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. 2008 Oct 16;40(4):464–473. doi: 10.1165/rcmb.2008-0255OC

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Figure 6. — CSE induced CK2-dependent HDAC2 phosphorylation in human bronchial epithelial and small airway epithelial cells. [A(i)] H292 cells were treated with CSE (2.5%) for 0.5, 1, 2, and 4 hours. Immunoprecipitated HDAC2 was analyzed for phosphorylation of serine residues using specific phospho-serine antibodies by SDS-polyacrylamide gel. CSE induced significant cyclical phosphorylation of HDAC2 on serine residues at 0.5, 1, and 4 hours. [A(ii)] Relative density of phospho-serine level normalized to immunoprecipitated HDAC2. [B(i)] SAECs were exposed to CSE (0.1%, 0.5%, and 1%) for 4 hours. Immunoprecipitated HDAC2 from whole cell lysates was probed for phosphorylation of serine residues. CSE induced a dose-dependent increase in HDAC2 serine phosphorylation. [B(ii)] Relative density of phospho-serine level normalized to immunoprecipitated HDAC2. (C) H292 cells were treated with or without specific CK2 inhibitor, TBB, for 1 hour, and cells were washed with PBS and then treated with freshly prepared CSE (2.5%) for 0.5 hours. Immunoprecipitated HDAC2 was assayed for phosphorylation on serine residues. TBB significantly inhibited CSE-induced HDAC2 phosphorylation. (D) Relative density of phospho-serine level normalized to immunoprecipitated HDAC2. Data expressed as mean ± SEM (n = 3). **P < 0.01, ***P < 0.001, significant compared with control treatments, or respective controls. ^##P < 0.01 significant compared with CSE + TBB versus CSE alone.

Figure 6. — CSE induced CK2-dependent HDAC2 phosphorylation in human bronchial epithelial and small airway epithelial cells. [A(i)] H292 cells were treated with CSE (2.5%) for 0.5, 1, 2, and 4 hours. Immunoprecipitated HDAC2 was analyzed for phosphorylation of serine residues using specific phospho-serine antibodies by SDS-polyacrylamide gel. CSE induced significant cyclical phosphorylation of HDAC2 on serine residues at 0.5, 1, and 4 hours. [A(ii)] Relative density of phospho-serine level normalized to immunoprecipitated HDAC2. [B(i)] SAECs were exposed to CSE (0.1%, 0.5%, and 1%) for 4 hours. Immunoprecipitated HDAC2 from whole cell lysates was probed for phosphorylation of serine residues. CSE induced a dose-dependent increase in HDAC2 serine phosphorylation. [B(ii)] Relative density of phospho-serine level normalized to immunoprecipitated HDAC2. (C) H292 cells were treated with or without specific CK2 inhibitor, TBB, for 1 hour, and cells were washed with PBS and then treated with freshly prepared CSE (2.5%) for 0.5 hours. Immunoprecipitated HDAC2 was assayed for phosphorylation on serine residues. TBB significantly inhibited CSE-induced HDAC2 phosphorylation. (D) Relative density of phospho-serine level normalized to immunoprecipitated HDAC2. Data expressed as mean ± SEM (n = 3). **P < 0.01, ***P < 0.001, significant compared with control treatments, or respective controls. ^##P < 0.01 significant compared with CSE + TBB versus CSE alone.