; Cancer; Inflammatory Bowel Diseases; Neurodegenerative Diseases; Stem Cells

  JOURNAL NAME: Advances in Bioscience and Biotechnology, Vol.4 No.7C, July 17, 2013

  ABSTRACT: IFN-γ is an extraordinarily pleotropic cytokine. It can not only heighten both the innate and adaptive immune response against pathogens and tumors, but also has the ability to maintain immune homeostasis. Since the effects of IFN-γ are cell and tissue specific, it is important to consider the recent advances in IFN-γ signaling in the context of different diseases. To this end, we review the involvement of IFN-γ in the pathogenesis of several inflammatory diseases, its therapeutic potential as an anti-tumor agent and its effects upon stem cells.