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Corning Life Sciences hek 293 t cells expressing ace2
Hek 293 T Cells Expressing Ace2, supplied by Corning Life Sciences, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/hek 293 t cells expressing ace2/product/Corning Life Sciences
Average 90 stars, based on 1 article reviews
hek 293 t cells expressing ace2 - by Bioz Stars, 2026-03
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Genecopoeia hek 293 t cells
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BEI Resources human ace2 receptor expressing hek 293 t target cells
Development of a vascularized micro-organ microphysiological system and SARS-CoV-2 pseudotyped virus. ( A ) Schematic of an individual microfluidic device unit. Hydrostatic pressure drives medium from the inlet (MI) through the microfluidic channels and tissue chamber (T1–T3) to the medium outlet (MO). Hydrogel is loaded via the gel loading inlet (GLI) and outlet (GLO) with the pressure regulator (PR) to prevent leak into the microfluidic channel in the case of over-pressure during injection. ( B ) Development of the vasculature over time. EC labeled red; fibroblasts unlabeled. ( C ) Perfusion of 70 kDa FITC-Dextran through the vasculature (EC eRFP) at day 8. ( D ) COMSOL modeling of the shear stress (dynes/cm 2 ) through each tissue chamber. ( E ) Quantification of fluid flow through each chamber (m/s). ( F ) Schematic of SARS-CoV-2 pseudotyped virus. SARS-CoV-2 spike protein is inserted into the membrane of an HIV-1 envelope with a Gag-iGFP construct. ( G ) Schematic showing infectivity of the pseudotyped virus into EC using <t>ACE2,</t> leading to GFP expression.
Human Ace2 Receptor Expressing Hek 293 T Target Cells, supplied by BEI Resources, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/human ace2 receptor expressing hek 293 t target cells/product/BEI Resources
Average 90 stars, based on 1 article reviews
human ace2 receptor expressing hek 293 t target cells - by Bioz Stars, 2026-03
90/100 stars
  Buy from Supplier

90
Corning Life Sciences hek 293 t cells expressing ace2
Development of a vascularized micro-organ microphysiological system and SARS-CoV-2 pseudotyped virus. ( A ) Schematic of an individual microfluidic device unit. Hydrostatic pressure drives medium from the inlet (MI) through the microfluidic channels and tissue chamber (T1–T3) to the medium outlet (MO). Hydrogel is loaded via the gel loading inlet (GLI) and outlet (GLO) with the pressure regulator (PR) to prevent leak into the microfluidic channel in the case of over-pressure during injection. ( B ) Development of the vasculature over time. EC labeled red; fibroblasts unlabeled. ( C ) Perfusion of 70 kDa FITC-Dextran through the vasculature (EC eRFP) at day 8. ( D ) COMSOL modeling of the shear stress (dynes/cm 2 ) through each tissue chamber. ( E ) Quantification of fluid flow through each chamber (m/s). ( F ) Schematic of SARS-CoV-2 pseudotyped virus. SARS-CoV-2 spike protein is inserted into the membrane of an HIV-1 envelope with a Gag-iGFP construct. ( G ) Schematic showing infectivity of the pseudotyped virus into EC using <t>ACE2,</t> leading to GFP expression.
Hek 293 T Cells Expressing Ace2, supplied by Corning Life Sciences, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/hek 293 t cells expressing ace2/product/Corning Life Sciences
Average 90 stars, based on 1 article reviews
hek 293 t cells expressing ace2 - by Bioz Stars, 2026-03
90/100 stars
  Buy from Supplier

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Development of a vascularized micro-organ microphysiological system and SARS-CoV-2 pseudotyped virus. ( A ) Schematic of an individual microfluidic device unit. Hydrostatic pressure drives medium from the inlet (MI) through the microfluidic channels and tissue chamber (T1–T3) to the medium outlet (MO). Hydrogel is loaded via the gel loading inlet (GLI) and outlet (GLO) with the pressure regulator (PR) to prevent leak into the microfluidic channel in the case of over-pressure during injection. ( B ) Development of the vasculature over time. EC labeled red; fibroblasts unlabeled. ( C ) Perfusion of 70 kDa FITC-Dextran through the vasculature (EC eRFP) at day 8. ( D ) COMSOL modeling of the shear stress (dynes/cm 2 ) through each tissue chamber. ( E ) Quantification of fluid flow through each chamber (m/s). ( F ) Schematic of SARS-CoV-2 pseudotyped virus. SARS-CoV-2 spike protein is inserted into the membrane of an HIV-1 envelope with a Gag-iGFP construct. ( G ) Schematic showing infectivity of the pseudotyped virus into EC using ACE2, leading to GFP expression.

Journal: Frontiers in Cardiovascular Medicine

Article Title: SARS-CoV-2 infection of endothelial cells, dependent on flow-induced ACE2 expression, drives hypercytokinemia in a vascularized microphysiological system

doi: 10.3389/fcvm.2024.1360364

Figure Lengend Snippet: Development of a vascularized micro-organ microphysiological system and SARS-CoV-2 pseudotyped virus. ( A ) Schematic of an individual microfluidic device unit. Hydrostatic pressure drives medium from the inlet (MI) through the microfluidic channels and tissue chamber (T1–T3) to the medium outlet (MO). Hydrogel is loaded via the gel loading inlet (GLI) and outlet (GLO) with the pressure regulator (PR) to prevent leak into the microfluidic channel in the case of over-pressure during injection. ( B ) Development of the vasculature over time. EC labeled red; fibroblasts unlabeled. ( C ) Perfusion of 70 kDa FITC-Dextran through the vasculature (EC eRFP) at day 8. ( D ) COMSOL modeling of the shear stress (dynes/cm 2 ) through each tissue chamber. ( E ) Quantification of fluid flow through each chamber (m/s). ( F ) Schematic of SARS-CoV-2 pseudotyped virus. SARS-CoV-2 spike protein is inserted into the membrane of an HIV-1 envelope with a Gag-iGFP construct. ( G ) Schematic showing infectivity of the pseudotyped virus into EC using ACE2, leading to GFP expression.

Article Snippet: Virus infectivity was determined by infecting 1 × 10 4 human ACE2 receptor expressing HEK 293 T target cells (BEI Resources) per well with a serial dilution of the CoV-2/HIV-1 pseudotyped virus particles.

Techniques: Virus, Injection, Labeling, Shear, Membrane, Construct, Infection, Expressing

Upregulated ACE2 expression in the vascularized micro-organ supports SARS-CoV-2 pseudotyped infectivity. qPCR analysis of ( A ) ACE2, ( B ) AGTR1, and ( C ) TMPRSS2, which are necessary for SARS-CoV-2 infectivity, comparing monolayer normal human lung fibroblasts (NHLF), monolayer EC, the vascularized micro-organ (VMO) before (D4) and after (D8) the formation of perfusable vasculature. ( D ) Immunofluorescence staining of a D8 VMO showing CD31/PECAM1 (red), DAPI (blue), and localization of ACE2 (green) and TMPRSS2 (purple) to the endothelium. Showing nonspecificity of secondary antibodies alone. ( E ) Infectivity efficiency (mean fluorescent intensity) of SARS-CoV-2 pseudotyped virus compared to a lentivirus expressing green fluorescent protein (GFP). ( F ) Titering of GFP SARS-CoV-2 pseudotyped virus in a perfused VMO. Infectivity is measured as an increase in the mean fluorescent intensity of the GFP channel. ( G ) Subset of a D8 VMO EC (mCherry) and background fluorescence or fluorescence induced by infection with SARS-CoV-2 pseudotyped virus (GFP). Ctrl, control; PV, pseudotyped virus. ( H ) qPCR analysis of ACE2 expression induced by shear stress in an ibidi microfluidic chip. *<0.05, **<0.01, ***<0.001.

Journal: Frontiers in Cardiovascular Medicine

Article Title: SARS-CoV-2 infection of endothelial cells, dependent on flow-induced ACE2 expression, drives hypercytokinemia in a vascularized microphysiological system

doi: 10.3389/fcvm.2024.1360364

Figure Lengend Snippet: Upregulated ACE2 expression in the vascularized micro-organ supports SARS-CoV-2 pseudotyped infectivity. qPCR analysis of ( A ) ACE2, ( B ) AGTR1, and ( C ) TMPRSS2, which are necessary for SARS-CoV-2 infectivity, comparing monolayer normal human lung fibroblasts (NHLF), monolayer EC, the vascularized micro-organ (VMO) before (D4) and after (D8) the formation of perfusable vasculature. ( D ) Immunofluorescence staining of a D8 VMO showing CD31/PECAM1 (red), DAPI (blue), and localization of ACE2 (green) and TMPRSS2 (purple) to the endothelium. Showing nonspecificity of secondary antibodies alone. ( E ) Infectivity efficiency (mean fluorescent intensity) of SARS-CoV-2 pseudotyped virus compared to a lentivirus expressing green fluorescent protein (GFP). ( F ) Titering of GFP SARS-CoV-2 pseudotyped virus in a perfused VMO. Infectivity is measured as an increase in the mean fluorescent intensity of the GFP channel. ( G ) Subset of a D8 VMO EC (mCherry) and background fluorescence or fluorescence induced by infection with SARS-CoV-2 pseudotyped virus (GFP). Ctrl, control; PV, pseudotyped virus. ( H ) qPCR analysis of ACE2 expression induced by shear stress in an ibidi microfluidic chip. *<0.05, **<0.01, ***<0.001.

Article Snippet: Virus infectivity was determined by infecting 1 × 10 4 human ACE2 receptor expressing HEK 293 T target cells (BEI Resources) per well with a serial dilution of the CoV-2/HIV-1 pseudotyped virus particles.

Techniques: Expressing, Infection, Immunofluorescence, Staining, Virus, Fluorescence, Control, Shear

Pharmacological intervention inhibits SARS-CoV-2 pseudotyped virus entry and reduces downstream nF κ B activation. ( A ) Recombinant ACE2 (rACE2) prevented pseudotyped infectivity through competitive binding of the SARS-CoV-2 spike protein. ( B ) VMOs were treated with SARS-CoV-2 pseudotyped virus and rACE2 or camostat mesylate (camostat). The mean fluorescent intensity of the GFP pseudotyped virus was measured. Camostat mesylate had minimal protective ability, and rACE2 prevented infection. ( C ) Effluent from non-treated and treated devices was placed on EC transduced with an NF κ B induced mCherry reporter. The mean fluorescent intensity of mCherry was measured. *<0.05, **<0.01, ***<0.001.

Journal: Frontiers in Cardiovascular Medicine

Article Title: SARS-CoV-2 infection of endothelial cells, dependent on flow-induced ACE2 expression, drives hypercytokinemia in a vascularized microphysiological system

doi: 10.3389/fcvm.2024.1360364

Figure Lengend Snippet: Pharmacological intervention inhibits SARS-CoV-2 pseudotyped virus entry and reduces downstream nF κ B activation. ( A ) Recombinant ACE2 (rACE2) prevented pseudotyped infectivity through competitive binding of the SARS-CoV-2 spike protein. ( B ) VMOs were treated with SARS-CoV-2 pseudotyped virus and rACE2 or camostat mesylate (camostat). The mean fluorescent intensity of the GFP pseudotyped virus was measured. Camostat mesylate had minimal protective ability, and rACE2 prevented infection. ( C ) Effluent from non-treated and treated devices was placed on EC transduced with an NF κ B induced mCherry reporter. The mean fluorescent intensity of mCherry was measured. *<0.05, **<0.01, ***<0.001.

Article Snippet: Virus infectivity was determined by infecting 1 × 10 4 human ACE2 receptor expressing HEK 293 T target cells (BEI Resources) per well with a serial dilution of the CoV-2/HIV-1 pseudotyped virus particles.

Techniques: Virus, Activation Assay, Recombinant, Infection, Binding Assay, Transduction