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. Author manuscript; available in PMC: 2011 Feb 1.
Published in final edited form as: Biochim Biophys Acta. 2010 Jan 15;1803(2):323–332. doi: 10.1016/j.bbamcr.2010.01.006

Figure 3. p38 kinase functions as the downstream effector of IKKα to mediate increased Cyclin D1 degradation in the UVB response.

Figure 3

(A) WT, IKKβ−/− and IKKα−/− cells were exposed to different doses of UVB and the activation status of p38K, ERKs and GSK3β was determined by western-blot assay 1 hr after UVB exposure. (B) WT, IKKα−/− and IKKα−/− (IKKα) cells were exposed to different doses of UVB and the activation status of p38K was determined by western-blot assay 1 hr after UVB exposure. (C) WT cells were pretreated with the inhibitors of JNKs (10 µM SP600125), ERKs (50 µM PD98059), p38K (20 µM SB202190) or their vehicle control (DMSO) for 1 hr and then left untreated or exposed to UVB irradiation (1.0 kJ/m2). After treatment with 10 µM CHX at the indicated time points, cells were harvested and Cyclin D1 levels were detected by western-blot assay. (D) WT cells were pretreated with 20µM SB202190 or DMSO for 1 hr and then exposed to UVB irradiation (1.0 kJ/m2). The phosphorylation and expression of Cyclin D1 were detected at the indicated time points after UVB exposure.