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TargetMol cftr function
( ETI) treatment on cystic fibrosis transmembrane conductance protein <t>(CFTR)</t> <t>function</t> and infection pattern in cystic fibrosis (CF) cultures. A) Fold change in TEER measurements after 24 hours of ETI treatement (+ ETI) or no treatement (-ETI) in ALI cultures from three CF donors homozygous for ΔF508 mutation. B) TEEC after CFTR stimulation in treated (+ ETI) and untreated (-ETI) cells. Each dot represents one independent donor. C) TEER change after 14 h of infection with PAO1 laboratory strain in treated (+ ETI) and untreated (-ETI). D) Bacterial growth (CFU) after 14 h of infection in the apical (non attached / free bacteria), attached to the epithelium, and basolateral compartment, along with the total number of bacteria. In A,C-D, each dot represents one independent experiment and the mean ± SD is included. Statistical significance was calculated by paired two-sided t-test where **p<0.01 and ****p<0.0001. E) Three-dimensional reconstruction of confocal microscopy images of immunofluorescent staining of CFTR protein in ALI cultures from the CF donors treated (+ ETI) and untreated (-ETI). Green: Anti-CFTR 570 (CFTR protein), Red: Phalloidin (F-actin), Blue: DAPI (nuclei). ALI: air-liquid interface; TEER: transepithelial electrical resistance; TEEC: transepithelial electrical conductance; CFU: colony-forming units.
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TargetMol cftr inhibitor ppq
( ETI) treatment on cystic fibrosis transmembrane conductance protein <t>(CFTR)</t> <t>function</t> and infection pattern in cystic fibrosis (CF) cultures. A) Fold change in TEER measurements after 24 hours of ETI treatement (+ ETI) or no treatement (-ETI) in ALI cultures from three CF donors homozygous for ΔF508 mutation. B) TEEC after CFTR stimulation in treated (+ ETI) and untreated (-ETI) cells. Each dot represents one independent donor. C) TEER change after 14 h of infection with PAO1 laboratory strain in treated (+ ETI) and untreated (-ETI). D) Bacterial growth (CFU) after 14 h of infection in the apical (non attached / free bacteria), attached to the epithelium, and basolateral compartment, along with the total number of bacteria. In A,C-D, each dot represents one independent experiment and the mean ± SD is included. Statistical significance was calculated by paired two-sided t-test where **p<0.01 and ****p<0.0001. E) Three-dimensional reconstruction of confocal microscopy images of immunofluorescent staining of CFTR protein in ALI cultures from the CF donors treated (+ ETI) and untreated (-ETI). Green: Anti-CFTR 570 (CFTR protein), Red: Phalloidin (F-actin), Blue: DAPI (nuclei). ALI: air-liquid interface; TEER: transepithelial electrical resistance; TEEC: transepithelial electrical conductance; CFU: colony-forming units.
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MedChemExpress cftr inhibitor 172
( ETI) treatment on cystic fibrosis transmembrane conductance protein <t>(CFTR)</t> <t>function</t> and infection pattern in cystic fibrosis (CF) cultures. A) Fold change in TEER measurements after 24 hours of ETI treatement (+ ETI) or no treatement (-ETI) in ALI cultures from three CF donors homozygous for ΔF508 mutation. B) TEEC after CFTR stimulation in treated (+ ETI) and untreated (-ETI) cells. Each dot represents one independent donor. C) TEER change after 14 h of infection with PAO1 laboratory strain in treated (+ ETI) and untreated (-ETI). D) Bacterial growth (CFU) after 14 h of infection in the apical (non attached / free bacteria), attached to the epithelium, and basolateral compartment, along with the total number of bacteria. In A,C-D, each dot represents one independent experiment and the mean ± SD is included. Statistical significance was calculated by paired two-sided t-test where **p<0.01 and ****p<0.0001. E) Three-dimensional reconstruction of confocal microscopy images of immunofluorescent staining of CFTR protein in ALI cultures from the CF donors treated (+ ETI) and untreated (-ETI). Green: Anti-CFTR 570 (CFTR protein), Red: Phalloidin (F-actin), Blue: DAPI (nuclei). ALI: air-liquid interface; TEER: transepithelial electrical resistance; TEEC: transepithelial electrical conductance; CFU: colony-forming units.
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Cayman Chemical cftr inhibitor cayman chemical (15545)
Pharmacological inhibitors and activators used in this study.
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Image Search Results


( ETI) treatment on cystic fibrosis transmembrane conductance protein (CFTR) function and infection pattern in cystic fibrosis (CF) cultures. A) Fold change in TEER measurements after 24 hours of ETI treatement (+ ETI) or no treatement (-ETI) in ALI cultures from three CF donors homozygous for ΔF508 mutation. B) TEEC after CFTR stimulation in treated (+ ETI) and untreated (-ETI) cells. Each dot represents one independent donor. C) TEER change after 14 h of infection with PAO1 laboratory strain in treated (+ ETI) and untreated (-ETI). D) Bacterial growth (CFU) after 14 h of infection in the apical (non attached / free bacteria), attached to the epithelium, and basolateral compartment, along with the total number of bacteria. In A,C-D, each dot represents one independent experiment and the mean ± SD is included. Statistical significance was calculated by paired two-sided t-test where **p<0.01 and ****p<0.0001. E) Three-dimensional reconstruction of confocal microscopy images of immunofluorescent staining of CFTR protein in ALI cultures from the CF donors treated (+ ETI) and untreated (-ETI). Green: Anti-CFTR 570 (CFTR protein), Red: Phalloidin (F-actin), Blue: DAPI (nuclei). ALI: air-liquid interface; TEER: transepithelial electrical resistance; TEEC: transepithelial electrical conductance; CFU: colony-forming units.

Journal: bioRxiv

Article Title: Infection dynamics and virulence potential of clinical Pseudomonas aeruginosa isolates in a human airway epithelium model system

doi: 10.1101/2025.04.11.644308

Figure Lengend Snippet: ( ETI) treatment on cystic fibrosis transmembrane conductance protein (CFTR) function and infection pattern in cystic fibrosis (CF) cultures. A) Fold change in TEER measurements after 24 hours of ETI treatement (+ ETI) or no treatement (-ETI) in ALI cultures from three CF donors homozygous for ΔF508 mutation. B) TEEC after CFTR stimulation in treated (+ ETI) and untreated (-ETI) cells. Each dot represents one independent donor. C) TEER change after 14 h of infection with PAO1 laboratory strain in treated (+ ETI) and untreated (-ETI). D) Bacterial growth (CFU) after 14 h of infection in the apical (non attached / free bacteria), attached to the epithelium, and basolateral compartment, along with the total number of bacteria. In A,C-D, each dot represents one independent experiment and the mean ± SD is included. Statistical significance was calculated by paired two-sided t-test where **p<0.01 and ****p<0.0001. E) Three-dimensional reconstruction of confocal microscopy images of immunofluorescent staining of CFTR protein in ALI cultures from the CF donors treated (+ ETI) and untreated (-ETI). Green: Anti-CFTR 570 (CFTR protein), Red: Phalloidin (F-actin), Blue: DAPI (nuclei). ALI: air-liquid interface; TEER: transepithelial electrical resistance; TEEC: transepithelial electrical conductance; CFU: colony-forming units.

Article Snippet: To subsequently inhibit CFTR function, a solution containing CFTR inhibitor PPQ-102 30 μM (TargetMol) was added to the apical side.

Techniques: Infection, Mutagenesis, Bacteria, Confocal Microscopy, Staining

Pharmacological inhibitors and activators used in this study.

Journal: Cells

Article Title: Effects of Akt Activator SC79 on Human M0 Macrophage Phagocytosis and Cytokine Production

doi: 10.3390/cells13110902

Figure Lengend Snippet: Pharmacological inhibitors and activators used in this study.

Article Snippet: CFTR inh 172 , CFTR inhibitor , Cayman Chemical (15545).

Techniques:

SC79 activates NO production via Akt. ( A ) Bar graph of endpoint DAF-FM fluorescence from 5 independent experiments using macrophages from different donors. Responses were tested with 0.1–10 µg/mL SC79 ± Akt inhibitors MK2206 (10 µg/mL) or GSK690693 (10 µM), PKC inhibitor Gö6983 (10 µM), PKA inhibitor H89 (10 µM), NOS inhibitor L-NAME (10 µM), or inactive D-NAME (10 µM). Significance was determined via one-way ANOVA with Dunnett’s post-test, comparing values to those for HBSS alone; * p < 0.05. ( B ) DAF-FM fluorescence data with 1 and 10 µg/mL SC79 ± 10 µM CFTR inh 172 pretreatment. No significant differences were determined via one-way ANOVA. ( C ) Representative real-time traces of DAF-FM fluorescence, ± L-NAME or D-NAME. Time of addition of the indicated drugs is denoted by the arrow. ( D ) Data from 5 independent experiments done similarly as in ( C ). Significance was determined via one-way ANOVA with Dunnett’s post-test, comparing values to those for SC79 alone; * p < 0.05.

Journal: Cells

Article Title: Effects of Akt Activator SC79 on Human M0 Macrophage Phagocytosis and Cytokine Production

doi: 10.3390/cells13110902

Figure Lengend Snippet: SC79 activates NO production via Akt. ( A ) Bar graph of endpoint DAF-FM fluorescence from 5 independent experiments using macrophages from different donors. Responses were tested with 0.1–10 µg/mL SC79 ± Akt inhibitors MK2206 (10 µg/mL) or GSK690693 (10 µM), PKC inhibitor Gö6983 (10 µM), PKA inhibitor H89 (10 µM), NOS inhibitor L-NAME (10 µM), or inactive D-NAME (10 µM). Significance was determined via one-way ANOVA with Dunnett’s post-test, comparing values to those for HBSS alone; * p < 0.05. ( B ) DAF-FM fluorescence data with 1 and 10 µg/mL SC79 ± 10 µM CFTR inh 172 pretreatment. No significant differences were determined via one-way ANOVA. ( C ) Representative real-time traces of DAF-FM fluorescence, ± L-NAME or D-NAME. Time of addition of the indicated drugs is denoted by the arrow. ( D ) Data from 5 independent experiments done similarly as in ( C ). Significance was determined via one-way ANOVA with Dunnett’s post-test, comparing values to those for SC79 alone; * p < 0.05.

Article Snippet: CFTR inh 172 , CFTR inhibitor , Cayman Chemical (15545).

Techniques: Fluorescence

SC79 enhancement of phagocytosis is not altered by CFTR inh 172. ( A ) The same type of FITC E. coli phagocytosis experiments as in , testing the SC79 ± CFTR inh 172 pretreatment. ( B ) The same type of phagocytosis experiments of pHrodo S. aureus as in , but testing SC79 ± CFTR inh 172 pretreatment. Significance was determined via one-way ANOVA with Bonferroni’s post-test with paired comparisons; * p < 0.05 vs. 0 µg/mL SC79 (HBSS + 0.1% DMSO vehicle control); n.s. means there was no statistical significance between bracketed groups. Data from 5–6 independent experiments per condition with macrophages from different donors.

Journal: Cells

Article Title: Effects of Akt Activator SC79 on Human M0 Macrophage Phagocytosis and Cytokine Production

doi: 10.3390/cells13110902

Figure Lengend Snippet: SC79 enhancement of phagocytosis is not altered by CFTR inh 172. ( A ) The same type of FITC E. coli phagocytosis experiments as in , testing the SC79 ± CFTR inh 172 pretreatment. ( B ) The same type of phagocytosis experiments of pHrodo S. aureus as in , but testing SC79 ± CFTR inh 172 pretreatment. Significance was determined via one-way ANOVA with Bonferroni’s post-test with paired comparisons; * p < 0.05 vs. 0 µg/mL SC79 (HBSS + 0.1% DMSO vehicle control); n.s. means there was no statistical significance between bracketed groups. Data from 5–6 independent experiments per condition with macrophages from different donors.

Article Snippet: CFTR inh 172 , CFTR inhibitor , Cayman Chemical (15545).

Techniques: Control