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. Author manuscript; available in PMC: 2011 Mar 1.
Published in final edited form as: Mol Cell Neurosci. 2010 Jan 4;43(3):315–325. doi: 10.1016/j.mcn.2009.12.005

Figure 6.

Figure 6

KChIP4a-mediated increase in stabilization of Kv4.2 requires PKA phosphorylation of S552. (A) Immunoblots of total protein from COS7 cells, which were co-transfected with Kv4.2 or Kv4.2S552A along with either control vector or KChIP4a for 48 hr. (B) Normalized total protein level of Kv4.2 was increased by co-expression with KChIP4a compared to Kv4.2 expression alone. In contrast, the total level of Kv4.2S552A was not different between KChIP4a and control vector co-expression. (C-D) Chronic forskolin treatment (10 μM, 24 hr) greatly enhanced the stability of total Kv4.2 protein levels when co-expressed with KChIP4a compared with control vector, but no differences were found in the total level of Kv4.2S552A with forskolin treatment between control and KChIP4a co-expression. Error bars represent S.E.M. (E) Enhanced stability of wild type Kv4.2 was found after co-expression with either KChIP isoform. Protein levels of Kv4.2S552A, however, were only increased after KChIP1 expression. KChIP4a but not KChIP1 therefore requires S552 phosphorylation of Kv4.2 to enhance protein stability (n = 4). Error bars represent S.E.M.