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Peptide Institute e 64d
E 64d, supplied by Peptide Institute, 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/product/e+64d/64d+e/pm41342557-123-17-22
Average 86 stars, based on 1 article reviews
e 64d - by Bioz Stars, 2026-09
86/100 stars

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Incubation:

Article Title: Autophagy Promotes Cell Death Induced by Hydrogen Peroxide in Physcomitrium patens.
Article Snippet: 1Graduate School of Science and Engineering, Saitama University, Saitama, 338-8570 Japan 2Department of Biochemistry and Molecular Biology, Bangladesh Agricultural University, Mymensingh 2202, Bangladesh 3Research Institute for Clinical Oncology, Saitama Cancer Center, Saitama, 362-0806 Japan 4Department of Neuroscience, University of Florida Scripps Biomedical Research, 130 Scripps Way, Jupiter, FL 33458, USA 5Department of Horticulture, Bangabandhu Sheikh Mujibur Rahman Agricultural University, Gazipur 1706, Bangladesh

Infection:

Article Title: Targeting envelope lipids with 2,6‑di‑ O ‑methyl‑3‑acetyl‑β‑cyclodextrin impairs infectivity of SARS‑CoV‑2 and Japanese encephalitis virus
Article Snippet: After 24 h, the cells were infected with the DMA-β-CyD-treated Wuhan variant and then incubated for an additional 72 h. Viral infectivity titers were then determined by the microscopic evaluation of CPE or by measuring absorbance using the CCK-8 assay. .. In addition, the infectivity titer of the DMA-β-CyD-treated Wuhan variant was also assessed in cells pretreated with E-64D (10 μM, 180 min; Peptide Institute, Inc.). .. To determine whether DMA-β-CyD inhibits the binding of the SARS-CoV-2 spike protein to ACE2, an ACE2:SARS-CoV-2 Spike S1 Inhibitor Screening Assay Kit (BPS Bioscience, Inc.) was used.

Article Title: Targeting envelope lipids with 2,6‑di‑ O ‑methyl‑3‑acetyl‑β‑cyclodextrin impairs infectivity of SARS‑CoV‑2 and Japanese encephalitis virus.
Article Snippet: After 24 h, the cells were infected with the DMA-β-CyD-treated Wuhan variant and then incubated for an additional 72 h. Viral infectivity titers were then determined by the microscopic evaluation of CPE or by measuring absorbance using the CCK-8 assay. .. In addition, the infectivity titer of the DMA-β-CyD-treated Wuhan variant was also assessed in cells pretreated with E-64D (10 μM, 180 min; Peptide Institute, Inc.). .. To determine whether DMA-β-CyD inhibits the binding of the SARS-CoV-2 spike protein to ACE2, an ACE2:SARS-CoV-2 Spike S1 Inhibitor Screening Assay Kit (BPS Bioscience, Inc.) was used.

Variant Assay:

Article Title: Targeting envelope lipids with 2,6‑di‑ O ‑methyl‑3‑acetyl‑β‑cyclodextrin impairs infectivity of SARS‑CoV‑2 and Japanese encephalitis virus
Article Snippet: After 24 h, the cells were infected with the DMA-β-CyD-treated Wuhan variant and then incubated for an additional 72 h. Viral infectivity titers were then determined by the microscopic evaluation of CPE or by measuring absorbance using the CCK-8 assay. .. In addition, the infectivity titer of the DMA-β-CyD-treated Wuhan variant was also assessed in cells pretreated with E-64D (10 μM, 180 min; Peptide Institute, Inc.). .. To determine whether DMA-β-CyD inhibits the binding of the SARS-CoV-2 spike protein to ACE2, an ACE2:SARS-CoV-2 Spike S1 Inhibitor Screening Assay Kit (BPS Bioscience, Inc.) was used.

Article Title: Targeting envelope lipids with 2,6‑di‑ O ‑methyl‑3‑acetyl‑β‑cyclodextrin impairs infectivity of SARS‑CoV‑2 and Japanese encephalitis virus.
Article Snippet: After 24 h, the cells were infected with the DMA-β-CyD-treated Wuhan variant and then incubated for an additional 72 h. Viral infectivity titers were then determined by the microscopic evaluation of CPE or by measuring absorbance using the CCK-8 assay. .. In addition, the infectivity titer of the DMA-β-CyD-treated Wuhan variant was also assessed in cells pretreated with E-64D (10 μM, 180 min; Peptide Institute, Inc.). .. To determine whether DMA-β-CyD inhibits the binding of the SARS-CoV-2 spike protein to ACE2, an ACE2:SARS-CoV-2 Spike S1 Inhibitor Screening Assay Kit (BPS Bioscience, Inc.) was used.

other:

Article Title: Increased Electrophoretic Mobility of Long-Type GATA-6 Transcription Factor upon Substitution of Its PEST Sequence
Article Snippet: MG115 and E-64d were from the Peptide Institute.



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Treatment of cells with camostat targeting the cell surface TMPRSS2 pathway and <t>E64d</t> targeting the endocytic cathepsin L pathway was used to block infectious virus entry via each pathway. Experiments with infectious virus (A) or pseudovirus (B) is shown for the different spike variants in VeroE6/TMPRSS2 cells. (A) Relative viral load was measured the RNA copies of MERS-CoV using the UpE assay in the cell supernatant at 48 hpi. (B) Relative cell entry was measured by RLU. (A-B) 2015/GD01 was the reference for comparison. Figures show the representative data from 2 independent experiments each with two biological replicates for each experiment each drug dose. An inhibition curve was fitted using the Hill equation with inhibition in Graphpad Prism. (C) RT-qPCR to measure RNA expression of DPP4, TMPRSS2 and CTSL gene among difference cell lines. Expressions were normalized by GAPDH gene for each cell line and relative fold changes were compared to 293T cells as reference. Flow cytometry analysis of surface expression of DPP4 and TMPRSS2 among different cell lines. Background levels were determined by isotype controls as indicated in grey. (D) Caco2 cells representing the TMPRSS2 entry pathway model and Huh7 cells representing the endosomal entry pathway model were pretreated with Camostat (25 μM), E64d (10 μM) or in both. Pseudoviruses were infected on drug treated cells in quadruplicate wells. Data shown are a representative of two independent repeats.
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Treatment of cells with camostat targeting the cell surface TMPRSS2 pathway and <t>E64d</t> targeting the endocytic cathepsin L pathway was used to block infectious virus entry via each pathway. Experiments with infectious virus (A) or pseudovirus (B) is shown for the different spike variants in VeroE6/TMPRSS2 cells. (A) Relative viral load was measured the RNA copies of MERS-CoV using the UpE assay in the cell supernatant at 48 hpi. (B) Relative cell entry was measured by RLU. (A-B) 2015/GD01 was the reference for comparison. Figures show the representative data from 2 independent experiments each with two biological replicates for each experiment each drug dose. An inhibition curve was fitted using the Hill equation with inhibition in Graphpad Prism. (C) RT-qPCR to measure RNA expression of DPP4, TMPRSS2 and CTSL gene among difference cell lines. Expressions were normalized by GAPDH gene for each cell line and relative fold changes were compared to 293T cells as reference. Flow cytometry analysis of surface expression of DPP4 and TMPRSS2 among different cell lines. Background levels were determined by isotype controls as indicated in grey. (D) Caco2 cells representing the TMPRSS2 entry pathway model and Huh7 cells representing the endosomal entry pathway model were pretreated with Camostat (25 μM), E64d (10 μM) or in both. Pseudoviruses were infected on drug treated cells in quadruplicate wells. Data shown are a representative of two independent repeats.
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Treatment of cells with camostat targeting the cell surface TMPRSS2 pathway and <t>E64d</t> targeting the endocytic cathepsin L pathway was used to block infectious virus entry via each pathway. Experiments with infectious virus (A) or pseudovirus (B) is shown for the different spike variants in VeroE6/TMPRSS2 cells. (A) Relative viral load was measured the RNA copies of MERS-CoV using the UpE assay in the cell supernatant at 48 hpi. (B) Relative cell entry was measured by RLU. (A-B) 2015/GD01 was the reference for comparison. Figures show the representative data from 2 independent experiments each with two biological replicates for each experiment each drug dose. An inhibition curve was fitted using the Hill equation with inhibition in Graphpad Prism. (C) RT-qPCR to measure RNA expression of DPP4, TMPRSS2 and CTSL gene among difference cell lines. Expressions were normalized by GAPDH gene for each cell line and relative fold changes were compared to 293T cells as reference. Flow cytometry analysis of surface expression of DPP4 and TMPRSS2 among different cell lines. Background levels were determined by isotype controls as indicated in grey. (D) Caco2 cells representing the TMPRSS2 entry pathway model and Huh7 cells representing the endosomal entry pathway model were pretreated with Camostat (25 μM), E64d (10 μM) or in both. Pseudoviruses were infected on drug treated cells in quadruplicate wells. Data shown are a representative of two independent repeats.
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Treatment of cells with camostat targeting the cell surface TMPRSS2 pathway and <t>E64d</t> targeting the endocytic cathepsin L pathway was used to block infectious virus entry via each pathway. Experiments with infectious virus (A) or pseudovirus (B) is shown for the different spike variants in VeroE6/TMPRSS2 cells. (A) Relative viral load was measured the RNA copies of MERS-CoV using the UpE assay in the cell supernatant at 48 hpi. (B) Relative cell entry was measured by RLU. (A-B) 2015/GD01 was the reference for comparison. Figures show the representative data from 2 independent experiments each with two biological replicates for each experiment each drug dose. An inhibition curve was fitted using the Hill equation with inhibition in Graphpad Prism. (C) RT-qPCR to measure RNA expression of DPP4, TMPRSS2 and CTSL gene among difference cell lines. Expressions were normalized by GAPDH gene for each cell line and relative fold changes were compared to 293T cells as reference. Flow cytometry analysis of surface expression of DPP4 and TMPRSS2 among different cell lines. Background levels were determined by isotype controls as indicated in grey. (D) Caco2 cells representing the TMPRSS2 entry pathway model and Huh7 cells representing the endosomal entry pathway model were pretreated with Camostat (25 μM), E64d (10 μM) or in both. Pseudoviruses were infected on drug treated cells in quadruplicate wells. Data shown are a representative of two independent repeats.
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Image Search Results


Treatment of cells with camostat targeting the cell surface TMPRSS2 pathway and E64d targeting the endocytic cathepsin L pathway was used to block infectious virus entry via each pathway. Experiments with infectious virus (A) or pseudovirus (B) is shown for the different spike variants in VeroE6/TMPRSS2 cells. (A) Relative viral load was measured the RNA copies of MERS-CoV using the UpE assay in the cell supernatant at 48 hpi. (B) Relative cell entry was measured by RLU. (A-B) 2015/GD01 was the reference for comparison. Figures show the representative data from 2 independent experiments each with two biological replicates for each experiment each drug dose. An inhibition curve was fitted using the Hill equation with inhibition in Graphpad Prism. (C) RT-qPCR to measure RNA expression of DPP4, TMPRSS2 and CTSL gene among difference cell lines. Expressions were normalized by GAPDH gene for each cell line and relative fold changes were compared to 293T cells as reference. Flow cytometry analysis of surface expression of DPP4 and TMPRSS2 among different cell lines. Background levels were determined by isotype controls as indicated in grey. (D) Caco2 cells representing the TMPRSS2 entry pathway model and Huh7 cells representing the endosomal entry pathway model were pretreated with Camostat (25 μM), E64d (10 μM) or in both. Pseudoviruses were infected on drug treated cells in quadruplicate wells. Data shown are a representative of two independent repeats.

Journal: PLOS Pathogens

Article Title: The impact of clade B lineage 5 MERS coronaviruses spike mutations from 2015 to 2023 on virus entry and replication competence

doi: 10.1371/journal.ppat.1013336

Figure Lengend Snippet: Treatment of cells with camostat targeting the cell surface TMPRSS2 pathway and E64d targeting the endocytic cathepsin L pathway was used to block infectious virus entry via each pathway. Experiments with infectious virus (A) or pseudovirus (B) is shown for the different spike variants in VeroE6/TMPRSS2 cells. (A) Relative viral load was measured the RNA copies of MERS-CoV using the UpE assay in the cell supernatant at 48 hpi. (B) Relative cell entry was measured by RLU. (A-B) 2015/GD01 was the reference for comparison. Figures show the representative data from 2 independent experiments each with two biological replicates for each experiment each drug dose. An inhibition curve was fitted using the Hill equation with inhibition in Graphpad Prism. (C) RT-qPCR to measure RNA expression of DPP4, TMPRSS2 and CTSL gene among difference cell lines. Expressions were normalized by GAPDH gene for each cell line and relative fold changes were compared to 293T cells as reference. Flow cytometry analysis of surface expression of DPP4 and TMPRSS2 among different cell lines. Background levels were determined by isotype controls as indicated in grey. (D) Caco2 cells representing the TMPRSS2 entry pathway model and Huh7 cells representing the endosomal entry pathway model were pretreated with Camostat (25 μM), E64d (10 μM) or in both. Pseudoviruses were infected on drug treated cells in quadruplicate wells. Data shown are a representative of two independent repeats.

Article Snippet: 3193) and E64d (Tocris, Cat. No. 4545) were serially diluted with 2% FBS DMEM medium and incubated on to VeroE6/TMPRSS2 cells for 2 hours prior infection.

Techniques: Blocking Assay, Virus, Comparison, Inhibition, Quantitative RT-PCR, RNA Expression, Flow Cytometry, Expressing, Infection