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. Author manuscript; available in PMC: 2011 Feb 7.
Published in final edited form as: Br J Haematol. 2009 Sep 29;148(1):132–143. doi: 10.1111/j.1365-2141.2009.07925.x

Fig 2.

Fig 2

MS-1020 inhibits JAK3/STAT signaling. L540 (A), HDLM-2 (B) and MDA-MB-468 (C) cells were cultured for 24 hours in the presence of either vehicle (DMSO) alone, MS-1020 at different concentrations or the JAK kinase inhibitor AG490 (150 μmol/L). Whole- cell extracts were processed for Western blot analysis using antibodies specific for the molecules indicated. Treatment with MS-1020 inhibited constitutively-active STAT3 in a cell type-dependent manner (lane 1 and 2). Interestingly, MS-1020 effectively decreased phosphotyrosine JAK3 levels, and showed selectivity for JAK3 over other JAK kinases and oncogenic pathway components, such as Src, Lyn, Akt, EGFR and ERK1/2 (lanes 3-13), suggesting the selectivity of MS-1020 for JAK3. These results are consistent with the finding that MS-1020 abrogated persistently-active STAT3 in cells only with hyper-activated JAK3, such as L540 cells. GAPDH serves as a loading control.