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ATCC human coronaviruses oc43

(a) PROTACs are bifunctional molecules, consisting of a target protein-binding ligand and an E3 ligase ligand attached via a linker. Upon binding of both targets, the E3 ligase catalyses ubiquitination of the target protein, inducing its degradation. (b) Structure of p38α/β-targeting PROTAC NR-7h. The shaded regions indicate the kinase-binding ligand (based on PH-797804) and the CRBN E3 ligase ligand. A549 cells treated with 10 μM NR-7h for 24 h show significant degradation of p38 kinase (c) but no effects on cell viability, as measured by MTS assay (d) . A549 cells infected with <t>OC43</t> (MOI=0.1) and treated with 10 μM NR-7h showed significant reduction of viral infectivity (e) and viral RNA (f) after 72 h. (g) NR-7h showed greater antiviral efficacy compared to two p38 kinase small molecule inhibitors (NR-7h, IC 50 1.0 nM; PH-797804, IC 50 >10 µM; LY2228820, IC 50 648.4 nM). Graphs show mean ± SEM (n=3); *, p≤0.05; **, p≤0.01; ***, p≤0.001.

Human Coronaviruses Oc43, supplied by ATCC, used in various techniques. Bioz Stars score: 98/100, based on 450 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 98 stars, based on 450 article reviews

human coronaviruses oc43 - by Bioz Stars, 2026-08

98/100 stars

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Article Title: Proof-of-concept of targeted degradation of p38α/β MAPK host-kinase as a potent inhibitor of coronaviruses

Journal: bioRxiv

doi: 10.64898/2026.04.29.721712

Figure Legend Snippet: (a) PROTACs are bifunctional molecules, consisting of a target protein-binding ligand and an E3 ligase ligand attached via a linker. Upon binding of both targets, the E3 ligase catalyses ubiquitination of the target protein, inducing its degradation. (b) Structure of p38α/β-targeting PROTAC NR-7h. The shaded regions indicate the kinase-binding ligand (based on PH-797804) and the CRBN E3 ligase ligand. A549 cells treated with 10 μM NR-7h for 24 h show significant degradation of p38 kinase (c) but no effects on cell viability, as measured by MTS assay (d) . A549 cells infected with OC43 (MOI=0.1) and treated with 10 μM NR-7h showed significant reduction of viral infectivity (e) and viral RNA (f) after 72 h. (g) NR-7h showed greater antiviral efficacy compared to two p38 kinase small molecule inhibitors (NR-7h, IC 50 1.0 nM; PH-797804, IC 50 >10 µM; LY2228820, IC 50 648.4 nM). Graphs show mean ± SEM (n=3); *, p≤0.05; **, p≤0.01; ***, p≤0.001.

Techniques Used: Protein Binding, Binding Assay, Ubiquitin Proteomics, MTS Assay, Infection

BHK-21 cells treated with 10 μM NR-7h for 24 h show significant degradation of p38 kinase (a) but no effects on cell viability, as measured by MTS assay (b) . BHK-21 cells infected with OC43 (MOI=0.1) and treated with 10 μM NR-7h showed significant reduction of viral infectivity (c) and viral RNA (d) after 72 h. (e) NR-7h showed greater inhibition in BHK-21 cells compared to two p38 kinase small molecule inhibitors (NR-7h, IC 50 9.9 nM; PH-797804, IC 50 3.5 µM; LY2228820, IC 50 69.3 nM). Graphs show mean ± SEM (n=3); *, p≤0.05; **, p≤0.01; ***, p≤0.001. Graphs show mean ± SEM (n=3); *, p≤0.05.

Figure Legend Snippet: BHK-21 cells treated with 10 μM NR-7h for 24 h show significant degradation of p38 kinase (a) but no effects on cell viability, as measured by MTS assay (b) . BHK-21 cells infected with OC43 (MOI=0.1) and treated with 10 μM NR-7h showed significant reduction of viral infectivity (c) and viral RNA (d) after 72 h. (e) NR-7h showed greater inhibition in BHK-21 cells compared to two p38 kinase small molecule inhibitors (NR-7h, IC 50 9.9 nM; PH-797804, IC 50 3.5 µM; LY2228820, IC 50 69.3 nM). Graphs show mean ± SEM (n=3); *, p≤0.05; **, p≤0.01; ***, p≤0.001. Graphs show mean ± SEM (n=3); *, p≤0.05.

Techniques Used: MTS Assay, Infection, Inhibition

(a) BHK-21 cells were infected with OC43, and treated with 10 µM NR-7h at 0, 1, 3, or 6 h post-infection, and quantified 14 h post-infection. (b) Quantification of infection was normalised to DMSO-treated cells. Inhibition of infection was not observed for any of these conditions. Graphs show mean ± SEM (n=3).

Figure Legend Snippet: (a) BHK-21 cells were infected with OC43, and treated with 10 µM NR-7h at 0, 1, 3, or 6 h post-infection, and quantified 14 h post-infection. (b) Quantification of infection was normalised to DMSO-treated cells. Inhibition of infection was not observed for any of these conditions. Graphs show mean ± SEM (n=3).

Techniques Used: Infection, Inhibition

Cell viability of A549 cells treated with (a) MG132 or (b) MLN4924, no cytotoxicity was observed up to 10 µM for both inhibitors. A549 cells treated with 10 µM NR-7h and (c) MG132 (5 µM) or (d) MLN4924 (3 µM) showed no degradation of p38 kinase compared to when no inhibitors were present. A549 cells infected with OC43 (MOI=0.1) showed significant reduction in infection 72 h after treatment in presence of NR-7h, but infectivity was recovered in presence of (e) MG132 (5 µM) or (f) MLN4924 (3 µM). Graphs show mean ± SEM (n=3); **, p≤0.01; ***, p≤0.001.

Figure Legend Snippet: Cell viability of A549 cells treated with (a) MG132 or (b) MLN4924, no cytotoxicity was observed up to 10 µM for both inhibitors. A549 cells treated with 10 µM NR-7h and (c) MG132 (5 µM) or (d) MLN4924 (3 µM) showed no degradation of p38 kinase compared to when no inhibitors were present. A549 cells infected with OC43 (MOI=0.1) showed significant reduction in infection 72 h after treatment in presence of NR-7h, but infectivity was recovered in presence of (e) MG132 (5 µM) or (f) MLN4924 (3 µM). Graphs show mean ± SEM (n=3); **, p≤0.01; ***, p≤0.001.

Techniques Used: Infection

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Journal: bioRxiv

Article Title: Proof-of-concept of targeted degradation of p38α/β MAPK host-kinase as a potent inhibitor of coronaviruses

doi: 10.64898/2026.04.29.721712

Figure Lengend Snippet: (a) PROTACs are bifunctional molecules, consisting of a target protein-binding ligand and an E3 ligase ligand attached via a linker. Upon binding of both targets, the E3 ligase catalyses ubiquitination of the target protein, inducing its degradation. (b) Structure of p38α/β-targeting PROTAC NR-7h. The shaded regions indicate the kinase-binding ligand (based on PH-797804) and the CRBN E3 ligase ligand. A549 cells treated with 10 μM NR-7h for 24 h show significant degradation of p38 kinase (c) but no effects on cell viability, as measured by MTS assay (d) . A549 cells infected with OC43 (MOI=0.1) and treated with 10 μM NR-7h showed significant reduction of viral infectivity (e) and viral RNA (f) after 72 h. (g) NR-7h showed greater antiviral efficacy compared to two p38 kinase small molecule inhibitors (NR-7h, IC 50 1.0 nM; PH-797804, IC 50 >10 µM; LY2228820, IC 50 648.4 nM). Graphs show mean ± SEM (n=3); *, p≤0.05; **, p≤0.01; ***, p≤0.001.

Article Snippet: Human coronaviruses OC43 (ATCC VR-1558) stocks were grown in HCT-8 cells, and human coronavirus 229E (ATCC VR-740) stocks were grown and titred in MRC-5 cells.

Techniques: Protein Binding, Binding Assay, Ubiquitin Proteomics, MTS Assay, Infection

Journal: bioRxiv

Article Title: Proof-of-concept of targeted degradation of p38α/β MAPK host-kinase as a potent inhibitor of coronaviruses

doi: 10.64898/2026.04.29.721712

Figure Lengend Snippet: BHK-21 cells treated with 10 μM NR-7h for 24 h show significant degradation of p38 kinase (a) but no effects on cell viability, as measured by MTS assay (b) . BHK-21 cells infected with OC43 (MOI=0.1) and treated with 10 μM NR-7h showed significant reduction of viral infectivity (c) and viral RNA (d) after 72 h. (e) NR-7h showed greater inhibition in BHK-21 cells compared to two p38 kinase small molecule inhibitors (NR-7h, IC 50 9.9 nM; PH-797804, IC 50 3.5 µM; LY2228820, IC 50 69.3 nM). Graphs show mean ± SEM (n=3); *, p≤0.05; **, p≤0.01; ***, p≤0.001. Graphs show mean ± SEM (n=3); *, p≤0.05.

Article Snippet: Human coronaviruses OC43 (ATCC VR-1558) stocks were grown in HCT-8 cells, and human coronavirus 229E (ATCC VR-740) stocks were grown and titred in MRC-5 cells.

Techniques: MTS Assay, Infection, Inhibition

Journal: bioRxiv

Article Title: Proof-of-concept of targeted degradation of p38α/β MAPK host-kinase as a potent inhibitor of coronaviruses

doi: 10.64898/2026.04.29.721712

Figure Lengend Snippet: (a) BHK-21 cells were infected with OC43, and treated with 10 µM NR-7h at 0, 1, 3, or 6 h post-infection, and quantified 14 h post-infection. (b) Quantification of infection was normalised to DMSO-treated cells. Inhibition of infection was not observed for any of these conditions. Graphs show mean ± SEM (n=3).

Article Snippet: Human coronaviruses OC43 (ATCC VR-1558) stocks were grown in HCT-8 cells, and human coronavirus 229E (ATCC VR-740) stocks were grown and titred in MRC-5 cells.

Techniques: Infection, Inhibition

Journal: bioRxiv

Article Title: Proof-of-concept of targeted degradation of p38α/β MAPK host-kinase as a potent inhibitor of coronaviruses

doi: 10.64898/2026.04.29.721712

Figure Lengend Snippet: Cell viability of A549 cells treated with (a) MG132 or (b) MLN4924, no cytotoxicity was observed up to 10 µM for both inhibitors. A549 cells treated with 10 µM NR-7h and (c) MG132 (5 µM) or (d) MLN4924 (3 µM) showed no degradation of p38 kinase compared to when no inhibitors were present. A549 cells infected with OC43 (MOI=0.1) showed significant reduction in infection 72 h after treatment in presence of NR-7h, but infectivity was recovered in presence of (e) MG132 (5 µM) or (f) MLN4924 (3 µM). Graphs show mean ± SEM (n=3); **, p≤0.01; ***, p≤0.001.

Article Snippet: Human coronaviruses OC43 (ATCC VR-1558) stocks were grown in HCT-8 cells, and human coronavirus 229E (ATCC VR-740) stocks were grown and titred in MRC-5 cells.

Techniques: Infection

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