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Published in final edited form as: Int J Biochem Cell Biol. 2010 Aug 11;43(2):180–188. doi: 10.1016/j.biocel.2010.08.002

Fig 7 — SB220025 inhibits TNF-stimulated p38MAPK, ERK1/2 and MK2 activity and TNF-stimulated proliferation in vitro. Serum deprived AML12 were pre-treated with SB22002 at the indicated doses and then stimulated with TNF (20ng/ml) for 10 min. A) TNF-stimulated MK2 activity is inhibited with increasing concentrations of SB220025 from 0.01 to 5 µM. B) TNF-stimulated MK2 phosphorylation at T222 and T334 is inhibited by SB220025. C) Densitometry analysis of phospho-T222-MK2 and T334-MK2 relative to total levels of MK-2. Replicate samples (n=4–5) were analyzed. D) TNF-stimulated RIP2, ERK, and MK2 with increasing concentrations of SB220025. C) SB220025 inhibited TNF-stimulated cell proliferation as determined by thymidine incorporation as described in Materials and Methods.

Fig 7 — SB220025 inhibits TNF-stimulated p38MAPK, ERK1/2 and MK2 activity and TNF-stimulated proliferation in vitro. Serum deprived AML12 were pre-treated with SB22002 at the indicated doses and then stimulated with TNF (20ng/ml) for 10 min. A) TNF-stimulated MK2 activity is inhibited with increasing concentrations of SB220025 from 0.01 to 5 µM. B) TNF-stimulated MK2 phosphorylation at T222 and T334 is inhibited by SB220025. C) Densitometry analysis of phospho-T222-MK2 and T334-MK2 relative to total levels of MK-2. Replicate samples (n=4–5) were analyzed. D) TNF-stimulated RIP2, ERK, and MK2 with increasing concentrations of SB220025. C) SB220025 inhibited TNF-stimulated cell proliferation as determined by thymidine incorporation as described in Materials and Methods.