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    ACE2 is a carboxypeptidase which converts angiotensin I to angiotensin 1-9, a peptide of unknown function, and angiotensin II to angiotensin 1-7, a vasodilator. Also able to hydrolyze apelin-13 and dynorphin-13 with high efficiency. May
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    N/A
    An aporphine alkaloid that has been isolated from Corydalis and exhibits inhibitory activity against enzymes such as tyrosine 3-monooxygenase and diamine oxidase.
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    86
    Biomol GmbH anti hace2 antibody
    Binding inhibition of S1 spike protein to human <t>HEK293-hACE2</t> cells by extract pre-incubation. Cells were pre-incubated for the indicated times with 10 mg/mL T. officinale (TO), its HMW fraction, equal to 10 mg/mL extract (HMW), and 10 mg/mL C. intybus (CI) or solvent control (a.d.) and subsequently treated with His-tagged S1 spike protein for 1 h without a washing step in between at 4 °C. Binding inhibition was assessed using flow cytometry. N = 3, bars are means + SD. Upper left: cytogram of gated HEK-hACE2 cells. Middle: overlay of representative fluorescence intensity histograms for ACE2 surface expression. Upper right: overlay of representative fluorescence intensity histograms for spike-binding inhibition by the extracts or a.d.; positive control: 20 µg/mL soluble hACE2. Cells were stained with anti-His-tag Alexa Fluor 647 conjugated monoclonal antibody; ** p < 0.01. Significance of difference was calculated relative to the solvent control by one-way ANOVA.
    Anti Hace2 Antibody, supplied by Biomol GmbH, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti hace2 antibody/product/Biomol GmbH
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti hace2 antibody - by Bioz Stars, 2024-04
    86/100 stars
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    86
    Bio-Techne corporation anti human ace2 antibodies
    A large fraction of serum sACE2 is inactive and binds the SARS-CoV-2 spike (A) <t>ACE2</t> was pulled down from indicated volumes of serum from patients and HDs using RBD-coupled beads. Recombinant ACE2 (rACE2) was loaded as control. Markers (M) in kDa. ∗Unspecific bands. (B) Specificity confirmed by a mutant RBD (A475R/G496R) lacking ACE2 binding and by an HIV gp140 control. (C) Percent inhibition (%) of 50 ng/mL rACE2 after addition to serum plotted against a-sACE2. Significance indicates a likelihood ratio test to compare a two-degree polynomial model with linear regression for moderate or severe COVID-19. (D) Activity of rACE2 spike-in (%) determined in serum fractions collected after ultrafiltration with indicated cut-off values. (E) Determination of a-sACE2 in indicated reciprocal serum dilutions. (F) Pearson correlation with a 95% confidence interval of a-sACE2 in undiluted samples and maximum a-sACE2 detected after serum dilution. (C), (E), and (F) include measurements of repeated longitudinal blood drawings. For gel source data, see <xref ref-type=Figure S11 . " width="250" height="auto" />
    Anti Human Ace2 Antibodies, supplied by Bio-Techne corporation, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti human ace2 antibodies/product/Bio-Techne corporation
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti human ace2 antibodies - by Bioz Stars, 2024-04
    86/100 stars
      Buy from Supplier

    N/A
    The membrane-associated protein ABCB7 is a member of the superfamily of ATP-binding cassette (ABC) transporters. ABC proteins transport various molecules across extra- and intra-cellular membranes. ABC genes are divided into seven distinct subfamilies (ABC1, MDR/TAP,
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    Binding inhibition of S1 spike protein to human HEK293-hACE2 cells by extract pre-incubation. Cells were pre-incubated for the indicated times with 10 mg/mL T. officinale (TO), its HMW fraction, equal to 10 mg/mL extract (HMW), and 10 mg/mL C. intybus (CI) or solvent control (a.d.) and subsequently treated with His-tagged S1 spike protein for 1 h without a washing step in between at 4 °C. Binding inhibition was assessed using flow cytometry. N = 3, bars are means + SD. Upper left: cytogram of gated HEK-hACE2 cells. Middle: overlay of representative fluorescence intensity histograms for ACE2 surface expression. Upper right: overlay of representative fluorescence intensity histograms for spike-binding inhibition by the extracts or a.d.; positive control: 20 µg/mL soluble hACE2. Cells were stained with anti-His-tag Alexa Fluor 647 conjugated monoclonal antibody; ** p < 0.01. Significance of difference was calculated relative to the solvent control by one-way ANOVA.

    Journal: Pharmaceuticals

    Article Title: In Vitro Effect of Taraxacum officinale Leaf Aqueous Extract on the Interaction between ACE2 Cell Surface Receptor and SARS-CoV-2 Spike Protein D614 and Four Mutants

    doi: 10.3390/ph14101055

    Figure Lengend Snippet: Binding inhibition of S1 spike protein to human HEK293-hACE2 cells by extract pre-incubation. Cells were pre-incubated for the indicated times with 10 mg/mL T. officinale (TO), its HMW fraction, equal to 10 mg/mL extract (HMW), and 10 mg/mL C. intybus (CI) or solvent control (a.d.) and subsequently treated with His-tagged S1 spike protein for 1 h without a washing step in between at 4 °C. Binding inhibition was assessed using flow cytometry. N = 3, bars are means + SD. Upper left: cytogram of gated HEK-hACE2 cells. Middle: overlay of representative fluorescence intensity histograms for ACE2 surface expression. Upper right: overlay of representative fluorescence intensity histograms for spike-binding inhibition by the extracts or a.d.; positive control: 20 µg/mL soluble hACE2. Cells were stained with anti-His-tag Alexa Fluor 647 conjugated monoclonal antibody; ** p < 0.01. Significance of difference was calculated relative to the solvent control by one-way ANOVA.

    Article Snippet: Anti-hACE2 antibody (Biomol, NSJ-F49433) was used as reference for transduction inhibition assay.

    Techniques: Binding Assay, Inhibition, Incubation, Flow Cytometry, Fluorescence, Expressing, Positive Control, Staining

    Binding inhibition of spike D614, and its mutants D614G, N501Y or mix (N501Y, K417N and E484K) to human HEK293-hACE2 and A549-hACE2-TMPRSS2 cells by extract pre- or post-incubation. Overlay of fluorescence intensity histogram for ( A ) unstained HEK cells, staining control (anti-His-tag Alexa Fluor 647), and cells incubated with His-tag-labelled spike D614, D614G or N501Y for 1 h at 4 °C. ( B , C ) cells pre-incubated with solvent control (a.d.), 10 mg/mL T. officinale (TO) or 10 mg/mL C. intybus (CI) for 30–60 s, and then treated with His-tag-labelled S1 spike D614, D614G or N501Y protein for 1 h without a washing step in between at 4 °C. ( D – G ) Effect of extract incubation on HEK or A549 cells either before or after incubation with His-tag-labelled spike D614, D614G, N501Y or mix (N501Y, K417N and E484K) protein at 37 °C. ( H ) Plant extracts were incubated in saliva from four human donors for 0.5 h at 37 °C. Afterwards, cells were pre-treated with 5 mg/mL extracts for 60 s at 37 °C before incubation with His-tag-labelled spike D614 protein for 0.5 h at 37 °C. Spike-binding inhibition to human cells was assessed using flow cytometric analysis of cells stained with anti-His-tag Alexa Fluor 647 conjugated monoclonal antibody. Bars are means +SD; * p < 0.05, ** p < 0.01. Significance of difference was calculated relative to the respective solvent control by one-way ANOVA.

    Journal: Pharmaceuticals

    Article Title: In Vitro Effect of Taraxacum officinale Leaf Aqueous Extract on the Interaction between ACE2 Cell Surface Receptor and SARS-CoV-2 Spike Protein D614 and Four Mutants

    doi: 10.3390/ph14101055

    Figure Lengend Snippet: Binding inhibition of spike D614, and its mutants D614G, N501Y or mix (N501Y, K417N and E484K) to human HEK293-hACE2 and A549-hACE2-TMPRSS2 cells by extract pre- or post-incubation. Overlay of fluorescence intensity histogram for ( A ) unstained HEK cells, staining control (anti-His-tag Alexa Fluor 647), and cells incubated with His-tag-labelled spike D614, D614G or N501Y for 1 h at 4 °C. ( B , C ) cells pre-incubated with solvent control (a.d.), 10 mg/mL T. officinale (TO) or 10 mg/mL C. intybus (CI) for 30–60 s, and then treated with His-tag-labelled S1 spike D614, D614G or N501Y protein for 1 h without a washing step in between at 4 °C. ( D – G ) Effect of extract incubation on HEK or A549 cells either before or after incubation with His-tag-labelled spike D614, D614G, N501Y or mix (N501Y, K417N and E484K) protein at 37 °C. ( H ) Plant extracts were incubated in saliva from four human donors for 0.5 h at 37 °C. Afterwards, cells were pre-treated with 5 mg/mL extracts for 60 s at 37 °C before incubation with His-tag-labelled spike D614 protein for 0.5 h at 37 °C. Spike-binding inhibition to human cells was assessed using flow cytometric analysis of cells stained with anti-His-tag Alexa Fluor 647 conjugated monoclonal antibody. Bars are means +SD; * p < 0.05, ** p < 0.01. Significance of difference was calculated relative to the respective solvent control by one-way ANOVA.

    Article Snippet: Anti-hACE2 antibody (Biomol, NSJ-F49433) was used as reference for transduction inhibition assay.

    Techniques: Binding Assay, Inhibition, Incubation, Fluorescence, Staining

    Effect of T. officinale extract on ACE2 enzyme activity and protein expression. ( A ) Viability of A549-hACE2-TMPRSS2 cells was determined using trypan blue cell staining after 84 h exposure to the extract. ( B ) Cells were incubated with TO extract or 500 ng/mL S1 protein and analyzed for enzyme activity using a fluorescence kit. ( C , D ) Cells were exposed for 6 h or 24 h to extract without (white bars) or with (black bars) 500 ng/mL S1 protein and analyzed for ACE2 protein expression using a human ACE2 ELISA kit; a.d.: solvent control. Bars are means + SD, N ≥ 3 independent experiments; * p < 0.05, ** p < 0.01. Significance of difference was calculated relative to the respective control by one-way ANOVA.

    Journal: Pharmaceuticals

    Article Title: In Vitro Effect of Taraxacum officinale Leaf Aqueous Extract on the Interaction between ACE2 Cell Surface Receptor and SARS-CoV-2 Spike Protein D614 and Four Mutants

    doi: 10.3390/ph14101055

    Figure Lengend Snippet: Effect of T. officinale extract on ACE2 enzyme activity and protein expression. ( A ) Viability of A549-hACE2-TMPRSS2 cells was determined using trypan blue cell staining after 84 h exposure to the extract. ( B ) Cells were incubated with TO extract or 500 ng/mL S1 protein and analyzed for enzyme activity using a fluorescence kit. ( C , D ) Cells were exposed for 6 h or 24 h to extract without (white bars) or with (black bars) 500 ng/mL S1 protein and analyzed for ACE2 protein expression using a human ACE2 ELISA kit; a.d.: solvent control. Bars are means + SD, N ≥ 3 independent experiments; * p < 0.05, ** p < 0.01. Significance of difference was calculated relative to the respective control by one-way ANOVA.

    Article Snippet: Anti-hACE2 antibody (Biomol, NSJ-F49433) was used as reference for transduction inhibition assay.

    Techniques: Activity Assay, Expressing, Staining, Incubation, Fluorescence, Enzyme-linked Immunosorbent Assay

    Viral transduction inhibition of A549-hACE2-TMPRSS2 cells by T. officinale extract. ( A ) Cells were pre-treated with T. officinale (TO) or HMW extract for 0.5 h before infection with 7500 TU/mL SARS-CoV-2 spike D614 or Delta (B.1.617.2) variant for 24 h; ( B , C ) Cells were transduced with 7500 TU/mL SARS-CoV-2 for (B) 3 h before addition of TO for another 21 h or (C) 24 h. After transduction, the medium was exchanged with fresh medium containing TO or HMW extract at the indicated concentrations and post-incubated for 60 h. ( D ) Cells were pre-treated with 40 mg/mL TO for 3 h before transduction with the indicated virus titer for 24 h. After that, the medium was exchanged with fresh medium and incubated for another 48 h. Luminescence was then detected within 1 h. 0.35 mg/mL HMW extract equals to 20 mg/mL TO extract. Transduction control: (−) negative control: bald lentiviral pseudovirion; (+) positive control: firefly luciferase lentivirus; inhibitor positive control: 100 µg/mL anti-hACE2 antibody. ( E ) Pro-inflammatory IL-6 cytokine secretion analysis was done either after 24 h virus transduction together with extract (left), after 24 h + 60 h post-infection with extract (middle) or after 60 h post-infection with extract (right) using multiplexing flow cytometric analysis. Solvent control: distilled water (a.d.). N ≥ 3 independent experiments; * p < 0.05, ** p < 0.01. Significance of difference was calculated relative to the solvent control by one-way ANOVA.

    Journal: Pharmaceuticals

    Article Title: In Vitro Effect of Taraxacum officinale Leaf Aqueous Extract on the Interaction between ACE2 Cell Surface Receptor and SARS-CoV-2 Spike Protein D614 and Four Mutants

    doi: 10.3390/ph14101055

    Figure Lengend Snippet: Viral transduction inhibition of A549-hACE2-TMPRSS2 cells by T. officinale extract. ( A ) Cells were pre-treated with T. officinale (TO) or HMW extract for 0.5 h before infection with 7500 TU/mL SARS-CoV-2 spike D614 or Delta (B.1.617.2) variant for 24 h; ( B , C ) Cells were transduced with 7500 TU/mL SARS-CoV-2 for (B) 3 h before addition of TO for another 21 h or (C) 24 h. After transduction, the medium was exchanged with fresh medium containing TO or HMW extract at the indicated concentrations and post-incubated for 60 h. ( D ) Cells were pre-treated with 40 mg/mL TO for 3 h before transduction with the indicated virus titer for 24 h. After that, the medium was exchanged with fresh medium and incubated for another 48 h. Luminescence was then detected within 1 h. 0.35 mg/mL HMW extract equals to 20 mg/mL TO extract. Transduction control: (−) negative control: bald lentiviral pseudovirion; (+) positive control: firefly luciferase lentivirus; inhibitor positive control: 100 µg/mL anti-hACE2 antibody. ( E ) Pro-inflammatory IL-6 cytokine secretion analysis was done either after 24 h virus transduction together with extract (left), after 24 h + 60 h post-infection with extract (middle) or after 60 h post-infection with extract (right) using multiplexing flow cytometric analysis. Solvent control: distilled water (a.d.). N ≥ 3 independent experiments; * p < 0.05, ** p < 0.01. Significance of difference was calculated relative to the solvent control by one-way ANOVA.

    Article Snippet: Anti-hACE2 antibody (Biomol, NSJ-F49433) was used as reference for transduction inhibition assay.

    Techniques: Transduction, Inhibition, Infection, Variant Assay, Incubation, Negative Control, Positive Control, Luciferase, Multiplexing

    A large fraction of serum sACE2 is inactive and binds the SARS-CoV-2 spike (A) ACE2 was pulled down from indicated volumes of serum from patients and HDs using RBD-coupled beads. Recombinant ACE2 (rACE2) was loaded as control. Markers (M) in kDa. ∗Unspecific bands. (B) Specificity confirmed by a mutant RBD (A475R/G496R) lacking ACE2 binding and by an HIV gp140 control. (C) Percent inhibition (%) of 50 ng/mL rACE2 after addition to serum plotted against a-sACE2. Significance indicates a likelihood ratio test to compare a two-degree polynomial model with linear regression for moderate or severe COVID-19. (D) Activity of rACE2 spike-in (%) determined in serum fractions collected after ultrafiltration with indicated cut-off values. (E) Determination of a-sACE2 in indicated reciprocal serum dilutions. (F) Pearson correlation with a 95% confidence interval of a-sACE2 in undiluted samples and maximum a-sACE2 detected after serum dilution. (C), (E), and (F) include measurements of repeated longitudinal blood drawings. For gel source data, see <xref ref-type=Figure S11 . " width="100%" height="100%">

    Journal: iScience

    Article Title: Soluble ACE2 correlates with severe COVID-19 and can impair antibody responses

    doi: 10.1016/j.isci.2024.109330

    Figure Lengend Snippet: A large fraction of serum sACE2 is inactive and binds the SARS-CoV-2 spike (A) ACE2 was pulled down from indicated volumes of serum from patients and HDs using RBD-coupled beads. Recombinant ACE2 (rACE2) was loaded as control. Markers (M) in kDa. ∗Unspecific bands. (B) Specificity confirmed by a mutant RBD (A475R/G496R) lacking ACE2 binding and by an HIV gp140 control. (C) Percent inhibition (%) of 50 ng/mL rACE2 after addition to serum plotted against a-sACE2. Significance indicates a likelihood ratio test to compare a two-degree polynomial model with linear regression for moderate or severe COVID-19. (D) Activity of rACE2 spike-in (%) determined in serum fractions collected after ultrafiltration with indicated cut-off values. (E) Determination of a-sACE2 in indicated reciprocal serum dilutions. (F) Pearson correlation with a 95% confidence interval of a-sACE2 in undiluted samples and maximum a-sACE2 detected after serum dilution. (C), (E), and (F) include measurements of repeated longitudinal blood drawings. For gel source data, see Figure S11 .

    Article Snippet: The membrane was stained in 5 ml anti-human ACE2 antibodies (R&D Systems, #AF933; #F49433, NSJ Bioreagents, #3215, ProSci Incorporated, #AHP888 Bio-Rad Laboratories) diluted to 0.2 μg/ml at +4°C overnight with constant mixing on the roller.

    Techniques: Recombinant, Mutagenesis, Binding Assay, Inhibition, Activity Assay

    Serology suggests that sACE2 impairs generation of antibodies preventing RBD-ACE2 interaction (A) Scheme depicting SARS-CoV-2 spike epitope masking by sACE2. (B) Serum IgG binding to RBD (ED50, serum dilution corresponding to 50% of maximum binding activity) of HDs (blue, N = 151), moderate (yellow, N = 120) and severe (red, N = 198) patients collected >20 PSO. Patients are stratified into the respective WHO class at the time of sampling. Statistical analyses by two-sided Mann–Whitney test (∗∗∗∗p < 0.0001, ∗∗∗p < 0.001, ∗∗p < 0.01, and ∗p < 0.05; ns, not significant). Boxplots depict median +/− interquartile range. Whisker length is 1.5 interquartile ranges. (C) Blocking of ACE2-RBD interaction (BD50, serum dilution corresponding to 50% of maximum blocking activity) plotted against a-sACE2 for moderate and (D) severe COVID-19. Data for individual samples are shown; samples drawn after 15 days PSO are selected. Spearman correlation performed with a 95% confidence interval. (E) ED50 of anti-RBD IgG plotted against blocking of ACE2-binding (BD50). (F) ACE2 competition, (G) anti-RBD IgG, and (H) anti-nucleocapsid IgG confirmed for two sample groups with high (gray, N = 12) versus low (black line, N = 5) RBD titers. Positive and negative controls in blue and red, respectively. (I) Structural depiction of the RBD bound to CC12.1 and P2B-2F6. PDB: 6XDG , 7BWJ , and 6XC2 . (J) RBD binding of recombinant antibodies in competition with class 1 nAb CC12.1 and class 2 nAb P2B-2F6. (K) Localization of class 1 and 2 abrogating RBD mutations F456A and E484K. ACE2 footprint shown in blue. (L) RBD high versus low binding sera cleared by a pull-down with RBD WT, RBD-F456A, RBD-E484K, and MERS-CoV RBD as control. Remaining IgG binding to RBD and ACE2 competition is depicted in %.

    Journal: iScience

    Article Title: Soluble ACE2 correlates with severe COVID-19 and can impair antibody responses

    doi: 10.1016/j.isci.2024.109330

    Figure Lengend Snippet: Serology suggests that sACE2 impairs generation of antibodies preventing RBD-ACE2 interaction (A) Scheme depicting SARS-CoV-2 spike epitope masking by sACE2. (B) Serum IgG binding to RBD (ED50, serum dilution corresponding to 50% of maximum binding activity) of HDs (blue, N = 151), moderate (yellow, N = 120) and severe (red, N = 198) patients collected >20 PSO. Patients are stratified into the respective WHO class at the time of sampling. Statistical analyses by two-sided Mann–Whitney test (∗∗∗∗p < 0.0001, ∗∗∗p < 0.001, ∗∗p < 0.01, and ∗p < 0.05; ns, not significant). Boxplots depict median +/− interquartile range. Whisker length is 1.5 interquartile ranges. (C) Blocking of ACE2-RBD interaction (BD50, serum dilution corresponding to 50% of maximum blocking activity) plotted against a-sACE2 for moderate and (D) severe COVID-19. Data for individual samples are shown; samples drawn after 15 days PSO are selected. Spearman correlation performed with a 95% confidence interval. (E) ED50 of anti-RBD IgG plotted against blocking of ACE2-binding (BD50). (F) ACE2 competition, (G) anti-RBD IgG, and (H) anti-nucleocapsid IgG confirmed for two sample groups with high (gray, N = 12) versus low (black line, N = 5) RBD titers. Positive and negative controls in blue and red, respectively. (I) Structural depiction of the RBD bound to CC12.1 and P2B-2F6. PDB: 6XDG , 7BWJ , and 6XC2 . (J) RBD binding of recombinant antibodies in competition with class 1 nAb CC12.1 and class 2 nAb P2B-2F6. (K) Localization of class 1 and 2 abrogating RBD mutations F456A and E484K. ACE2 footprint shown in blue. (L) RBD high versus low binding sera cleared by a pull-down with RBD WT, RBD-F456A, RBD-E484K, and MERS-CoV RBD as control. Remaining IgG binding to RBD and ACE2 competition is depicted in %.

    Article Snippet: The membrane was stained in 5 ml anti-human ACE2 antibodies (R&D Systems, #AF933; #F49433, NSJ Bioreagents, #3215, ProSci Incorporated, #AHP888 Bio-Rad Laboratories) diluted to 0.2 μg/ml at +4°C overnight with constant mixing on the roller.

    Techniques: Binding Assay, Activity Assay, Sampling, MANN-WHITNEY, Whisker Assay, Blocking Assay, Recombinant

    Soluble ACE2 interferes with the germinal center reaction in silico (A) Scheme depicting the germinal center (GC) response: GC reaction starts with an influx of low-affinity seeder cells. These cells are in a pro-apoptotic state and must acquire survival signals by antigen acquisition and T follicular helper cell (Tfh cell) signaling. Ag binding probability (P Ag ) is proportional to the mutational distance of the BCR to the Ag (MutDist, see and ). The Tfh cells preferentially provide signal to B cells that acquire larger amounts of antigen. Some of the selected B cells exit the GC and become output cells, whereas the rest recycle back and proliferate with mutations, resulting in daughter cells of higher affinity. These new cells again compete for survival signals, resulting in progressive B cell affinity increase. Serum sACE2 and the antibodies produced by output B cells can feedback to the GC by making antigen acquisition harder (mechanisms in B and C). (B) Epitope masking mechanism (scenario A): sACE2 and antibodies can bind to the antigen and mask it, thus lowering the amount of antigen available for B cells. (C) Epitope masking and mean field Ab-B cell competition mechanism (scenario B): BCR probability of binding the unmasked Ag is reduced depending on the average affinity of sACE2 and endogenous Abs (ACE2/Ab affinity). (D–K) Simulation results for different sACE2 concentrations (0, 1, 10, and 50 nM constant concentration in D–G; 0, 0.05, 0.23 nM constant concentration and 0.05–0.23 nM linear increase in H–K): IP (D, H) and GC size (E, I) with scenario A; IP (F, J) and GC size (G, K) with mean field Ab-B cell competition. (L–S) Simulation results for different sACE2 affinities (0.475, 1.9, and 3.8 nM in L–O; 5, 25, 125 nM in P–S): IP (L, P) and GC size (M, Q) with epitope masking only; IP (N, R) and GC size (O, S) with scenario B. Mean (continuous lines) and standard deviation (shaded area) of simulations for a total of 20 simulated GCs are shown. Schemes (A–C) are created with BioRender.

    Journal: iScience

    Article Title: Soluble ACE2 correlates with severe COVID-19 and can impair antibody responses

    doi: 10.1016/j.isci.2024.109330

    Figure Lengend Snippet: Soluble ACE2 interferes with the germinal center reaction in silico (A) Scheme depicting the germinal center (GC) response: GC reaction starts with an influx of low-affinity seeder cells. These cells are in a pro-apoptotic state and must acquire survival signals by antigen acquisition and T follicular helper cell (Tfh cell) signaling. Ag binding probability (P Ag ) is proportional to the mutational distance of the BCR to the Ag (MutDist, see and ). The Tfh cells preferentially provide signal to B cells that acquire larger amounts of antigen. Some of the selected B cells exit the GC and become output cells, whereas the rest recycle back and proliferate with mutations, resulting in daughter cells of higher affinity. These new cells again compete for survival signals, resulting in progressive B cell affinity increase. Serum sACE2 and the antibodies produced by output B cells can feedback to the GC by making antigen acquisition harder (mechanisms in B and C). (B) Epitope masking mechanism (scenario A): sACE2 and antibodies can bind to the antigen and mask it, thus lowering the amount of antigen available for B cells. (C) Epitope masking and mean field Ab-B cell competition mechanism (scenario B): BCR probability of binding the unmasked Ag is reduced depending on the average affinity of sACE2 and endogenous Abs (ACE2/Ab affinity). (D–K) Simulation results for different sACE2 concentrations (0, 1, 10, and 50 nM constant concentration in D–G; 0, 0.05, 0.23 nM constant concentration and 0.05–0.23 nM linear increase in H–K): IP (D, H) and GC size (E, I) with scenario A; IP (F, J) and GC size (G, K) with mean field Ab-B cell competition. (L–S) Simulation results for different sACE2 affinities (0.475, 1.9, and 3.8 nM in L–O; 5, 25, 125 nM in P–S): IP (L, P) and GC size (M, Q) with epitope masking only; IP (N, R) and GC size (O, S) with scenario B. Mean (continuous lines) and standard deviation (shaded area) of simulations for a total of 20 simulated GCs are shown. Schemes (A–C) are created with BioRender.

    Article Snippet: The membrane was stained in 5 ml anti-human ACE2 antibodies (R&D Systems, #AF933; #F49433, NSJ Bioreagents, #3215, ProSci Incorporated, #AHP888 Bio-Rad Laboratories) diluted to 0.2 μg/ml at +4°C overnight with constant mixing on the roller.

    Techniques: In Silico, Binding Assay, Produced, Concentration Assay, Standard Deviation

    Journal: iScience

    Article Title: Soluble ACE2 correlates with severe COVID-19 and can impair antibody responses

    doi: 10.1016/j.isci.2024.109330

    Figure Lengend Snippet:

    Article Snippet: The membrane was stained in 5 ml anti-human ACE2 antibodies (R&D Systems, #AF933; #F49433, NSJ Bioreagents, #3215, ProSci Incorporated, #AHP888 Bio-Rad Laboratories) diluted to 0.2 μg/ml at +4°C overnight with constant mixing on the roller.

    Techniques: Recombinant, Magnetic Beads, Software, In Silico