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. Author manuscript; available in PMC: 2013 Sep 1.
Published in final edited form as: Nat Immunol. 2012 Aug 5;13(9):823–831. doi: 10.1038/ni.2378

Figure 1.

Figure 1

NLRC3 inhibits MyD88- and TRAF6-dependent activation of NF-κB. (a) Luciferase activity in HEK293T cells transfected with a luciferase reporter vector driven by an NF-κB-responsive promoter, plus empty vector (EV) or vector encoding MyD88, IRAK, TRAF6, IKKα or p65, and increasing concentrations (wedges) of a vector encoding NLRC3; results are presented relative to results obtained in the absence of NLRC3. *P < 0.001 and **P < 0.0001 (Student’s t-test). (b, c) Expression of TNF and IL6 in THP-1 cell lines stably transduced with retrovirus expressing empty vector or Flag-tagged NLRC3 (b) or empty vector or shNLRC3 (c) and stimulated with LPS; results were normalized to the expression of ACTB (encoding β-actin) and are presented relative to those of untreated cells. (d, e) Production of TNF and IL-6 by THP-1 cells transduced as in b(d) or c(e) and simulated with LPS. (f) Immunoblot analysis of total and phosphorylated (p-) IκBα in THP-1 cells transduced as in b, c and simulated with LPS; actin serves as a loading control throughout. Data are representative of at least three independent experiments (mean and s.e.m. in a–e).