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. Author manuscript; available in PMC: 2011 Mar 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2010 Feb 5;30(3):395–402. doi: 10.1161/ATVBAHA.109.191395

Figure 1.

Figure 1

SMC TNFR-1 and LTβR signaling differentially activates classical and alternative NF-κB pathways. SMC were stimulated with 1 ng/mL TNF or 10 μg/mL α-LTβR or buffer for the indicated time points. A, Immunoblot analysis of TNF-induced p100 accumulation and IκBα degradation (left) and α-LTβR–induced p100 to p52 processing (right) in total cell homogenates. *,>Unspecific bands. B, Immunoblot analysis of TNF-induced and α-LTβR–induced nuclear translocation of RelA and RelB in SMC. C, Electrophoretic mobility shift assay/super-shift analysis of TNF-induced RelA complexes and α-LTβR–induced RelA and RelB complexes. Open arrow, shifted complexes; closed arrow, RelA complexes; arrowhead, RelB complexes; control, pre-immune serum. D, Combined stimulation of TNFR-1 and LTβR in SMC hyperinduces p52 and RelB nuclear translocation. Immunoblot analysis of cytoplasmic and nuclear p100, p52, RelB, and RelA levels in untreated (un) and in 24-hour α-LTβR–stimulated (L), TNF-stimulated (T), or α-LTβR+TNF–stimulated (LT) SMC. Actin and polymerase II Western blotting for cytoplasmic and nuclear extracts, respectively (Ctrl in D), or by Coomassie staining of immunoblots (A–C; not shown) served as loading controls.

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