Viral Vectors & Particles

Please note this product may be subject to fees, we invite you to contact your local office. NLR family Pyrin domain containing 3 (NLRP3) is expressed in macrophages and is a component of inflammasomes. NLRP3 detects uric acid and extracellular ATP in damaged tissue and interacts with a pro-apoptotic protein that recruits caspases. This complex is also an upstream activator of NF-κB signaling and triggers an immune response as part of the innate immune system. Mutations in NLRP3 are known to cause autoinflammatory and neuroinflammatory diseases, such as Alzheimer's, Parkinson's, and prion disease.  The NLRP3 CRISPR/Cas9 Lentiviruses are replication incompetent, HIV-based VSV-G pseudo-typed lentiviral particles ready to infect most types of mammalian cells, including primary and non-dividing cells. The particles contain a CRISPR/Cas9 gene driven by an EF1a promoter, along with 5 sgRNA (single guide RNA) targeting human NLRP3 (Figure 1 and Table 1), allowing the knockdown of NLRP3 in tra

Please note this product may be subject to fees, we invite you to contact your local office. NLR family Pyrin domain containing 3 (NLRP3) is expressed in macrophages and is a component of inflammasomes. NLRP3 detects uric acid and extracellular ATP in damaged tissue and interacts with a pro-apoptotic protein that recruits caspases. This complex is also an upstream activator of NF-κB signaling and triggers an immune response as part of the innate immune system. Mutations in NLRP3 are known to cause autoinflammatory and neuroinflammatory diseases such as Alzheimer's, Parkinson's, and prion disease.  The NLRP3 CRISPR/Cas9 Lentiviruses are replication incompetent, HIV-based VSV-G pseudo-typed lentiviral particles ready to be transduced into most  types of mammalian cells, including primary and non-dividing cells. The particles contain a CRISPR/Cas9 gene driven by an EF1a promoter, along with 5 sgRNA (single guide RNA) targeting human NLRP3 (Figure 1 and Table 1), allowing the knockdown of

The anti-CD20 CAR lentiviruses are replication incompetent, HIV-based, VSV-G-pseudotyped lentiviral particles that are ready to infect almost all types of mammalian cells, including primary and non-dividing cells. These viruses transduce the ScFv (single-chain variable fragment) of anti-CD20 (clone Leu-16) linked to a 2^nd generation CAR (Chimeric Antigen Receptor) containing CD8 hinge and transmembrane domains, and the 4-1BB and CD3ζ signaling domains .

The anti-CD22 CAR lentiviruses are replication incompetent, HIV-based, VSV-G-pseudotyped lentiviral particles that are ready to infect almost all types of mammalian cells, including primary and non-dividing cells. These viruses transduce the ScFv (single-chain variable fragment) of anti-CD22 (clone m971) linked to a 2^nd generation CAR (Chimeric Antigen Receptor) containing CD8 hinge and transmembrane domains, and the 4-1BB and CD3ζ signaling domains (below).

The pandemic coronavirus disease 2019 (COVID-19) is caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). As the first step of the viral replication, the virus attaches to the host cell surface before entering the cell. The viral Spike protein recognizes and attaches to the Angiotensin-Converting Enzyme 2 (ACE2) receptor found on the surface of type I and II pneumocytes, endothelial cells, and ciliated bronchial epithelial cells. Drugs targeting the interaction between the Spike protein of SARS-CoV-2 and human ACE2 may offer protection against the viral infection. Numerous SARS-CoV-2 variants have been identified so far. These variants contain a number of mutations that may increase morbidity and mortality and allow the virus to spread more easily and quickly than the original strain. BPS Bioscience has launched a series of Spike Variants (SARS-CoV-2) Pseudotyped Lentivirus (Luc reporter). The Spike (SARS-CoV-2) Pseudotyped Lentiviruses were produced with SARS-CoV-2 S

The pandemic coronavirus disease 2019 (COVID-19) is caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). As the first step of the viral replication, the virus attaches to the host cell surface before entering the cell. The viral Spike protein recognizes and attaches to the Angiotensin-Converting Enzyme 2 (ACE2) receptor found on the surface of type I and II pneumocytes, endothelial cells, and ciliated bronchial epithelial cells. Drugs targeting the interaction between the Spike protein of SARS-CoV-2 and ACE2 may offer protection against the viral infection. A variant called B.1.621 (also known as the Mu Variant) was first identified in Columbia in early 2021. This variant has a number of mutations that may increase morbidity and mortality and allow the virus to spread more easily and quickly than other variants. The Spike (B.1.621, Mu Variant) (SARS-CoV-2) Pseudotyped Lentiviruses were produced with SARS-CoV-2 B.1.621 Variant Spike (Genbank Accession #QHD43416.1 with

The pandemic coronavirus disease 2019 (COVID-19) is caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). As the first step of the viral replication, the virus attaches to the host cell surface before entering the cell. The viral Spike protein recognizes and attaches to the Angiotensin-Converting Enzyme 2 (ACE2) receptor found on the surface of type I and II pneumocytes, endothelial cells, and ciliated bronchial epithelial cells. Drugs targeting the interaction between the Spike protein of SARS-CoV-2 and ACE2 may offer protection against the viral infection. A variant called B.1.621 (also known as the Mu Variant) was first identified in Columbia in early 2021. This variant has a number of mutations that may increase morbidity and mortality and allow the virus to spread more easily and quickly than other variants. The Spike (B.1.621, Mu Variant) (SARS-CoV-2) Pseudotyped Lentiviruses were produced with SARS-CoV-2 B.1.621 Variant Spike (Genbank Accession #QHD43416.1 with

The pandemic coronavirus disease 2019 (COVID-19) is caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). As the first step of the viral replication, the virus attaches to the host cell surface before entering the cell. The viral Spike protein recognizes and attaches to the Angiotensin-Converting Enzyme 2 (ACE2) receptor found on the surface of type I and II pneumocytes, endothelial cells, and ciliated bronchial epithelial cells. Drugs targeting the interaction between the Spike protein of SARS-CoV-2 and ACE2 may offer protection against the viral infection. A variant called B.1.1.529 BA.1 (also known as the Omicron Variant) was identified in South Africa in November of 2021. This variant has a large number of mutations that allow the virus to spread more easily and quickly than other variants. A sub-lineage of BA.1 with an R346K substitution in the spike protein is classified as B.1.1.529 BA.1.1. The Spike (B.1.1.529 BA.1.1, Omicron Variant R346K) (SARS-CoV-2) Pseudo

Please note this product may be subject to fees, we invite you to contact your local office. The UAS (Upstream Activation Sequence) Luciferase Reporter Lentiviruses are replication incompetent, HIV-based, VSV-G pseudotyped lentiviral particles that are ready to transduce almost all types of mammalian cells, including primary and non-dividing cells. The particles contain a firefly luciferase gene driven by a multimerized GAL4 upstream activation sequence (UAS) located upstream of the minimal TATA promoter and an antibiotic selection gene (puromycin) for the selection of stable clones. After transduction, the UAS-controlled signaling pathway in the target cells can be monitored by measuring the luciferase activity.