antimyc tag 9b11 mouse monoclonal (Cell Signaling Technology Inc)
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Cell Signaling Technology Inc
antimyc tag 9b11 mouse monoclonal
Antimyc Tag 9b11 Mouse Monoclonal, supplied by Cell Signaling Technology Inc, 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/antimyc+9b11/pm41053424-270-46-50
Average 86 stars, based on 1 article reviews
Antimyc Tag 9b11 Mouse Monoclonal, supplied by Cell Signaling Technology Inc, 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/antimyc+9b11/pm41053424-270-46-50
Average 86 stars, based on 1 article reviews
antimyc tag 9b11 mouse monoclonal - by Bioz Stars,
2026-10
86/100 stars
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Western Blot:Article Title: Expression of SARS-CoV-2 Nonstructural Proteins 3 and 4 Can Tune the Unfolded Protein Response in Cell Culture. Article Snippet: Coronaviruses (CoV), including SARS-CoV-2, modulate host proteostasis through the activation of stress-responsive signaling pathways such as the Unfolded Protein Response (UPR), which remedies misfolded protein accumulation by attenuating translation and increasing protein folding capacity.. While CoV nonstructural proteins (nsps) are essential for infection, little is known about the role of nsps in modulating the UPR.. We characterized the impact of overexpression of SARS-CoV-2 nsp4, a key driver of replication, on the UPR in cell culture using quantitative proteomics to sensitively detect pathway-wide upregulation of effector proteins. Blocking Assay:Article Title: Expression of SARS-CoV-2 Nonstructural Proteins 3 and 4 Can Tune the Unfolded Protein Response in Cell Culture. Article Snippet: Coronaviruses (CoV), including SARS-CoV-2, modulate host proteostasis through the activation of stress-responsive signaling pathways such as the Unfolded Protein Response (UPR), which remedies misfolded protein accumulation by attenuating translation and increasing protein folding capacity.. While CoV nonstructural proteins (nsps) are essential for infection, little is known about the role of nsps in modulating the UPR.. We characterized the impact of overexpression of SARS-CoV-2 nsp4, a key driver of replication, on the UPR in cell culture using quantitative proteomics to sensitively detect pathway-wide upregulation of effector proteins. |