l aspartic acid Search Results


94
MedChemExpress orotidine
Uridine antagonizes the antiviral potency of Antimycin A. (A-C) Inhibitory effect of Antimycin A on BHV-1 infection was counteracted by excess uridine supplementation: MDBK cells were treated with different concentrations of Antimycin A in the presence of excess uridine at the time of BHV-1 infection (MOI = 0.5). (A) Viral infection was quantified at 24 hpi using a Gaussia Luciferase Flash Assay. Statistical significance was determined using a two-tailed unpaired Student's t -test: ****p < 0.0001, ns = no significant difference. (B) eGFP fluorescent expression in infected cells at the same time point (hpi) was visualized. Representative images are shown. Scale bars, 300 µm. Magnification, ×10. (C) Western blot was performed to quantify infection using anti-BHV-1 serum. β-actin was used as a loading control. (D) Schematic of the pyrimidine biosynthesis pathway: The de novo pathway generates uridine triphosphate (UTP) from cellular L-glutamine, while the salvage pathway can support pyrimidine synthesis by recycling preexisting nucleotides from extracellular sources, such as uridine. (E-H) Effect of pyrimidine intermediates on Antimycin A treatment: MDBK cells were treated with Antimycin A along with 100 μM of L-Aspartic acid (E), L-Hydroorotic acid (F), Orotic acid (G), or <t>Orotidine</t> (H) at the time of BHV-1 infection (MOI = 0.5). Infection was quantified at 24 hpi using a Gaussia Luciferase Flash Assay. Statistical significance was assessed using a two-tailed unpaired Student's t -test: ****p < 0.0001.
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BOC Sciences n boc l aspartic acid
Uridine antagonizes the antiviral potency of Antimycin A. (A-C) Inhibitory effect of Antimycin A on BHV-1 infection was counteracted by excess uridine supplementation: MDBK cells were treated with different concentrations of Antimycin A in the presence of excess uridine at the time of BHV-1 infection (MOI = 0.5). (A) Viral infection was quantified at 24 hpi using a Gaussia Luciferase Flash Assay. Statistical significance was determined using a two-tailed unpaired Student's t -test: ****p < 0.0001, ns = no significant difference. (B) eGFP fluorescent expression in infected cells at the same time point (hpi) was visualized. Representative images are shown. Scale bars, 300 µm. Magnification, ×10. (C) Western blot was performed to quantify infection using anti-BHV-1 serum. β-actin was used as a loading control. (D) Schematic of the pyrimidine biosynthesis pathway: The de novo pathway generates uridine triphosphate (UTP) from cellular L-glutamine, while the salvage pathway can support pyrimidine synthesis by recycling preexisting nucleotides from extracellular sources, such as uridine. (E-H) Effect of pyrimidine intermediates on Antimycin A treatment: MDBK cells were treated with Antimycin A along with 100 μM of L-Aspartic acid (E), L-Hydroorotic acid (F), Orotic acid (G), or <t>Orotidine</t> (H) at the time of BHV-1 infection (MOI = 0.5). Infection was quantified at 24 hpi using a Gaussia Luciferase Flash Assay. Statistical significance was assessed using a two-tailed unpaired Student's t -test: ****p < 0.0001.
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BOC Sciences aspartic acid
Uridine antagonizes the antiviral potency of Antimycin A. (A-C) Inhibitory effect of Antimycin A on BHV-1 infection was counteracted by excess uridine supplementation: MDBK cells were treated with different concentrations of Antimycin A in the presence of excess uridine at the time of BHV-1 infection (MOI = 0.5). (A) Viral infection was quantified at 24 hpi using a Gaussia Luciferase Flash Assay. Statistical significance was determined using a two-tailed unpaired Student's t -test: ****p < 0.0001, ns = no significant difference. (B) eGFP fluorescent expression in infected cells at the same time point (hpi) was visualized. Representative images are shown. Scale bars, 300 µm. Magnification, ×10. (C) Western blot was performed to quantify infection using anti-BHV-1 serum. β-actin was used as a loading control. (D) Schematic of the pyrimidine biosynthesis pathway: The de novo pathway generates uridine triphosphate (UTP) from cellular L-glutamine, while the salvage pathway can support pyrimidine synthesis by recycling preexisting nucleotides from extracellular sources, such as uridine. (E-H) Effect of pyrimidine intermediates on Antimycin A treatment: MDBK cells were treated with Antimycin A along with 100 μM of L-Aspartic acid (E), L-Hydroorotic acid (F), Orotic acid (G), or <t>Orotidine</t> (H) at the time of BHV-1 infection (MOI = 0.5). Infection was quantified at 24 hpi using a Gaussia Luciferase Flash Assay. Statistical significance was assessed using a two-tailed unpaired Student's t -test: ****p < 0.0001.
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Revvity aspartate
Uridine antagonizes the antiviral potency of Antimycin A. (A-C) Inhibitory effect of Antimycin A on BHV-1 infection was counteracted by excess uridine supplementation: MDBK cells were treated with different concentrations of Antimycin A in the presence of excess uridine at the time of BHV-1 infection (MOI = 0.5). (A) Viral infection was quantified at 24 hpi using a Gaussia Luciferase Flash Assay. Statistical significance was determined using a two-tailed unpaired Student's t -test: ****p < 0.0001, ns = no significant difference. (B) eGFP fluorescent expression in infected cells at the same time point (hpi) was visualized. Representative images are shown. Scale bars, 300 µm. Magnification, ×10. (C) Western blot was performed to quantify infection using anti-BHV-1 serum. β-actin was used as a loading control. (D) Schematic of the pyrimidine biosynthesis pathway: The de novo pathway generates uridine triphosphate (UTP) from cellular L-glutamine, while the salvage pathway can support pyrimidine synthesis by recycling preexisting nucleotides from extracellular sources, such as uridine. (E-H) Effect of pyrimidine intermediates on Antimycin A treatment: MDBK cells were treated with Antimycin A along with 100 μM of L-Aspartic acid (E), L-Hydroorotic acid (F), Orotic acid (G), or <t>Orotidine</t> (H) at the time of BHV-1 infection (MOI = 0.5). Infection was quantified at 24 hpi using a Gaussia Luciferase Flash Assay. Statistical significance was assessed using a two-tailed unpaired Student's t -test: ****p < 0.0001.
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94
Thermo Fisher l aspartic acid
Uridine antagonizes the antiviral potency of Antimycin A. (A-C) Inhibitory effect of Antimycin A on BHV-1 infection was counteracted by excess uridine supplementation: MDBK cells were treated with different concentrations of Antimycin A in the presence of excess uridine at the time of BHV-1 infection (MOI = 0.5). (A) Viral infection was quantified at 24 hpi using a Gaussia Luciferase Flash Assay. Statistical significance was determined using a two-tailed unpaired Student's t -test: ****p < 0.0001, ns = no significant difference. (B) eGFP fluorescent expression in infected cells at the same time point (hpi) was visualized. Representative images are shown. Scale bars, 300 µm. Magnification, ×10. (C) Western blot was performed to quantify infection using anti-BHV-1 serum. β-actin was used as a loading control. (D) Schematic of the pyrimidine biosynthesis pathway: The de novo pathway generates uridine triphosphate (UTP) from cellular L-glutamine, while the salvage pathway can support pyrimidine synthesis by recycling preexisting nucleotides from extracellular sources, such as uridine. (E-H) Effect of pyrimidine intermediates on Antimycin A treatment: MDBK cells were treated with Antimycin A along with 100 μM of L-Aspartic acid (E), L-Hydroorotic acid (F), Orotic acid (G), or <t>Orotidine</t> (H) at the time of BHV-1 infection (MOI = 0.5). Infection was quantified at 24 hpi using a Gaussia Luciferase Flash Assay. Statistical significance was assessed using a two-tailed unpaired Student's t -test: ****p < 0.0001.
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93
MedChemExpress aspartic acid
Uridine antagonizes the antiviral potency of Antimycin A. (A-C) Inhibitory effect of Antimycin A on BHV-1 infection was counteracted by excess uridine supplementation: MDBK cells were treated with different concentrations of Antimycin A in the presence of excess uridine at the time of BHV-1 infection (MOI = 0.5). (A) Viral infection was quantified at 24 hpi using a Gaussia Luciferase Flash Assay. Statistical significance was determined using a two-tailed unpaired Student's t -test: ****p < 0.0001, ns = no significant difference. (B) eGFP fluorescent expression in infected cells at the same time point (hpi) was visualized. Representative images are shown. Scale bars, 300 µm. Magnification, ×10. (C) Western blot was performed to quantify infection using anti-BHV-1 serum. β-actin was used as a loading control. (D) Schematic of the pyrimidine biosynthesis pathway: The de novo pathway generates uridine triphosphate (UTP) from cellular L-glutamine, while the salvage pathway can support pyrimidine synthesis by recycling preexisting nucleotides from extracellular sources, such as uridine. (E-H) Effect of pyrimidine intermediates on Antimycin A treatment: MDBK cells were treated with Antimycin A along with 100 μM of L-Aspartic acid (E), L-Hydroorotic acid (F), Orotic acid (G), or <t>Orotidine</t> (H) at the time of BHV-1 infection (MOI = 0.5). Infection was quantified at 24 hpi using a Gaussia Luciferase Flash Assay. Statistical significance was assessed using a two-tailed unpaired Student's t -test: ****p < 0.0001.
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Santa Cruz Biotechnology aspartic acid
Uridine antagonizes the antiviral potency of Antimycin A. (A-C) Inhibitory effect of Antimycin A on BHV-1 infection was counteracted by excess uridine supplementation: MDBK cells were treated with different concentrations of Antimycin A in the presence of excess uridine at the time of BHV-1 infection (MOI = 0.5). (A) Viral infection was quantified at 24 hpi using a Gaussia Luciferase Flash Assay. Statistical significance was determined using a two-tailed unpaired Student's t -test: ****p < 0.0001, ns = no significant difference. (B) eGFP fluorescent expression in infected cells at the same time point (hpi) was visualized. Representative images are shown. Scale bars, 300 µm. Magnification, ×10. (C) Western blot was performed to quantify infection using anti-BHV-1 serum. β-actin was used as a loading control. (D) Schematic of the pyrimidine biosynthesis pathway: The de novo pathway generates uridine triphosphate (UTP) from cellular L-glutamine, while the salvage pathway can support pyrimidine synthesis by recycling preexisting nucleotides from extracellular sources, such as uridine. (E-H) Effect of pyrimidine intermediates on Antimycin A treatment: MDBK cells were treated with Antimycin A along with 100 μM of L-Aspartic acid (E), L-Hydroorotic acid (F), Orotic acid (G), or <t>Orotidine</t> (H) at the time of BHV-1 infection (MOI = 0.5). Infection was quantified at 24 hpi using a Gaussia Luciferase Flash Assay. Statistical significance was assessed using a two-tailed unpaired Student's t -test: ****p < 0.0001.
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93
Santa Cruz Biotechnology cat sc 285170
Uridine antagonizes the antiviral potency of Antimycin A. (A-C) Inhibitory effect of Antimycin A on BHV-1 infection was counteracted by excess uridine supplementation: MDBK cells were treated with different concentrations of Antimycin A in the presence of excess uridine at the time of BHV-1 infection (MOI = 0.5). (A) Viral infection was quantified at 24 hpi using a Gaussia Luciferase Flash Assay. Statistical significance was determined using a two-tailed unpaired Student's t -test: ****p < 0.0001, ns = no significant difference. (B) eGFP fluorescent expression in infected cells at the same time point (hpi) was visualized. Representative images are shown. Scale bars, 300 µm. Magnification, ×10. (C) Western blot was performed to quantify infection using anti-BHV-1 serum. β-actin was used as a loading control. (D) Schematic of the pyrimidine biosynthesis pathway: The de novo pathway generates uridine triphosphate (UTP) from cellular L-glutamine, while the salvage pathway can support pyrimidine synthesis by recycling preexisting nucleotides from extracellular sources, such as uridine. (E-H) Effect of pyrimidine intermediates on Antimycin A treatment: MDBK cells were treated with Antimycin A along with 100 μM of L-Aspartic acid (E), L-Hydroorotic acid (F), Orotic acid (G), or <t>Orotidine</t> (H) at the time of BHV-1 infection (MOI = 0.5). Infection was quantified at 24 hpi using a Gaussia Luciferase Flash Assay. Statistical significance was assessed using a two-tailed unpaired Student's t -test: ****p < 0.0001.
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91
Santa Cruz Biotechnology sc 22839
Uridine antagonizes the antiviral potency of Antimycin A. (A-C) Inhibitory effect of Antimycin A on BHV-1 infection was counteracted by excess uridine supplementation: MDBK cells were treated with different concentrations of Antimycin A in the presence of excess uridine at the time of BHV-1 infection (MOI = 0.5). (A) Viral infection was quantified at 24 hpi using a Gaussia Luciferase Flash Assay. Statistical significance was determined using a two-tailed unpaired Student's t -test: ****p < 0.0001, ns = no significant difference. (B) eGFP fluorescent expression in infected cells at the same time point (hpi) was visualized. Representative images are shown. Scale bars, 300 µm. Magnification, ×10. (C) Western blot was performed to quantify infection using anti-BHV-1 serum. β-actin was used as a loading control. (D) Schematic of the pyrimidine biosynthesis pathway: The de novo pathway generates uridine triphosphate (UTP) from cellular L-glutamine, while the salvage pathway can support pyrimidine synthesis by recycling preexisting nucleotides from extracellular sources, such as uridine. (E-H) Effect of pyrimidine intermediates on Antimycin A treatment: MDBK cells were treated with Antimycin A along with 100 μM of L-Aspartic acid (E), L-Hydroorotic acid (F), Orotic acid (G), or <t>Orotidine</t> (H) at the time of BHV-1 infection (MOI = 0.5). Infection was quantified at 24 hpi using a Gaussia Luciferase Flash Assay. Statistical significance was assessed using a two-tailed unpaired Student's t -test: ****p < 0.0001.
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Santa Cruz Biotechnology aga substrate asp amc
Uridine antagonizes the antiviral potency of Antimycin A. (A-C) Inhibitory effect of Antimycin A on BHV-1 infection was counteracted by excess uridine supplementation: MDBK cells were treated with different concentrations of Antimycin A in the presence of excess uridine at the time of BHV-1 infection (MOI = 0.5). (A) Viral infection was quantified at 24 hpi using a Gaussia Luciferase Flash Assay. Statistical significance was determined using a two-tailed unpaired Student's t -test: ****p < 0.0001, ns = no significant difference. (B) eGFP fluorescent expression in infected cells at the same time point (hpi) was visualized. Representative images are shown. Scale bars, 300 µm. Magnification, ×10. (C) Western blot was performed to quantify infection using anti-BHV-1 serum. β-actin was used as a loading control. (D) Schematic of the pyrimidine biosynthesis pathway: The de novo pathway generates uridine triphosphate (UTP) from cellular L-glutamine, while the salvage pathway can support pyrimidine synthesis by recycling preexisting nucleotides from extracellular sources, such as uridine. (E-H) Effect of pyrimidine intermediates on Antimycin A treatment: MDBK cells were treated with Antimycin A along with 100 μM of L-Aspartic acid (E), L-Hydroorotic acid (F), Orotic acid (G), or <t>Orotidine</t> (H) at the time of BHV-1 infection (MOI = 0.5). Infection was quantified at 24 hpi using a Gaussia Luciferase Flash Assay. Statistical significance was assessed using a two-tailed unpaired Student's t -test: ****p < 0.0001.
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92
BOC Sciences t boc l aspartic acid
Uridine antagonizes the antiviral potency of Antimycin A. (A-C) Inhibitory effect of Antimycin A on BHV-1 infection was counteracted by excess uridine supplementation: MDBK cells were treated with different concentrations of Antimycin A in the presence of excess uridine at the time of BHV-1 infection (MOI = 0.5). (A) Viral infection was quantified at 24 hpi using a Gaussia Luciferase Flash Assay. Statistical significance was determined using a two-tailed unpaired Student's t -test: ****p < 0.0001, ns = no significant difference. (B) eGFP fluorescent expression in infected cells at the same time point (hpi) was visualized. Representative images are shown. Scale bars, 300 µm. Magnification, ×10. (C) Western blot was performed to quantify infection using anti-BHV-1 serum. β-actin was used as a loading control. (D) Schematic of the pyrimidine biosynthesis pathway: The de novo pathway generates uridine triphosphate (UTP) from cellular L-glutamine, while the salvage pathway can support pyrimidine synthesis by recycling preexisting nucleotides from extracellular sources, such as uridine. (E-H) Effect of pyrimidine intermediates on Antimycin A treatment: MDBK cells were treated with Antimycin A along with 100 μM of L-Aspartic acid (E), L-Hydroorotic acid (F), Orotic acid (G), or <t>Orotidine</t> (H) at the time of BHV-1 infection (MOI = 0.5). Infection was quantified at 24 hpi using a Gaussia Luciferase Flash Assay. Statistical significance was assessed using a two-tailed unpaired Student's t -test: ****p < 0.0001.
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94
MedChemExpress l aspartic acid β hydroxamate
Uridine antagonizes the antiviral potency of Antimycin A. (A-C) Inhibitory effect of Antimycin A on BHV-1 infection was counteracted by excess uridine supplementation: MDBK cells were treated with different concentrations of Antimycin A in the presence of excess uridine at the time of BHV-1 infection (MOI = 0.5). (A) Viral infection was quantified at 24 hpi using a Gaussia Luciferase Flash Assay. Statistical significance was determined using a two-tailed unpaired Student's t -test: ****p < 0.0001, ns = no significant difference. (B) eGFP fluorescent expression in infected cells at the same time point (hpi) was visualized. Representative images are shown. Scale bars, 300 µm. Magnification, ×10. (C) Western blot was performed to quantify infection using anti-BHV-1 serum. β-actin was used as a loading control. (D) Schematic of the pyrimidine biosynthesis pathway: The de novo pathway generates uridine triphosphate (UTP) from cellular L-glutamine, while the salvage pathway can support pyrimidine synthesis by recycling preexisting nucleotides from extracellular sources, such as uridine. (E-H) Effect of pyrimidine intermediates on Antimycin A treatment: MDBK cells were treated with Antimycin A along with 100 μM of L-Aspartic acid (E), L-Hydroorotic acid (F), Orotic acid (G), or <t>Orotidine</t> (H) at the time of BHV-1 infection (MOI = 0.5). Infection was quantified at 24 hpi using a Gaussia Luciferase Flash Assay. Statistical significance was assessed using a two-tailed unpaired Student's t -test: ****p < 0.0001.
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Image Search Results


Uridine antagonizes the antiviral potency of Antimycin A. (A-C) Inhibitory effect of Antimycin A on BHV-1 infection was counteracted by excess uridine supplementation: MDBK cells were treated with different concentrations of Antimycin A in the presence of excess uridine at the time of BHV-1 infection (MOI = 0.5). (A) Viral infection was quantified at 24 hpi using a Gaussia Luciferase Flash Assay. Statistical significance was determined using a two-tailed unpaired Student's t -test: ****p < 0.0001, ns = no significant difference. (B) eGFP fluorescent expression in infected cells at the same time point (hpi) was visualized. Representative images are shown. Scale bars, 300 µm. Magnification, ×10. (C) Western blot was performed to quantify infection using anti-BHV-1 serum. β-actin was used as a loading control. (D) Schematic of the pyrimidine biosynthesis pathway: The de novo pathway generates uridine triphosphate (UTP) from cellular L-glutamine, while the salvage pathway can support pyrimidine synthesis by recycling preexisting nucleotides from extracellular sources, such as uridine. (E-H) Effect of pyrimidine intermediates on Antimycin A treatment: MDBK cells were treated with Antimycin A along with 100 μM of L-Aspartic acid (E), L-Hydroorotic acid (F), Orotic acid (G), or Orotidine (H) at the time of BHV-1 infection (MOI = 0.5). Infection was quantified at 24 hpi using a Gaussia Luciferase Flash Assay. Statistical significance was assessed using a two-tailed unpaired Student's t -test: ****p < 0.0001.

Journal: Journal of Advanced Research

Article Title: Antimycin A inhibits alpha-herpesvirus replication by disrupting the formation of pyrimidinosomes

doi: 10.1016/j.jare.2025.05.016

Figure Lengend Snippet: Uridine antagonizes the antiviral potency of Antimycin A. (A-C) Inhibitory effect of Antimycin A on BHV-1 infection was counteracted by excess uridine supplementation: MDBK cells were treated with different concentrations of Antimycin A in the presence of excess uridine at the time of BHV-1 infection (MOI = 0.5). (A) Viral infection was quantified at 24 hpi using a Gaussia Luciferase Flash Assay. Statistical significance was determined using a two-tailed unpaired Student's t -test: ****p < 0.0001, ns = no significant difference. (B) eGFP fluorescent expression in infected cells at the same time point (hpi) was visualized. Representative images are shown. Scale bars, 300 µm. Magnification, ×10. (C) Western blot was performed to quantify infection using anti-BHV-1 serum. β-actin was used as a loading control. (D) Schematic of the pyrimidine biosynthesis pathway: The de novo pathway generates uridine triphosphate (UTP) from cellular L-glutamine, while the salvage pathway can support pyrimidine synthesis by recycling preexisting nucleotides from extracellular sources, such as uridine. (E-H) Effect of pyrimidine intermediates on Antimycin A treatment: MDBK cells were treated with Antimycin A along with 100 μM of L-Aspartic acid (E), L-Hydroorotic acid (F), Orotic acid (G), or Orotidine (H) at the time of BHV-1 infection (MOI = 0.5). Infection was quantified at 24 hpi using a Gaussia Luciferase Flash Assay. Statistical significance was assessed using a two-tailed unpaired Student's t -test: ****p < 0.0001.

Article Snippet: The specific compounds used in this study included Antimycin A (MS0070-10MG; Maokang Biotechnology), Ara-C (MCE, HY-13605), Uridine (MCE, HY-B1449), Orotate (MCE, HY-N8060A), Dihydroorotate (MCE, HY-N0157), Aspartic Acid (MCE, HY-N0666R), Orotidine (MCE, 113226), Ascorbic Acid (MCE, B0166R), and BQR (MCE, 108325).

Techniques: Infection, Luciferase, Two Tailed Test, Expressing, Western Blot, Control