Lentivirus

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. 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. As of May 2022, Omicron variants have been divided into seven distinct sub-lineages: BA.1, BA.1.1, BA.2, BA.3, BA.2.12.1, BA.4, and BA.5. The Spike (BA.2.12.1, Omicron Variant) (SARS-CoV-2) Pseudotyped Lentiviruses were produced

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. 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. As of May 2022, Omicron variants have been divided into seven distinct sub-lineages: BA.1, BA.1.1, BA.2, BA.3, BA.2.12.1, BA.4, and BA.5. Among them, BA.4 and BA.5 have identical mutations on their spike protein. The spike prote

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. 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. As of May 2022, Omicron variants have been divided into seven distinct sub-lineages: BA.1, BA.1.1, BA.2, BA.3, BA.2.12.1, BA.4, and BA.5. Among them, BA.4 and BA.5 have identical mutations on their spike protein. The spike prote

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. 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. As of May 2022, Omicron variants have been divided into seven distinct sub-lineages: BA.1, BA.1.1, BA.2, BA.3, BA.2.12.1, BA.4, and BA.5. Among them, BA.4 and BA.5 have identical mutations on their spike protein. The spike prote

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. 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. As of May 2022, Omicron variants have been divided into seven distinct sub-lineages: BA.1, BA.1.1, BA.2, BA.3, BA.2.12.1, BA.4, and BA.5. Among them, BA.4 and BA.5 have identical mutations on their spike protein. The spike prote

Please note this product may be subject to fees, we invite you to contact your local office. CD8 (cluster of differentiation 8) is a cell surface glycoprotein found on most cytotoxic T lymphocytes that functions within the immune system to mediate cell-cell interactions. The functional forms of CD8 consist of either a heterodimer of two isoforms, CD8α and CD8β, or a homodimer of two CD8α molecules. CD8 acts as a coreceptor to facilitate binding between the T-cell Receptor (TCR) and the class I Major Histocompatibility Complex (MHC). Studying CD8 and its importance in isoimmunity can further our understanding of post-transplant recognition. The CD8a/CD8b (CD8α/CD8β) 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 P2A-linked CD8a (NM_001768.6) and CD8b (NM_004931.5) driven by an EF1a promoter and a puromycin selection

Cereblon (CRBN) forms an E3 ubiquitin ligase complex which is responsible for ubiquitinating proteins that regulate various developmental processes. CRBN also binds to Calcium Activated Potassium Channel subunit alpha-1 (KCNMA1) to regulate ion transport. Moreover, mutations in CRBN may play an underlying role in tumor cells acquiring resistance to immunotherapy. The CRBN CRISPR/Cas9 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 CRISPR/Cas9 gene driven by an EF1a promoter, along with 5 sgRNA (single guide RNA) targeting human CRBN. The DNA transduced by this lentivirus integrates randomly into the cellular genome to express both Cas9 and sgRNA. Puromycin selection increases the knockout efficiency by forcing high expression levels of both Cas9 and the sgRNA, and can be used with the integrating lentivirus to quic

Cereblon (CRBN) forms an E3 ubiquitin ligase complex which is responsible for ubiquitinating proteins that regulate various developmental processes. CRBN also binds to Calcium Activated Potassium Channel subunit alpha-1 (KCNMA1) to regulate ion transport. Moreover, mutations in CRBN may play an underlying role in tumor cells acquiring resistance to immunotherapy. The CRBN CRISPR/Cas9 Lentiviruses are replication incompetent, HIV-based VSV-G pseudo-typed lentiviral particles that are ready to transduce into almost all 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 CRBN. The non-integrating lentivirus is made with a mutated integrase, resulting in only transient expression of the Cas9 and sgRNA. Although using the non-integrating lentivirus results in lower knockdown efficiency, the Cas9 is not permanently expressed, which lowers the risk of off-

Beta-2 Microglobulin (B2M) is a required component of Major Histocompatibility Complex (MHC) class 1 molecules, which present peptide fragments from within the cell to cytotoxic T-cells as part of the adaptive immune system. The B2M CRISPR/Cas9 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. The particles contain a CRISPR/Cas9 gene driven by an EF1a promoter, along with 5 sgRNA (single guide RNAs) targeting human B2M driven by a U6 promoter. The integrating lentivirus integrates randomly into the cellular genome to express both Cas9 and the sgRNA. Puromycin selection forces high expression levels of both Cas9 and the sgRNA, and can be used with the integrating lentivirus to quickly and easily achieve high knockdown efficiencies in a cell pool. Efficiencies will depend on the cell type and the gene of interest.