anti par1 pe  (R&D Systems)

Journal: Data in Brief

Article Title: Data regarding the effects of thrombin and dabigatran-inhibited thrombin on protease-activated receptor 1 and activation of human atrial fibroblasts

doi: 10.1016/j.dib.2018.05.124

Figure Lengend Snippet: (A) Representative pictures of primary human atrial Fib from patients without AF, immunostained for PAR1 after no treatment or exposure to thrombin (Th), dabigatran followed by thrombin (Dab + Th), or dabigatran alone (Dab). ( B ) Representative pictures of immunofluorescence for PAR1 in primary Fib from non-fibrillating atria, transfected with negative control siRNA (siCTR) or siRNA targeting human PAR1 (siPAR1), with or without subsequent incubation with dabigatran (Dab). Magnification is 200×, bars indicate 50 μm. ( C ) Western blot for PAR1, confirming the knockdown of PAR1 protein after transfection with siPAR1, but not siCTR.

Article Snippet: Cells were incubated for 1 h with a mouse monoclonal primary antibody against Arg27-Thr102 and Ser375-Thr425 of human PAR1 (clone 731115, R&D Systems, Minneapolis, MN, USA), then for 30 min with an Alexa Fluor® 488-conjugated secondary antibody (ThermoFisher Scientific).

Techniques: Immunofluorescence, Transfection, Negative Control, Incubation, Western Blot, Knockdown

Journal: Data in Brief

Article Title: Data regarding the effects of thrombin and dabigatran-inhibited thrombin on protease-activated receptor 1 and activation of human atrial fibroblasts

doi: 10.1016/j.dib.2018.05.124

Figure Lengend Snippet: Representative images ( A ) and quantification ( B ) of immunofluorescence for αSMA in primary human atrial Fib left untreated (CTR), incubated with thrombin (Th) and/or dabigatran (Dab), or transfected with a control (siCTR) or a PAR1-targeting (siPAR1) siRNA with or without subsequent exposure to Th or Dab as indicated. Fib were obtained from subjects with no history of AF. Magnification 200×, bars 50 μm. Data in B are from three independent replicates and were compared by the Kruskal-Wallis test.

Article Snippet: Cells were incubated for 1 h with a mouse monoclonal primary antibody against Arg27-Thr102 and Ser375-Thr425 of human PAR1 (clone 731115, R&D Systems, Minneapolis, MN, USA), then for 30 min with an Alexa Fluor® 488-conjugated secondary antibody (ThermoFisher Scientific).

Techniques: Immunofluorescence, Incubation, Transfection, Control

Journal: Data in Brief

Article Title: Data regarding the effects of thrombin and dabigatran-inhibited thrombin on protease-activated receptor 1 and activation of human atrial fibroblasts

doi: 10.1016/j.dib.2018.05.124

Figure Lengend Snippet: Primary atrial Fib from subjects without AF were left untreated (CTR), exposed to thrombin (Th) and/or dabigatran (Dab), or transfected with a control (siCTR) or a PAR1-targeting (siPAR1) siRNA with or without subsequent incubation with Th or Dab. At the end of treatments, cells were stained with Picro-Sirius red. Representative images of the staining in conventional and polarized light microscopy are given in ( A ) and ( B ), respectively, while quantification of the red signal in conventional light microscopy is presented in ( C ). Magnification is 200× and bars correspond to 50 μm. Data in the graph are from three independent replicates and were compared by using the Kruskal-Wallis test.

Article Snippet: Cells were incubated for 1 h with a mouse monoclonal primary antibody against Arg27-Thr102 and Ser375-Thr425 of human PAR1 (clone 731115, R&D Systems, Minneapolis, MN, USA), then for 30 min with an Alexa Fluor® 488-conjugated secondary antibody (ThermoFisher Scientific).

Techniques: Transfection, Control, Incubation, Staining, Light Microscopy

Journal: Data in Brief

Article Title: Data regarding the effects of thrombin and dabigatran-inhibited thrombin on protease-activated receptor 1 and activation of human atrial fibroblasts

doi: 10.1016/j.dib.2018.05.124

Figure Lengend Snippet:

Article Snippet: Cells were incubated for 1 h with a mouse monoclonal primary antibody against Arg27-Thr102 and Ser375-Thr425 of human PAR1 (clone 731115, R&D Systems, Minneapolis, MN, USA), then for 30 min with an Alexa Fluor® 488-conjugated secondary antibody (ThermoFisher Scientific).

Techniques: Microscopy, Fluorescence, Light Microscopy, Software, Knockdown, Expressing, Immunofluorescence, Western Blot, Staining, Activation Assay

Journal: Oncotarget

Article Title: Exogenous cathepsin G upregulates cell surface MHC class I molecules on immune and glioblastoma cells

doi: 10.18632/oncotarget.12980

Figure Lengend Snippet: A. SC35, SC38, and SC40 were incubated with CatG, LF, CatGinh., DMSO, CatG with LF, CatG with LF and CatG inhibitor (CatGinh.), CatG with LF and DMSO, or CatG with CatGinh. for 24h at 37°C. Cell surface expression of A . PAR1 or B. MHC I was determined by flow cytometry. All values were normalized to the isotype control. Eight independent experiments were performed ( n = 8) and summarized in a bar diagram. SC35, SC38, and SC40 were treated with different proteases (CatG, CatS, NE, PAR3, and thrombin) for 24h at 37°C and levels of PAR1 C. or MHC I D. were analyzed by flow cytometry. Nine independent experiments were performed ( n = 9) and values were normalized to the isotype control.

Article Snippet: Cell surface MHC I or PAR1 (anti-human PAR1, PE conjugated, monoclonal mouse IgG2B, R&D Systems, Abingdon, UK) was determined by flow cytometry as described above.

Techniques: Incubation, Expressing, Flow Cytometry, Control