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(A) Ifn-β−/− BMDMs were infected with Mtb H37Rv at MOI of 3 for 4h and flow cytometry was conducted at 4hpi to measure surface receptor expression levels of IFNAR1 and <t>IFNAR2.</t> (B and C) Ifn-β−/− BMDMs were infected as described in the presence of 300pg/ml IFN-β. Cell lysates were collected at 20 min post infection and immunoblotted for pJAK1 (Y1022/1023), total JAK1, pTYK2 (Y1054/1055), and total TYK2. (D and E) Ifn-β−/− BMDMs were infected as described in the presence of 300pg/ml IFN-γ. Cell lysates were collected at 20 min post infection and immunoblotted for pJAK1 (Y1022/1023), total JAK1, pTYK2 (Y1054/1055), and total TYK2. (F) Ifn-β BMDMs were treated with DMSO or increasing amounts of a JAK inhibitor for 1 hour, then stimulated with 200pg/ml IFN-β for 4 hours. Cell lysates were then collected and immunoblotted for pSTAT1 (Y701), total STAT1, and β-actin. Densitometry was performed using ImageJ software and phosphorylated protein bands were normalized to loading control for each condition. Densitometric ratios are relative to the UI +IFNβ or the UI +IFNγ conditions. Data and densities shown represent one representative experiment out of three.
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Modulation in chemokine and cytokine expression in DBMSCs after treatment with MDA231 cells.

Journal: Cells

Article Title: Partial Inhibition of Epithelial-to-Mesenchymal Transition (EMT) Phenotypes by Placenta-Derived DBMSCs in Human Breast Cancer Cell Lines, In Vitro

doi: 10.3390/cells13242131

Figure Lengend Snippet: Modulation in chemokine and cytokine expression in DBMSCs after treatment with MDA231 cells.

Article Snippet: Anti-Interferon Alpha/Beta Receptor 2 Antibody (FITC), Cat# 10359-MM07T-F, was purchased from SinoBiological (Houston, TX, USA).

Techniques: Expressing, Migration, Activity Assay

Modulation in expression of EMT genes in MDA231 cells after treatment with DBMSC cells (IC).

Journal: Cells

Article Title: Partial Inhibition of Epithelial-to-Mesenchymal Transition (EMT) Phenotypes by Placenta-Derived DBMSCs in Human Breast Cancer Cell Lines, In Vitro

doi: 10.3390/cells13242131

Figure Lengend Snippet: Modulation in expression of EMT genes in MDA231 cells after treatment with DBMSC cells (IC).

Article Snippet: Anti-Interferon Alpha/Beta Receptor 2 Antibody (FITC), Cat# 10359-MM07T-F, was purchased from SinoBiological (Houston, TX, USA).

Techniques: Expressing, Binding Assay, Activity Assay, Inhibition, Migration, Marker, Activation Assay, Transformation Assay

(A) Ifn-β−/− BMDMs were infected with Mtb H37Rv at MOI of 3 for 4h and flow cytometry was conducted at 4hpi to measure surface receptor expression levels of IFNAR1 and IFNAR2. (B and C) Ifn-β−/− BMDMs were infected as described in the presence of 300pg/ml IFN-β. Cell lysates were collected at 20 min post infection and immunoblotted for pJAK1 (Y1022/1023), total JAK1, pTYK2 (Y1054/1055), and total TYK2. (D and E) Ifn-β−/− BMDMs were infected as described in the presence of 300pg/ml IFN-γ. Cell lysates were collected at 20 min post infection and immunoblotted for pJAK1 (Y1022/1023), total JAK1, pTYK2 (Y1054/1055), and total TYK2. (F) Ifn-β BMDMs were treated with DMSO or increasing amounts of a JAK inhibitor for 1 hour, then stimulated with 200pg/ml IFN-β for 4 hours. Cell lysates were then collected and immunoblotted for pSTAT1 (Y701), total STAT1, and β-actin. Densitometry was performed using ImageJ software and phosphorylated protein bands were normalized to loading control for each condition. Densitometric ratios are relative to the UI +IFNβ or the UI +IFNγ conditions. Data and densities shown represent one representative experiment out of three.

Journal: Journal of immunology (Baltimore, Md. : 1950)

Article Title: Mycobacterium tuberculosis inhibits autocrine type I interferon signaling to increase intracellular survival.

doi: 10.4049/jimmunol.1801303

Figure Lengend Snippet: (A) Ifn-β−/− BMDMs were infected with Mtb H37Rv at MOI of 3 for 4h and flow cytometry was conducted at 4hpi to measure surface receptor expression levels of IFNAR1 and IFNAR2. (B and C) Ifn-β−/− BMDMs were infected as described in the presence of 300pg/ml IFN-β. Cell lysates were collected at 20 min post infection and immunoblotted for pJAK1 (Y1022/1023), total JAK1, pTYK2 (Y1054/1055), and total TYK2. (D and E) Ifn-β−/− BMDMs were infected as described in the presence of 300pg/ml IFN-γ. Cell lysates were collected at 20 min post infection and immunoblotted for pJAK1 (Y1022/1023), total JAK1, pTYK2 (Y1054/1055), and total TYK2. (F) Ifn-β BMDMs were treated with DMSO or increasing amounts of a JAK inhibitor for 1 hour, then stimulated with 200pg/ml IFN-β for 4 hours. Cell lysates were then collected and immunoblotted for pSTAT1 (Y701), total STAT1, and β-actin. Densitometry was performed using ImageJ software and phosphorylated protein bands were normalized to loading control for each condition. Densitometric ratios are relative to the UI +IFNβ or the UI +IFNγ conditions. Data and densities shown represent one representative experiment out of three.

Article Snippet: After infection, BMDMs were blocked with 5% FCS and rat anti-mouse CD16/CD32 Fc Block (BD Biosciences, 553141) for 15 min followed by incubation with either PE-conjugated mouse anti-IFNAR1 (Biolegend, 127311) or PE-conjugated goat anti-IFNAR2 (R&D Systems, FAB1083P) for 30 min on ice.

Techniques: Infection, Flow Cytometry, Expressing, Software