Bhk T7-9 Cells
Bhk T7-9 Cells - Related Videos
03:44
Generation of GFP-Tagged Recombinant Respiratory Syncytial Virus Using a T7 Expression System
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2026
Source: Bouillier, C. et. al., Amplification, and Titration of Recombinant Respiratory Syncytial Viruses. J. Vis. Exp. (2019)This video demonstrates the generation of a green fluorescent protein (GFP)-expressing recombinant respiratory syncytial virus using a T7-based reverse genetics system. The co-transfection of plasmids encoding viral proteins and a GFP-tagged genome leads to protein expression and initiates virus rescue.
10:09
Inducible T7 RNA Polymerase-mediated Multigene Expression System, pMGX
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2017
This study describes methods for the T7-mediated co-expression of multiple genes from a single plasmid in Escherichia coli using the pMGX plasmid system.
05:42
Quantitative PCR of T7 Bacteriophage from Biopanning
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Cited by 7 •
2018
A reproducible, accurate, and time efficient quantitative PCR (qPCR) method to enumerate T7 bacteriophage is described here. The protocol clearly describes phage genomic DNA preparation, PCR reaction preparation, qPCR cycling conditions, and qPCR data analysis.
05:18
Quantification of Immunostained Caspase-9 in Retinal Tissue
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Cited by 4 •
2022
Presented here is a detailed immunohistochemistry protocol to identify, validate, and target functionally relevant caspases in complex tissues.
08:11
Quantitative Methods to Study Protein Arginine Methyltransferase 1-9 Activity in Cells
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Cited by 1 •
2021
These protocols provide the methodology used to assess the enzymatic activity of individual members of the protein arginine methyltransferase (PRMT) family in cells. Detailed guidelines on assessing PRMT activity using endogenous and exogenous biomarkers, methyl-arginine recognizing antibodies, and inhibitor tool compounds are described.
FAQs
The central enabling event is transcription from a T7 promoter. When researchers introduce a plasmid carrying that promoter, the constitutively expressed T7 RNA polymerase recognizes it and produces the specified RNA inside the cell. That RNA can then support target protein production, providing a defined route for studying viral gene expression.
Reverse-genetics experiments can change a defined viral gene before introducing the relevant constructs, allowing investigators to connect a specific sequence with a measurable phenotype. T7-driven transcription generates the viral or target RNAs required by the experimental system. Comparing altered and unaltered versions helps assess effects on infectivity, immune evasion, or disease-related phenotypes.
The immediate output of T7 polymerase activity is RNA, but the experimental endpoint can differ. In one design, the transcribed RNA directs production of a target protein. In another, a compatible set of viral components can use the transcripts to enable recovery of recombinant virus. Thus, the same transcriptional platform supports distinct goals when the viral system is suitable.
A typical experiment begins by introducing plasmid DNA containing T7 promoter sequences into BHK T7-9 cells. Constitutive polymerase expression then drives transcription of the encoded viral or target sequences. Investigators can examine protein production or, when the system permits, recombinant-virus recovery. Subsequent infection studies can relate those outputs to replication or host responses.
They are particularly useful when a study needs controlled expression of viral genes alongside infection-related readouts. The platform supports investigations of viral replication, host responses, and pathogen-host interactions, making it relevant to immunology and infection research. It also suits experiments that ask how altering a defined viral gene changes immune evasion or disease-related behavior.
Comparisons between constructs carrying different viral gene versions can reveal whether a gene influences infectivity, immune evasion, or disease-related phenotypes. Because the system permits transcription from introduced T7-promoter plasmids, researchers can examine defined genetic changes rather than treating the virus as an unchanged whole. These findings help connect viral genotype with replication and host-interaction outcomes.