Human Cytomegalovirus miR-US5-2 Downregulation of GAB1 Regulates Cellular Proliferation and UL138 Expression through Modulation of Epidermal Growth Factor Receptor Signaling Pathways
Regulation of the epidermal growth factor (EGF) receptor (EGFR) signaling is essential for the replication of human cytomegalovirus (HCMV) and the latency and reactivation in CD34 + hematopoietic progenitor cells. HCMV microRNAs (miRNAs) provide a means to modulate the signal is activated by EGF through targeting EGFR signaling pathway components.
Here, we show that miR-US5-2 HCMV immediate critical downregulates EGFR GAB1 adapter proteins that mediate sustained activation and signals through phosphatidylinositol 3-kinase (PI3K) and MEK / extracellular signal-regulated kinase (ERK) pathway and cell proliferation in response to EGF. UL138 HCMV expression is regulated by the transcription factor early growth response gene 1 (EGR1) downstream of EGFR-induced MEK / ERK signaling. We show that by targeting GAB1 and smoothes the MEK / ERK signaling, mir-US5-2 indirectly regulating the expression EGR1 and UL138, which implicates critical miRNA regulation latency.IMPORTANCE HCMV Human cytomegalovirus (HCMV) causes significant illness in immunocompromised individuals, including transplant patients.
HCMV establishes latency in the hematopoietic stem cells in the bone marrow. The mechanisms that regulate the latency and reactivation of viral replication is complex and not fully understood. HCMV-encoded miRNAs are small regulatory RNA that reduces expression of the protein. In this study, we found that HCMV miRNA miR-US5-2 targeting the epidermal growth factor receptor (EGFR) protein GAB1 adapter that directly affect downstream cellular signaling pathways activated by EGF.
As a result, mir-US5-2 block EGF-mediated proliferation of human fibroblasts. early growth response gene 1 (EGR1) is a transcription factor activated by EGFR signaling that regulates the expression of HCMV UL138. We show that miR-UL138 US5-2 regulates expression via downregulation GAB1-mediated signaling pathways that lead to the expression of EGR1. These data demonstrate that miR-US5-2, through downregulation of GAB1, can play an important role during the reactivation from latency by reducing the proliferation and expression of UL138.
Human Cytomegalovirus miR-US5-2 Downregulation of GAB1 Regulates Cellular Proliferation and UL138 Expression through Modulation of Epidermal Growth Factor Receptor Signaling Pathways
early diagnosis and successful treatment of cytomegalovirus peritonitis in children with primary nephrotic syndrome: a case series and review of the literature
Cytomegalovirus (CMV) is a major pathogen in immunocompromised population and CMV infections in immunocompromised patients cause of morbidity and mortality are quite large. Common clinical manifestations of CMV infection is pneumonia, hepatitis, colitis and so on, while CMV without intestinal perforation peritonitis rarely occurs. Reviewing the literature, CMV peritonitis in patients with nephrotic syndrome (NS) has not been reported. Only four cases of peritonitis CMV without bowel perforation reported in adults with other illnesses.
Two cases were diagnosed by reverse-transcription polymerase chain reaction (RT-PCR) of ascites while two other cases with histopathological examination of peritoneal tissue. We report four cases of primary nephrotic syndrome complicated with CMV peritonitis. Four cases were all diagnosed by RT-PCR from ascites (659-455000 copies / mL).
Description: The NFAT Reporter - Jurkat Cell Line contains a firefly luciferase gene under the control of the_x000D_NFAT response element stably integrated into Jurkat cells. This cell line has been validated for_x000D_response to thapsigargin, ionomycin, and phorbol 12-myristate 13-acetate (PMA). It is useful as_x000D_a control cell line for other NFAT reporter cell lines expressing various immune checkpoint_x000D_receptors.
Description: The GAL4 Reporter (Luc) - HEK293 Cell Line contains a firefly luciferase gene under the control of a multimerized GAL4 upstream activation sequence (UAS) stably integrated into HEK293 cells. The cell line does not contain any exogenous activators of the GAL4 reporter and can be used alongside BPS Cat. #60655 as a control.
Human GFAP Differentiation Reporter (pGreenZeo, Virus) Puro
Description: The STAT5 Reporter (Luc)-Ba/F3 cell line is designed for monitoring STAT5 signal transduction pathways. It contains a firefly luciferase gene driven by the STAT5 response element located upstream of the minimal TATA promoter. After activation by cytokines or growth factors, endogenous STAT5 binds to the DNA response elements, inducing transcription of the luciferase reporter gene.
Description: The Interferon Regulatory Factor (IRF) reporter (Luc)-THP-1 cell line is designed to study the activation and signaling of Cytosolic DNA Sensors (CDS) in human monocytic cell line THP-1. It contains a firefly luciferase gene driven by multimerized ISRE (Interferon Stimulated Response Element) located upstream of the minimal TATA promoter. _x000D_The cGAS-STING pathway acts to detect cytosolic DNA and induce an immune response. Briefly, upon binding DNA, the protein cGAS (cyclic GMP-AMP Synthase) triggers reaction of GTP and ATP to form cGAMP. cGAMP binds to STING (Stimulator of Interferon Genes) which triggers phosphorylation of IRF3 via TBK1. IRF3 can then bind to interferon-stimulated responsive elements (ISRE) in the nucleus and leads to IFN-α/β production. The IRF reporter (Luc)-THP-1 cell line is highly responsive to STING and CDS ligands.
Description: NF-B luciferase reporter construct is stably integrated into the genome of HCT-116 cells. The firefly luciferase gene is controlled by 4 copies of NF-κB response element located upstream of the TATA promoter. Following activation by stimulants, endogenous NF-κB transcription factors bind to the DNA response elements to induce transcription of the luciferase gene._x000D_The NF-κB-luciferase/HCT-116 cell line is suitable for monitoring the activity of NF-κB signaling in response to stimulants such as the cytokines TNF and IL-1β, pathogen-associated molecular pattern (PAMP) (i.e. flagellin) or endogenous damage-associated molecular pattern (DAMP) molecules (i.e. NOD1 ligand) (see application references). It is also suitable for establishing cell-based screens for inhibitors that target specific NF-κB stimulating molecules. This cell line can be further modified to allow investigation of downstream NF-κB activities as a result of targeted genetic mutation(s).
Description: The NF-κB reporter (Luc) HEK293 cell line is designed to monitor nuclear factor Kappa B (NF-κB) activity. It contains a firefly luciferase gene driven by four copies of the NF-κB response element located upstream of the minimal TATA promoter. After activation by pro-inflammatory cytokines or agonists of lymphokine receptors, endogenous NF-κB transcription factors bind to the DNA response elements, inducing transcription of the luciferase reporter gene. The cell line has been functionally validated in response to human TNF-α, IL-1β, and IL-17.
Description: The NF-κB reporter (Luc)-Raw 264.7 cell line is designed for monitoring nuclear factor Kappa B (NF-κB) signal transduction pathways. It contains a firefly luciferase gene driven by four copies of the NF-κB response element located upstream of the minimal TATA promoter. After activation by pro-inflammatory cytokines or stimulants of lymphokine receptors, endogenous NF-κB transcription factors bind to the DNA response elements, inducing transcription of the luciferase reporter gene.
Description: The NF-κB reporter (Luc)-THP-1 cell line is designed for monitoring nuclear factor Kappa B (NF-κB) signal transduction pathways. It contains a firefly luciferase gene driven by four copies of the NF-κB response element located upstream of the minimal TATA promoter. After activation by pro-inflammatory cytokines or stimulants of lymphokine receptors, endogenous NF-κB transcription factors bind to the DNA response elements, inducing transcription of the luciferase reporter gene.
Description: PAI-1 Reporter (Luc)-Mv1 Lu cell line is designed for monitoring transforming growth factor β (TGF-β)-induced plasminogen activator inhibitor-1 (PAI-1) expression. Transforming growth factor-β (TGF-β) is a potent regulator of cellular differentiation, proliferation, migration, and protein expression._x000D__x000D_PAI-1 Reporter (Luc) -Mv1 Lu cell line contains a firefly luciferase gene under the control of PAI-1 responsive elements stably integrated into Mv1 Lu (NBL-7) cells, showing TGF-β pathway response. This cell line is validated for the TGF-β response to the induction of PAI-1 gene expression through luciferase activity. _x000D_
Description: The NF-κB reporter (Luc)-NIH/3T3 cell line is designed for monitoring nuclear factor Kappa B (NF-κB) signal transduction pathways. It contains a firefly luciferase gene driven by four copies of the NF-κB response element located upstream of the minimal TATA promoter. After activation by pro-inflammatory cytokines or stimulants of lymphokine receptors, endogenous NF-κB transcription factors bind to the DNA response elements, inducing transcription of the luciferase reporter gene.
Description: An NF-κB luciferase reporter construct is stably integrated into the genome of CHO-K1 cells. The firefly luciferase gene is controlled by the NF-κB response element located upstream of the TATA promoter. Following activation by stimulants, endogenous NF-κB transcription factors bind to the DNA response elements to induce transcription of the luciferase gene._x000D_The NF-κB-luciferase / CHO-K1 cell line is suitable for monitoring the activity of NF-κB transcription factor through luminescence readout.). This cell line responds to human cytokine IL-1β, responds moderately to human TNF, and does not respond to human IFN-λ (2 µg/ml). Reducing the amount of serum during incubation period may increase the sensitivity to cytokines. Since CHO-K1 cells do not express endogenous human proteins, this cell line provides an excellent platform to enable exogenous expression of a protein of interest to study its downstream effect on NF-κB signaling.
Description: The bald lentiviral pseudovirion was produced without envelope glycoproteins such as VSV-G or SARS-CoV-2 spike. It contains a firefly luciferase and eGFP cassette (Luc-P2A-eGFP) as the reporters, driven by a CMV promoter. The bald lentiviral pseudovirion can serve as a negative control when studying virus entry initiated by specific interactions between virus particles and receptors._x000D_
STAT3 Reporter (Luc) - HEK293 Cell line (Puromycin)
Description: The STAT3 Reporter (Luc)-HEK293 cell line is designed for monitoring STAT3 signal transduction pathway. It contains a firefly luciferase gene driven by STAT3 response elements located upstream of the minimal TATA promoter. After activation by cytokines and growth factors, endogenous STAT3 binds to the DNA response elements, inducing transcription of the luciferase reporter gene.
Description: The STAT5 Reporter (Luc)-U937 cell line is designed for monitoring STAT5 signal transduction pathway in the U937 cell line. It contains a firefly luciferase gene driven by the STAT5 response element located upstream of the minimal TATA promoter. After activation by GM-CSF, endogenous STAT5 binds to the DNA response elements, inducing transcription of the luciferase reporter gene.
Description: NF-κB luciferase reporter construct is stably integrated into the genome of A549 cells. The firefly luciferase gene is controlled by 4 copies of NF-κB response element located upstream of the TATA promoter. Following activation by stimulants, endogenous NF-κB transcription factors bind to the DNA response elements to induce transcription of the luciferase gene.
Description: Human Foxp3 luciferase reporter construct is stably integrated into the genome of Jurkat T- cells. The firefly luciferase gene is controlled by a human Foxp3 promoter and an enhancer-like conserved noncoding sequence upstream of the Foxp3 promoter.
Description: A polyclonal antibody against AASDHPPT. Recognizes AASDHPPT from Human, Mouse, Rat. This antibody is Unconjugated. Tested in the following application: ELISA, WB;WB:1:500-1:3000
Description: A polyclonal antibody against AASDHPPT. Recognizes AASDHPPT from Human, Mouse, Rat. This antibody is Unconjugated. Tested in the following application: ELISA, WB;WB:1:500-1:3000
Description: A polyclonal antibody against AASDHPPT. Recognizes AASDHPPT from Human. This antibody is Unconjugated. Tested in the following application: ELISA, WB, IHC; Recommended dilution: WB:1:200-1:1000, IHC:1:20-1:200
Description: A polyclonal antibody against AASDHPPT. Recognizes AASDHPPT from Human, Mouse, Rat. This antibody is Unconjugated. Tested in the following application: ELISA, WB, IHC;ELISA:1:2000-1:5000, WB:1:500-1:2000, IHC:1:50-1:200
Description: A polyclonal antibody against AASDHPPT. Recognizes AASDHPPT from Human, Mouse, Rat. This antibody is Unconjugated. Tested in the following application: ELISA, WB, IHC;ELISA:1:2000-1:5000, WB:1:500-1:2000, IHC:1:50-1:200
Description: A polyclonal antibody against AASDHPPT. Recognizes AASDHPPT from Human, Mouse, Rat. This antibody is Unconjugated. Tested in the following application: WB, IHC, ELISA;WB:1/500-1/2000.IHC:1/100-1/300.ELISA:1/40000
Human Alpha-Actin 2, ACTA2 Differentiation Reporter (pGreenZeo, virus)
Description: The Spike (B.1.429 Variant) (SARS-CoV-2) Pseudotyped Lentiviruses were produced with SARS-CoV-2 B.1.429 Variant Spike (Genbank Accession #QHD43416.1 with B.1.429 variant mutations; see below for details) as the envelope glycoproteins instead of the commonly used VSV-G. These pseudovirions contain the firefly luciferase gene driven by a CMV promoter, therefore, the spike-mediated cell entry can be measured via luciferase activity. The Spike (B.1.429 Variant) (SARS-CoV-2) pseudotyped lentivirus can be used to measure the activity of neutralizing antibody against SARS-CoV-2 B.1.429 variant in a Biosafety Level 2 facility.Spike Mutations in B.1.429 Variant: S13I W152C L452R D614G
Description: The Spike (B.1.429 Variant) (SARS-CoV-2) Pseudotyped Lentiviruses were produced with SARS-CoV-2 B.1.429 Variant Spike (Genbank Accession #QHD43416.1 with B.1.429 variant mutations; see below for details) as the envelope glycoproteins instead of the commonly used VSV-G. These pseudovirions contain the firefly luciferase gene driven by a CMV promoter, therefore, the spike-mediated cell entry can be measured via luciferase activity. The Spike (B.1.429 Variant) (SARS-CoV-2) pseudotyped lentivirus can be used to measure the activity of neutralizing antibody against SARS-CoV-2 B.1.429 variant in a Biosafety Level 2 facility.Spike Mutations in B.1.429 Variant: S13I W152C L452R D614G
Description: 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.1.617 (Kappa, Delta lineage) was identified in India in the spring of 2021. This variant has a number of mutations that allow the virus to spread more easily and quickly than other variants. The Spike (B.1.617 Variant) (SARS-CoV-2) Pseudotyped Lentivirus were produced with SARS-CoV-2 B.1.617 Variant Spike (Genbank Accession #QHD43416.1 with B.1.617 mutations; see below for details) as the envelope glycoproteins instead of the commonly used VSV-G. These pseudovirions contain the firefly luciferase gene driven by a CMV promoter, therefore, the spike-mediated cell entry can be measured via luciferase activity. The Spike (B.1.617 Variant) (SARS-CoV-2) pseudotyped lentivirus can be used to measure the activity of neutralizing antibody against SARS-CoV-2 B.1.617 variant in a Biosafety Level 2 facility.
Description: 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.1.617 (Kappa, Delta lineage) was identified in India in the spring of 2021. This variant has a number of mutations that allow the virus to spread more easily and quickly than other variants. The Spike (B.1.617 Variant) (SARS-CoV-2) Pseudotyped Lentivirus were produced with SARS-CoV-2 B.1.617 Variant Spike (Genbank Accession #QHD43416.1 with B.1.617 mutations; see below for details) as the envelope glycoproteins instead of the commonly used VSV-G. These pseudovirions contain the firefly luciferase gene driven by a CMV promoter, therefore, the spike-mediated cell entry can be measured via luciferase activity. The Spike (B.1.617 Variant) (SARS-CoV-2) pseudotyped lentivirus can be used to measure the activity of neutralizing antibody against SARS-CoV-2 B.1.617 variant in a Biosafety Level 2 facility.
Description: 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.1.617.1 (also known as the Kappa Variant) was identified in India in the spring of 2021. This variant has a number of mutations that allow the virus to spread more easily and quickly than other variants. The Spike (B.1.617.1 Variant) (SARS-CoV-2) Pseudotyped Lentivirus were produced with SARS-CoV-2 B.1.617.1 Variant Spike (Genbank Accession #QHD43416.1 with B.1.617.1 mutations; see below for details) as the envelope glycoproteins instead of the commonly used VSV-G. These pseudovirions contain the firefly luciferase gene driven by a CMV promoter, therefore, the spike-mediated cell entry can be measured via luciferase activity. The Spike (B.1.617.1 Variant) (SARS-CoV-2) pseudotyped lentivirus can be used to measure the activity of neutralizing antibody against SARS-CoV-2 B.1.617.1 variant in a Biosafety Level 2 facility. Spike Mutations in B.1.617.1 Variant:G142DE154KL452RE484QD614GP681RQ1071H
Description: 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.1.617.1 (also known as the Kappa Variant) was identified in India in the spring of 2021. This variant has a number of mutations that allow the virus to spread more easily and quickly than other variants. The Spike (B.1.617.1 Variant) (SARS-CoV-2) Pseudotyped Lentivirus were produced with SARS-CoV-2 B.1.617.1 Variant Spike (Genbank Accession #QHD43416.1 with B.1.617.1 mutations; see below for details) as the envelope glycoproteins instead of the commonly used VSV-G. These pseudovirions contain the firefly luciferase gene driven by a CMV promoter, therefore, the spike-mediated cell entry can be measured via luciferase activity. The Spike (B.1.617.1 Variant) (SARS-CoV-2) pseudotyped lentivirus can be used to measure the activity of neutralizing antibody against SARS-CoV-2 B.1.617.1 variant in a Biosafety Level 2 facility. Spike Mutations in B.1.617.1 Variant:G142DE154KL452RE484QD614GP681RQ1071H
Description: 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.1.618 was identified in India in the spring of 2021. This variant has a number of mutations that allow the virus to spread more easily and quickly than other variants. The Spike (B.1.618 Variant) (SARS-CoV-2) Pseudotyped Lentivirus were produced with SARS-CoV-2 B.1.618 Variant Spike (Genbank Accession #QHD43416.1 with B.1.618 mutations; see below for details) as the envelope glycoproteins instead of the commonly used VSV-G. These pseudovirions contain the firefly luciferase gene driven by a CMV promoter, therefore, the spike-mediated cell entry can be measured via luciferase activity. The Spike (B.1.618 Variant) (SARS-CoV-2) pseudotyped lentivirus can be used to measure the activity of neutralizing antibody against SARS-CoV-2 B.1.618 variant in a Biosafety Level 2 facility. Spike Mutations in B.1.618 Variant:Y145delH146delE484KD614G
Description: 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.1.618 was identified in India in the spring of 2021. This variant has a number of mutations that allow the virus to spread more easily and quickly than other variants. The Spike (B.1.618 Variant) (SARS-CoV-2) Pseudotyped Lentivirus were produced with SARS-CoV-2 B.1.618 Variant Spike (Genbank Accession #QHD43416.1 with B.1.618 mutations; see below for details) as the envelope glycoproteins instead of the commonly used VSV-G. These pseudovirions contain the firefly luciferase gene driven by a CMV promoter, therefore, the spike-mediated cell entry can be measured via luciferase activity. The Spike (B.1.618 Variant) (SARS-CoV-2) pseudotyped lentivirus can be used to measure the activity of neutralizing antibody against SARS-CoV-2 B.1.618 variant in a Biosafety Level 2 facility. Spike Mutations in B.1.618 Variant:Y145delH146delE484KD614G
Description: 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.1.617.2 (also known as the Delta Variant) was identified in India in the spring of 2021. This variant has a number of mutations that increase morbidity and mortality and allow the virus to spread more easily and quickly than other variants.The Spike (B.1.617.2 Variant) (SARS-CoV-2) Pseudotyped Lentiviruses were produced with SARS-CoV-2 B.1.617.2 Variant Spike (Genbank Accession #QHD43416.1 with B.1.617.2 mutations; see below for details) as the envelope glycoproteins instead of the commonly used VSV-G. These pseudovirions contain the firefly luciferase gene driven by a CMV promoter, therefore, the spike-mediated cell entry can be measured via luciferase activity. The Spike (B.1.617.2 Variant) (SARS-CoV-2) pseudotyped lentivirus can be used to measure the activity of neutralizing antibody against SARS-CoV-2 B.1.617.2 variant in a Biosafety Level 2 facility.
Description: 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.1.617.2 (also known as the Delta Variant) was identified in India in the spring of 2021. This variant has a number of mutations that increase morbidity and mortality and allow the virus to spread more easily and quickly than other variants.The Spike (B.1.617.2 Variant) (SARS-CoV-2) Pseudotyped Lentiviruses were produced with SARS-CoV-2 B.1.617.2 Variant Spike (Genbank Accession #QHD43416.1 with B.1.617.2 mutations; see below for details) as the envelope glycoproteins instead of the commonly used VSV-G. These pseudovirions contain the firefly luciferase gene driven by a CMV promoter, therefore, the spike-mediated cell entry can be measured via luciferase activity. The Spike (B.1.617.2 Variant) (SARS-CoV-2) pseudotyped lentivirus can be used to measure the activity of neutralizing antibody against SARS-CoV-2 B.1.617.2 variant in a Biosafety Level 2 facility.
Description: Severe acute respiratory syndrome (SARS) was the first new infectious disease identified in the twenty-first century. It is a viral respiratory disease caused by severe acute respiratory syndrome coronavirus (SARS-CoV-1). The first known cases occurred in November 2002, and the syndrome caused the 2002-2004 SARS outbreak. Since 2004, no cases of SARS-CoV-1 have been reported worldwide. A virus very similar to SARS-CoV-1 was discovered in late 2019. This virus, named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is the causative pathogen of COVID-19, the spread of which started the COVID-19 pandemic.SARS-CoV-1 attaches to the host cell surface before entering the cell. The Spike protein on the virus recognizes and binds to the Angiotensin-Converting Enzyme 2 (ACE2) receptor found on the surface of human airway epithelia as well as lung parenchyma. Drugs targeting the interaction between the Spike protein of SARS-CoV-1 and ACE2 may offer protection against the viral infection.The Spike (SARS-CoV-1) Pseudotyped Lentiviruses were produced with SARS-CoV-1 Spike (Genbank Accession #YP_009825051.1) as the envelope glycoprotein instead of the commonly used VSV-G. These pseudovirions contain the firefly luciferase gene driven by a CMV promoter, therefore, the spike-mediated cell entry can be measured via luciferase activity. The Spike (SARS-CoV-1) pseudovirus can be used to measure the activity of a neutralizing antibody against SARS-CoV-1 in a cellular context, using a Biosafety Level 2 facility.The Spike (SARS-CoV-1) Pseudotyped Lentiviruses has been validated for use with target cells ACE2-HEK293 (which overexpress ACE2; BPS Bioscience #79951).
Description: Severe acute respiratory syndrome (SARS) was the first new infectious disease identified in the twenty-first century. It is a viral respiratory disease caused by severe acute respiratory syndrome coronavirus (SARS-CoV-1). The first known cases occurred in November 2002, and the syndrome caused the 2002-2004 SARS outbreak. Since 2004, no cases of SARS-CoV-1 have been reported worldwide. A virus very similar to SARS-CoV-1 was discovered in late 2019. This virus, named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is the causative pathogen of COVID-19, the spread of which started the COVID-19 pandemic.SARS-CoV-1 attaches to the host cell surface before entering the cell. The Spike protein on the virus recognizes and binds to the Angiotensin-Converting Enzyme 2 (ACE2) receptor found on the surface of human airway epithelia as well as lung parenchyma. Drugs targeting the interaction between the Spike protein of SARS-CoV-1 and ACE2 may offer protection against the viral infection.The Spike (SARS-CoV-1) Pseudotyped Lentiviruses were produced with SARS-CoV-1 Spike (Genbank Accession #YP_009825051.1) as the envelope glycoprotein instead of the commonly used VSV-G. These pseudovirions contain the firefly luciferase gene driven by a CMV promoter, therefore, the spike-mediated cell entry can be measured via luciferase activity. The Spike (SARS-CoV-1) pseudovirus can be used to measure the activity of a neutralizing antibody against SARS-CoV-1 in a cellular context, using a Biosafety Level 2 facility.The Spike (SARS-CoV-1) Pseudotyped Lentiviruses has been validated for use with target cells ACE2-HEK293 (which overexpress ACE2; BPS Bioscience #79951).
Human MLC-2v Differentiation Reporter (pGreenZeo, Virus), EF1-Neo Marker
Description: NF-κB luciferase reporter construct is stably integrated into the genome of Jurkat T- cells. The firefly luciferase gene is controlled by 4 copies of NF-kB response element located upstream of the TATA promoter. Following activation by stimulants, endogenous NF-κB transcription factors bind to the DNA response elements to induce transcription of the luciferase gene.
Description: Recombinant HEK293 cell line expressing full length human CD40 (Tumor necrosis factor receptor superfamily member 5; TNFRSF5). Expression is confirmed by real-time qPCR and Western Blot. This NF-κB luciferase reporter construct is stably integrated into the genome. The firefly luciferase gene is controlled by 4 copies of NF-κB response element located upstream of the TATA promoter. Following activation by human CD40 ligand, NF-κB transcription factor binds to the DNA response elements to induce transcription of the luciferase gene. _x000D_
Description: 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 and ACE2 may offer protection against the viral infection. A SARS-CoV-2 variant carrying the spike protein amino acid change D614G has become the most prevalent form in the global pandemic. The SARS-CoV-2 Spike D614G Pseudotyped Lentivirus were produced with SARS-CoV-2 Spike (Genbank Accession #QHD43416.1; with D614G mutation) as the envelope glycoproteins instead of the commonly used VSV-G. These pseudovirions contain the firefly luciferase gene driven by a CMV promoter, therefore, the spike-mediated cell entry can be measured via luciferase activity. The SARS-CoV-2 Spike D614G pseudotyped lentivirus can be used to measure the activity of neutralizing antibody against SARS-CoV-2 in a Biosafety Level 2 facility._x000D_
Description: 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 and ACE2 may offer protection against the viral infection. A SARS-CoV-2 variant carrying the spike protein amino acid change D614G has become the most prevalent form in the global pandemic. The SARS-CoV-2 Spike D614G Pseudotyped Lentivirus were produced with SARS-CoV-2 Spike (Genbank Accession #QHD43416.1; with D614G mutation) as the envelope glycoproteins instead of the commonly used VSV-G. These pseudovirions contain the firefly luciferase gene driven by a CMV promoter, therefore, the spike-mediated cell entry can be measured via luciferase activity. The SARS-CoV-2 Spike D614G pseudotyped lentivirus can be used to measure the activity of neutralizing antibody against SARS-CoV-2 in a Biosafety Level 2 facility._x000D_
Description: The Myc Reporter - HCT116 cell line contains the firefly luciferase gene under the control of Myc responsive elements stably integrated into HCT116 cells, a human colon cancer cell line. HCT116 contains a mutated beta-catenin which leads to the accumulation of β-catenin and constitutive activation of downstream Myc that induces the expression of Myc luciferase reporter. The cell line is validated for the inhibition of the expression of Myc luciferase reporter.
GITR / NF-κB-Luciferase Reporter (Luc) - Jurkat Cell Line
Description: This cell line expresses a surface human GITR (glucocorticoid-induced TNFR family related gene; TNFRSF18; CD357) and an NF-κB luciferase reporter construct that are stably integrated into the genome of Jurkat T-cells. The firefly luciferase gene is controlled by 4 copies of NF-κB response element located upstream of the TATA promoter. Following activation by stimulants, endogenous NF-κB transcription factors bind to the DNA response elements to induce transcription of the luciferase gene. The cells have been validated using purified human GITRL and anti-GITR neutralizing antibody.
Description: 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 (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.The Spike (B.1.1.529 Variant) (SARS-CoV-2) Pseudotyped Lentivirus were produced with SARS-CoV-2 B.1.1.529 Variant Spike (Genbank Accession #QHD43416.1 with B.1.1.529 mutations; see below for details) as the envelope glycoproteins instead of the commonly used VSV-G. These pseudovirions contain the firefly luciferase gene driven by a CMV promoter, therefore, the spike-mediated cell entry can be measured via luciferase activity. The Spike (B.1.1.529 Variant) (SARS-CoV-2) pseudotyped lentivirus can be used to measure the activity of neutralizing antibody against SARS-CoV-2 B.1.1.529 variant in a Biosafety Level 2 facility.The Spike Omicron pseudovirus has been validated for use with target cells ACE2-HEK293 (which overexpress ACE2; BPS Bioscience, #79951).
Description: 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 (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.The Spike (B.1.1.529 Variant) (SARS-CoV-2) Pseudotyped Lentivirus were produced with SARS-CoV-2 B.1.1.529 Variant Spike (Genbank Accession #QHD43416.1 with B.1.1.529 mutations; see below for details) as the envelope glycoproteins instead of the commonly used VSV-G. These pseudovirions contain the firefly luciferase gene driven by a CMV promoter, therefore, the spike-mediated cell entry can be measured via luciferase activity. The Spike (B.1.1.529 Variant) (SARS-CoV-2) pseudotyped lentivirus can be used to measure the activity of neutralizing antibody against SARS-CoV-2 B.1.1.529 variant in a Biosafety Level 2 facility.The Spike Omicron pseudovirus has been validated for use with target cells ACE2-HEK293 (which overexpress ACE2; BPS Bioscience, #79951).
Description: The GAS reporter (Luc)-HeLa cell line is designed to monitor the activity of interferon gamma-induced signal transduction pathways in cultured cells by measuring activated STAT1 homodimers. It contains a firefly luciferase gene driven by three copies of the interferon gamma-activated sites (GAS) located upstream of the minimal TATA promoter. IFNγ first binds to a heterodimeric receptor consisting of two chains, IFNGR1 and IFNGR2, causing its dimerization and the activation of specific Janus family kinases (JAK1 and JAK2). Two STAT1 molecules associate with this ligand-activated receptor complex and are activated by phosphorylation to form active homodimer. The active STAT1 homodimers translocate to the nucleus where they bind interferon gamma-activated sites (GAS) in the promoter of IFNγ inducible genes, including luciferase reporter gene.
Description: 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.1.617.2.1 (also known as the Delta Plus Variant) was identified in India in the spring of 2021. This variant has a number of mutations that increase morbidity and mortality and allow the virus to spread more easily and quickly than other variants.The Spike (B.1.617.2.1 Variant) (SARS-CoV-2) Pseudotyped Lentiviruses were produced with SARS-CoV-2 B.1.617.2.1 Variant Spike (Genbank Accession #QHD43416.1 with B.1.617.2.1 mutations; see below for details) as the envelope glycoproteins instead of the commonly used VSV-G. Compared to the Delta variant (B.1.617.2), variant Delta Plus has an additional mutation, K417N. These pseudovirions contain the firefly luciferase gene driven by a CMV promoter, therefore, the spike-mediated cell entry can be measured via luciferase activity. The Spike (B.1.617.2.1 Variant) (SARS-CoV-2) pseudotyped lentivirus can be used to measure the activity of neutralizing antibody against SARS-CoV-2 B.1.617.2.1 variant in a Biosafety Level 2 facility.
Spike (B.1.617.2.1; Delta Plus Variant) Pseudotyped Lentivirus (Luc Reporter)
Description: 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.1.617.2.1 (also known as the Delta Plus Variant) was identified in India in the spring of 2021. This variant has a number of mutations that increase morbidity and mortality and allow the virus to spread more easily and quickly than other variants.The Spike (B.1.617.2.1 Variant) (SARS-CoV-2) Pseudotyped Lentiviruses were produced with SARS-CoV-2 B.1.617.2.1 Variant Spike (Genbank Accession #QHD43416.1 with B.1.617.2.1 mutations; see below for details) as the envelope glycoproteins instead of the commonly used VSV-G. Compared to the Delta variant (B.1.617.2), variant Delta Plus has an additional mutation, K417N. These pseudovirions contain the firefly luciferase gene driven by a CMV promoter, therefore, the spike-mediated cell entry can be measured via luciferase activity. The Spike (B.1.617.2.1 Variant) (SARS-CoV-2) pseudotyped lentivirus can be used to measure the activity of neutralizing antibody against SARS-CoV-2 B.1.617.2.1 variant in a Biosafety Level 2 facility.
Description: The Spike (SARS-CoV-2, UK variant) Pseudotyped Lentivirus were produced with SARS-CoV-2 UK Variant Spike (Genbank Accession #QHD43416.1 with UK variant mutations; see below for details) as the envelope glycoproteins instead of the commonly used VSV-G. These pseudovirions contain the firefly luciferase gene driven by a CMV promoter, therefore, the spike-mediated cell entry can be measured via luciferase activity. The Spike (SARS-CoV-2, UK variant) pseudotyped lentivirus can be used to measure the activity of neutralizing antibody against SARS-CoV-2 UK variant in a Biosafety Level 2 facility._x000D_
Spike (SARS-CoV-2, UK Variant) Pseudotyped Lentivirus (Luc Reporter)
Description: The Spike (SARS-CoV-2, UK variant) Pseudotyped Lentivirus were produced with SARS-CoV-2 UK Variant Spike (Genbank Accession #QHD43416.1 with UK variant mutations; see below for details) as the envelope glycoproteins instead of the commonly used VSV-G. These pseudovirions contain the firefly luciferase gene driven by a CMV promoter, therefore, the spike-mediated cell entry can be measured via luciferase activity. The Spike (SARS-CoV-2, UK variant) pseudotyped lentivirus can be used to measure the activity of neutralizing antibody against SARS-CoV-2 UK variant in a Biosafety Level 2 facility._x000D_
Description: The pandemic coronavirus disease 2019 (COVID-19) is caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). As the first step of 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._x000D_ The SARS-CoV-2 Spike Pseudotyped Lentivirus (Luc-eGFP dual reporter) were produced by replacing the VSV-G fusion glycoprotein with SARS-CoV-2 Spike protein (Genbank Accession #QHD43416.1) as a surrogate viral envelope protein. These pseudovirions also contain a firefly luciferase and eGFP cassette (Luc-P2A-eGFP) driven by a CMV promoter. The luciferase and eGFP are coexpressed under the CMV promoter in the transduced cells. Therefore, the Spike-mediated entry into the target cell can be conveniently measured via luciferase reporter activity or eGFP expression. The SARS-CoV-2 Spike pseudotyped lentivirus can be used in a cellular assay to measure the activity of neutralizing antibody against SARS-CoV-2._x000D_
Description: The pandemic coronavirus disease 2019 (COVID-19) is caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). As the first step of 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._x000D_ The SARS-CoV-2 Spike Pseudotyped Lentivirus (Luc-eGFP dual reporter) were produced by replacing the VSV-G fusion glycoprotein with SARS-CoV-2 Spike protein (Genbank Accession #QHD43416.1) as a surrogate viral envelope protein. These pseudovirions also contain a firefly luciferase and eGFP cassette (Luc-P2A-eGFP) driven by a CMV promoter. The luciferase and eGFP are coexpressed under the CMV promoter in the transduced cells. Therefore, the Spike-mediated entry into the target cell can be conveniently measured via luciferase reporter activity or eGFP expression. The SARS-CoV-2 Spike pseudotyped lentivirus can be used in a cellular assay to measure the activity of neutralizing antibody against SARS-CoV-2._x000D_
We mainly discuss the diagnosis and treatment of CMV without intestinal perforation peritonitis.Human cytomegalovirus (HCMV) is a double-stranded DNA virus widely infected humans. Circular RNAs (circRNAs) is a non-coding RNA with most functions remain unknown, and the effects of HCMV infection in the host circRNA productive transcription remains unclear. In this study, we profiled 283 hosts a significant circRNAs amended by the productive infection of HCMV in human embryonic lung fibroblast (helf) by RNA deep sequencing and bioinformatics analysis. Among other things, circSP100, circMAP3K1, circPLEKHM1, and circTRIO validated for transcription and their sequence.
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