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. 2009 Nov 3;106(46):19328–19333. doi: 10.1073/pnas.0908797106

Fig. 4.

Fig. 4.

(A) Sequence of IκBα; the sites of stabilizing mutations are shown in bold. (B) Stabilized IκBα variants wild-type IκBα (•), IκBα (C186P, A220P) (■), IκBα (Q111G) (▴), IκBα (Y254L/Q255H) (○), and IκBα (Y254L/T257A) (+) were less able to enhance dissociation. (C) For 3 different promoter sequences (HIV-κB, MIP2, RANTES), decreases in the rate of active dissociation for IκBα (C186P, A220P) (○, HIV-κB; ▴, MIP2; ■, RANTES) were similar to those observed with wild-type IκBα (•, HIV-κB; +, MIP2; ♦, RANTES).