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A genetic Xenopus laevis tadpole model to study lymphangiogenesis
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Glucocorticoids repress NF-kappa B-driven genes by disturbing the interaction of p65 with the basal transcription machinery, irrespective of coactivator levels in the cell.
(2000) PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA. 97(8). p.3919-3924 -
The nuclear factor-kappa B engages CBP/p300 and histone acetyltransferase activity for transcriptional activation of the interleukin-6 gene promoter.
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p38 and extracellular signal-regulated kinase mitogen-activated protein kinase pathways are required for nuclear factor kappa B p65 transactivation mediated by tumor necrosis factor.
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Induction of unresponsiveness to tumor necrosis factor (TNF) after autocrine TNF expression requires TNF membrane retention.
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Recombination signal sequence binding protein J kappa is constitutively bound to the NF-kappa B site of the interleukin-6 promoter and acts as a negative regulatory factor.
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Tumour necrosis factor: intracellular mechanism of action
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The p38/RK mitogen-activated protein kinase pathway regulates interleukin-6 synthesis in response to tumour necrosis factor.
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TNF-induced intracellular signaling leading to gene induction or to cytotoxicity by necrosis or by apoptosis.