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Fig. 5 | Cell & Bioscience

Fig. 5

From: Functional characterization of SLC26A3 c.392C>G (p.P131R) mutation in intestinal barrier function using CRISPR/CAS9-created cell models

Fig. 5

Identification of SLC26A3 as a CFTR and ZO-1 binding partner and effects on their interaction. a Endogenous IP assays of Caco-2 WT, P131R and RWT cell lysates showing that SLC26A3 co-precipitated with ZO-1 and CFTR, as well as that the interaction between SLC26A3 and ZO-1 is significantly decreased in P131R-SLC26A3 cells (P < 0.05). IgG was used as a negative control, GAPDH was used as an input control. b Densitometry analysis of endogenous IP assays. c P131R promotes SLC26A3 ubiquitination. WT, P131R and RWT cells were untreated (left panel) or stimulated with 100 ng/ml of TNF-α for 20 h (right panel), and cell lysates were assayed for immunoprecipitation (IP), and levels of ubiquitinated SLC26A3 were assessed by immunoblotting (IB). d Ratio of ubiquitination of protein between control and TNF-α treated groups. *P < 0.05, **P < 0.01, ***P < 0.001

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