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. 2004 May 12;101(21):8221–8226. doi: 10.1073/pnas.0400459101

Fig. 4.

Fig. 4.

Transcomplementation is not a general consequence of sequestering Hsc70 or Hsp70 but requires a specific match between the CFTR mutation and the complementing fragment. (A) Steady-state amounts of Hsp70 and Hsc70 in COS-7 cells transfected with the indicated constructs. (B) CoIP of Hsc70 with ΔF508-CFTR expressed in the presence or absence of fragment 1–633. (C) Hcs70 coimmunoprecipitated with either an amino fragment (1–633V5) or a carboxy fragment (837–1,480) of CFTR. (D) ΔF508-CFTR was not transcomplemented by a carboxy fragment (837–1,480), whereas H1085R-CFTR, a cytosolic-loop-4-processing mutant that associates with severe disease, was complemented by fragment 837–1,480 but not by fragment 1–633. (E) Fragment 837-1,480 also had no effect on the processing of the TPM. (F) Quantitative analysis of the correction of CFTR mutant processing by the indicated constructs. Blots were analyzed by densitometry by using the scion program. In each case, the band C signal was normalized to the total band B plus band C signal. Numbers of experiments are shown in parentheses. Data are means ± SEMs.