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Chunk #24 — Results — NF-κB DNA binding activity

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Neuroadaptations in human chronic alcoholics: dysregulation of the NF-kappaB system.
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not recognize specific DNA sequences, and is present at high levels in the human brain [48], [49]. The levels of the constitutively active and total (active plus latent) NF-κB DNA-binding were measured in the presence of 0.03% and 0.6% DOC, respectively; at high concentration DOC dissociates complexes of NF-κB with the IκB inhibitory protein [24], [38], [47]. The NF-κB/complex I was induced by pre-incubation of extracts from the PFC of control subjects or alcoholics with 0.6% DOC only by 12% and 14%, respectively; thus NF-κB was virtually present in the activated form in this structure (Figure 3A, lane 4). 0.6% DOC slightly inhibited p50 homodimer binding to DNA. The p50 homodimer was a dominant κB binding factor in the human cortex; the levels of its DNA-binding activity exceeded those of NF-κB by 2.4–2.7 fold in the PFC and MC of controls and alcoholics (Student's t-test for dependent samples: PFC/controls, T1,10 = 8.56, P<0.0001, n = 11; PFC/alcoholics, T1,12 = 12.77, P<0.0001, n = 13 (see Figure 3B, lines 1, 2, 4–8); MC/controls, T1,10 = 10.83, P<0.0001, n = 11; MC/alcoholics, T1,12 = 8.48, P<0.0001, n = 13).