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. Author manuscript; available in PMC: 2009 Oct 19.
Published in final edited form as: Eur J Cell Biol. 2003 May;82(5):209–221. doi: 10.1078/0171-9335-00316

Fig. 6.

Fig. 6

Presence of a stable pool of immunoreactive Cx50 in cells transfected with hCx50P88S. (A, B) Immunoblots of homogenates from HeLa-wt hCx50 (A) or HeLa-hCx50P88S (B) cells that were left untreated (lanes 0) or treated with 40 µg/ml cycloheximide for 1, 3 or 21 h (lanes 1, 3, 21, respectively) using anti-Cx50 antibodies. (Exposure times for A and B were different). (C–F) Photomicrographs showing Cx50 immunoreactivity in HeLa cells transfected with wild-type hCx50 (C, E) or hCx50P88S (D, F) that were left untreated (C, D) or treated with cycloheximide for 12 hours (E, F). (G) Northern blot of Cx50 RNA from HeLa-wt hCx50 (lane 1) and HeLa-hCx50P88S (lane 2) cells hybridized with a hCx50 probe. (Because cells were transfected with DNAs encoding wt hCx50 or hCx50P88S in the same vector, pSFFV-neo, the mRNA sizes of wt hCx50 and hCx50P88S are identical). (H, I) Immunoblots of homogenates from HeLa-wt hCx50 (lanes 1) and HeLa-hCx50P88S (lanes 2) cells reacted with anti-Cx50 (H) or antivimentin (I) antibodies. Bar represents 29 µm in C, and 26 µm in D, E and F.