2010
DOI: 10.1074/jbc.m109.065847
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Azadirachtin Interacts with the Tumor Necrosis Factor (TNF) Binding Domain of Its Receptors and Inhibits TNF-induced Biological Responses

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Cited by 38 publications
(17 citation statements)
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“…It potentially inhibits TNF-induced NF-B DNA binding and NF-B-dependent gene expression. These data further support our previous observation where azadirachtin has been shown to interact with TNF receptors and block TNF binding (31). Inhibition of NF-B-dependent gene transcription has shown without inhibition of NF-B DNA binding but by deregulation of p65 phosphorylation.…”
Section: Discussionsupporting
confidence: 80%
“…It potentially inhibits TNF-induced NF-B DNA binding and NF-B-dependent gene expression. These data further support our previous observation where azadirachtin has been shown to interact with TNF receptors and block TNF binding (31). Inhibition of NF-B-dependent gene transcription has shown without inhibition of NF-B DNA binding but by deregulation of p65 phosphorylation.…”
Section: Discussionsupporting
confidence: 80%
“…NF-B, AP-1, NF-AT, and p53 DNA Binding Assay-DNA binding activity of NF-B, AP-1, NF-AT, and p53 was determined by EMSA (26). Briefly, after different treatments, cells, were used to prepare cytoplasmic extracts and nuclear extracts (NE).…”
Section: Methodsmentioning
confidence: 99%
“…We showed that binding of TNFα to its cell surface receptors leads to enhanced activity of the IKK complex, consistent with previous studies highlighting the importance of TNFα signaling to IKK [23, 24]. It should be noted that while preproET-1 levels were significantly elevated after exposure to TNFα, luciferase assays revealed that increases in transcription were comparatively modest.…”
Section: Discussionsupporting
confidence: 91%