The immunosuppressive fungal metabolite gliotoxin specifically inhibits transcription factor NF-kappaB.

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The immunosuppressive fungal metabolite gliotoxin specifically inhibits transcription factor NF-kappaB

Opportunistic infections, such as aspergillosis, are among the most serious complications suffered by immunocompromised patients. Aspergillus fumigatus and other pathogenic fungi synthesize a toxic epipolythiodioxopiperazine metabolite called gliotoxin. Gliotoxin exhibits profound immunosuppressive activity in vivo. It induces apoptosis in thymocytes, splenocytes, and mesenteric lymph node cell...

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The nuclear factor-kappaB (NF-kappaB): from a versatile transcription factor to a ubiquitous therapeutic target.

The nuclear factor-kappaB (NF-kappaB) transcription factors regulate a plethora of cellular pathways and processes including the immune response, inflammation, proliferation, apoptosis and calcium homeostasis. In addition to the complexity of its physiological roles, the composition and function of this family of proteins is very complicated. While the basic understanding of NF-kappaB signallin...

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The nuclear factor-kappaB (NF-κB): from a versatile transcription factor to a ubiquitous therapeutic target

The nuclear factor-κappaB (NF-κB) transcription factors regulate a plethora of cellular pathways and processes including the immune response, inflammation, proliferation, apoptosis and calcium homeostasis. In addition to the complexity of its physiological roles, the composition and function of this family of proteins is very complicated. While the basic understanding of NF-κB signalling is ext...

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Tumor necrosis factor (TNF)-alpha is a potent inducer of apoptotic cell death in various tissues, whereas the transcription factor nuclear factor (NF)-kappaB is essential to protect against TNF-alpha-induced apoptosis. Human hepatoma cell lines were used to investigate the effectiveness and specificity of the fungal metabolite gliotoxin in inhibiting TNF-alpha-induced NF-kappaB activation in tr...

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ژورنال

عنوان ژورنال: Journal of Experimental Medicine

سال: 1996

ISSN: 0022-1007,1540-9538

DOI: 10.1084/jem.183.4.1829