human igg fc capture biosensor Search Results


hcmv igg/igm kit antibody  (Dia Pro Diagnostic Bioprobes Srl)
90
Dia Pro Diagnostic Bioprobes Srl hcmv igg/igm kit antibody
(A) Kasumi-3 and CD34 + HPCs were efficiently infected with the NR-1 strain of <t>HCMV.</t> Kasumi-3 and HPCs were either mock-infected or infected with a GFP-expressing NR-1 strain at the indicated multiplicities of infection (MOIs). Two days later, the cells were analyzed for GFP expression by flow cytometry. An MOI of 5 was used for the following experiment. (B) The maintenance of the NR-1 genome, the suppression of viral IE1 and the presence of latency-associated UL138 over a 10-day time course. DNA and total RNA were isolated from Kasumi-3 cells and HPCs at various time points after infection. Viral genomic DNA was assayed by PCR, and RNA molecules encoding IE1 and UL138 were assayed by RT-PCR. In both cases, gel electrophoresis was used to detect the products of the reactions. (C) Reactivation of NR-1 virus in infected Kasumi-3 cells and HPCs. Kasumi-3 cells and HPCs were latently infected along a 10-day time course. Then, a subset of each cell population was cultured for an additional 2 days under conditions favoring lytic reactivation: Kasumi-3 cells were exposed to TPA, while HPCs were grown in reactivation medium. Following this, total RNA was extracted from the cells, and the ratio of IE1 to UL138 cDNA expression was assessed by qRT-PCR in triplicate. (D) Release of infectious progeny virions in latently infected Kasumi-3 cells and HPCs following reactivation treatment. Latently infected or mock-infected Kasumi-3 cells and HPCs were cultured under conditions favoring lytic reactivation (described above) or control conditions for 6 days, after which the cells were washed with PBS and co-cultured with HFFs for 2 days. Then, the Kasumi-3 cells were removed from the co-cultures, and the HFFs were washed with PBS and cultured for an additional 5 days for fluorescence microscopy analysis of GFP-positive plaques. (E) miR-UL148D showed robust accumulation during the establishment of experimental HCMV latency in Kasumi-3 cells. In total, 20,000 infected cells were harvested for the isolation of total RNA and DNA at each indicted time point along the 10-day time course. Viral DNA was first quantified by qPCR, and then absolute viral genomes copies were calculated by generating a standard curve. HCMV miRNAs were then assayed with a HCMV miRNA probe kit, and their levels were calculated using a standard curve. The HCMV miRNA level per virus was calculated by dividing the amount of each HCMV miRNA by the virus copy number. (F) miR-UL148D accumulated in HPCs latently infected with NR-1. HCMV miRNA levels in NR-1-infected HPCs were determined as described above. Values are shown as the mean ± SEM (n = 3). **, P<0.01.
Hcmv Igg/Igm Kit Antibody, supplied by Dia Pro Diagnostic Bioprobes Srl, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+igg+fc+capture+biosensor/cmv+igm+capture+immunoassay/pmc05100954-321-13-16
Average 90 stars, based on 1 article reviews
hcmv igg/igm kit antibody - by Bioz Stars, 2026-10
90/100 stars
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control fc protein  (Jackson Immuno)
93
Jackson Immuno control fc protein
(A) Kasumi-3 and CD34 + HPCs were efficiently infected with the NR-1 strain of <t>HCMV.</t> Kasumi-3 and HPCs were either mock-infected or infected with a GFP-expressing NR-1 strain at the indicated multiplicities of infection (MOIs). Two days later, the cells were analyzed for GFP expression by flow cytometry. An MOI of 5 was used for the following experiment. (B) The maintenance of the NR-1 genome, the suppression of viral IE1 and the presence of latency-associated UL138 over a 10-day time course. DNA and total RNA were isolated from Kasumi-3 cells and HPCs at various time points after infection. Viral genomic DNA was assayed by PCR, and RNA molecules encoding IE1 and UL138 were assayed by RT-PCR. In both cases, gel electrophoresis was used to detect the products of the reactions. (C) Reactivation of NR-1 virus in infected Kasumi-3 cells and HPCs. Kasumi-3 cells and HPCs were latently infected along a 10-day time course. Then, a subset of each cell population was cultured for an additional 2 days under conditions favoring lytic reactivation: Kasumi-3 cells were exposed to TPA, while HPCs were grown in reactivation medium. Following this, total RNA was extracted from the cells, and the ratio of IE1 to UL138 cDNA expression was assessed by qRT-PCR in triplicate. (D) Release of infectious progeny virions in latently infected Kasumi-3 cells and HPCs following reactivation treatment. Latently infected or mock-infected Kasumi-3 cells and HPCs were cultured under conditions favoring lytic reactivation (described above) or control conditions for 6 days, after which the cells were washed with PBS and co-cultured with HFFs for 2 days. Then, the Kasumi-3 cells were removed from the co-cultures, and the HFFs were washed with PBS and cultured for an additional 5 days for fluorescence microscopy analysis of GFP-positive plaques. (E) miR-UL148D showed robust accumulation during the establishment of experimental HCMV latency in Kasumi-3 cells. In total, 20,000 infected cells were harvested for the isolation of total RNA and DNA at each indicted time point along the 10-day time course. Viral DNA was first quantified by qPCR, and then absolute viral genomes copies were calculated by generating a standard curve. HCMV miRNAs were then assayed with a HCMV miRNA probe kit, and their levels were calculated using a standard curve. The HCMV miRNA level per virus was calculated by dividing the amount of each HCMV miRNA by the virus copy number. (F) miR-UL148D accumulated in HPCs latently infected with NR-1. HCMV miRNA levels in NR-1-infected HPCs were determined as described above. Values are shown as the mean ± SEM (n = 3). **, P<0.01.
Control Fc Protein, supplied by Jackson Immuno, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+igg+fc+capture+biosensor/ChromPure+Human+IgG%2C+Fc+fragment/pm38078382-108-6-9
Average 93 stars, based on 1 article reviews
control fc protein - by Bioz Stars, 2026-10
93/100 stars
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anti human igg fc capture ahc biosensors  (R&D Systems)
97
R&D Systems anti human igg fc capture ahc biosensors
(A) Kasumi-3 and CD34 + HPCs were efficiently infected with the NR-1 strain of <t>HCMV.</t> Kasumi-3 and HPCs were either mock-infected or infected with a GFP-expressing NR-1 strain at the indicated multiplicities of infection (MOIs). Two days later, the cells were analyzed for GFP expression by flow cytometry. An MOI of 5 was used for the following experiment. (B) The maintenance of the NR-1 genome, the suppression of viral IE1 and the presence of latency-associated UL138 over a 10-day time course. DNA and total RNA were isolated from Kasumi-3 cells and HPCs at various time points after infection. Viral genomic DNA was assayed by PCR, and RNA molecules encoding IE1 and UL138 were assayed by RT-PCR. In both cases, gel electrophoresis was used to detect the products of the reactions. (C) Reactivation of NR-1 virus in infected Kasumi-3 cells and HPCs. Kasumi-3 cells and HPCs were latently infected along a 10-day time course. Then, a subset of each cell population was cultured for an additional 2 days under conditions favoring lytic reactivation: Kasumi-3 cells were exposed to TPA, while HPCs were grown in reactivation medium. Following this, total RNA was extracted from the cells, and the ratio of IE1 to UL138 cDNA expression was assessed by qRT-PCR in triplicate. (D) Release of infectious progeny virions in latently infected Kasumi-3 cells and HPCs following reactivation treatment. Latently infected or mock-infected Kasumi-3 cells and HPCs were cultured under conditions favoring lytic reactivation (described above) or control conditions for 6 days, after which the cells were washed with PBS and co-cultured with HFFs for 2 days. Then, the Kasumi-3 cells were removed from the co-cultures, and the HFFs were washed with PBS and cultured for an additional 5 days for fluorescence microscopy analysis of GFP-positive plaques. (E) miR-UL148D showed robust accumulation during the establishment of experimental HCMV latency in Kasumi-3 cells. In total, 20,000 infected cells were harvested for the isolation of total RNA and DNA at each indicted time point along the 10-day time course. Viral DNA was first quantified by qPCR, and then absolute viral genomes copies were calculated by generating a standard curve. HCMV miRNAs were then assayed with a HCMV miRNA probe kit, and their levels were calculated using a standard curve. The HCMV miRNA level per virus was calculated by dividing the amount of each HCMV miRNA by the virus copy number. (F) miR-UL148D accumulated in HPCs latently infected with NR-1. HCMV miRNA levels in NR-1-infected HPCs were determined as described above. Values are shown as the mean ± SEM (n = 3). **, P<0.01.
Anti Human Igg Fc Capture Ahc Biosensors, supplied by R&D Systems, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+igg+fc+capture+biosensor/Human+IgG+Fc+Antibody/bio_rxiv__2025__09__03__674085-282-0-23
Average 97 stars, based on 1 article reviews
anti human igg fc capture ahc biosensors - by Bioz Stars, 2026-10
97/100 stars
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antihuman igg fc biosensors  (Gator Bio Inc)
94
Gator Bio Inc antihuman igg fc biosensors
(A) Kasumi-3 and CD34 + HPCs were efficiently infected with the NR-1 strain of <t>HCMV.</t> Kasumi-3 and HPCs were either mock-infected or infected with a GFP-expressing NR-1 strain at the indicated multiplicities of infection (MOIs). Two days later, the cells were analyzed for GFP expression by flow cytometry. An MOI of 5 was used for the following experiment. (B) The maintenance of the NR-1 genome, the suppression of viral IE1 and the presence of latency-associated UL138 over a 10-day time course. DNA and total RNA were isolated from Kasumi-3 cells and HPCs at various time points after infection. Viral genomic DNA was assayed by PCR, and RNA molecules encoding IE1 and UL138 were assayed by RT-PCR. In both cases, gel electrophoresis was used to detect the products of the reactions. (C) Reactivation of NR-1 virus in infected Kasumi-3 cells and HPCs. Kasumi-3 cells and HPCs were latently infected along a 10-day time course. Then, a subset of each cell population was cultured for an additional 2 days under conditions favoring lytic reactivation: Kasumi-3 cells were exposed to TPA, while HPCs were grown in reactivation medium. Following this, total RNA was extracted from the cells, and the ratio of IE1 to UL138 cDNA expression was assessed by qRT-PCR in triplicate. (D) Release of infectious progeny virions in latently infected Kasumi-3 cells and HPCs following reactivation treatment. Latently infected or mock-infected Kasumi-3 cells and HPCs were cultured under conditions favoring lytic reactivation (described above) or control conditions for 6 days, after which the cells were washed with PBS and co-cultured with HFFs for 2 days. Then, the Kasumi-3 cells were removed from the co-cultures, and the HFFs were washed with PBS and cultured for an additional 5 days for fluorescence microscopy analysis of GFP-positive plaques. (E) miR-UL148D showed robust accumulation during the establishment of experimental HCMV latency in Kasumi-3 cells. In total, 20,000 infected cells were harvested for the isolation of total RNA and DNA at each indicted time point along the 10-day time course. Viral DNA was first quantified by qPCR, and then absolute viral genomes copies were calculated by generating a standard curve. HCMV miRNAs were then assayed with a HCMV miRNA probe kit, and their levels were calculated using a standard curve. The HCMV miRNA level per virus was calculated by dividing the amount of each HCMV miRNA by the virus copy number. (F) miR-UL148D accumulated in HPCs latently infected with NR-1. HCMV miRNA levels in NR-1-infected HPCs were determined as described above. Values are shown as the mean ± SEM (n = 3). **, P<0.01.
Antihuman Igg Fc Biosensors, supplied by Gator Bio Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+igg+fc+capture+biosensor/Anti-Human+IgG+Fc+(HFC)+Probes/pm38172096-282-7-11
Average 94 stars, based on 1 article reviews
antihuman igg fc biosensors - by Bioz Stars, 2026-10
94/100 stars
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anti human igg fc capture ahc sensor  (Sartorius AG)
97
Sartorius AG anti human igg fc capture ahc sensor
(A) Kasumi-3 and CD34 + HPCs were efficiently infected with the NR-1 strain of <t>HCMV.</t> Kasumi-3 and HPCs were either mock-infected or infected with a GFP-expressing NR-1 strain at the indicated multiplicities of infection (MOIs). Two days later, the cells were analyzed for GFP expression by flow cytometry. An MOI of 5 was used for the following experiment. (B) The maintenance of the NR-1 genome, the suppression of viral IE1 and the presence of latency-associated UL138 over a 10-day time course. DNA and total RNA were isolated from Kasumi-3 cells and HPCs at various time points after infection. Viral genomic DNA was assayed by PCR, and RNA molecules encoding IE1 and UL138 were assayed by RT-PCR. In both cases, gel electrophoresis was used to detect the products of the reactions. (C) Reactivation of NR-1 virus in infected Kasumi-3 cells and HPCs. Kasumi-3 cells and HPCs were latently infected along a 10-day time course. Then, a subset of each cell population was cultured for an additional 2 days under conditions favoring lytic reactivation: Kasumi-3 cells were exposed to TPA, while HPCs were grown in reactivation medium. Following this, total RNA was extracted from the cells, and the ratio of IE1 to UL138 cDNA expression was assessed by qRT-PCR in triplicate. (D) Release of infectious progeny virions in latently infected Kasumi-3 cells and HPCs following reactivation treatment. Latently infected or mock-infected Kasumi-3 cells and HPCs were cultured under conditions favoring lytic reactivation (described above) or control conditions for 6 days, after which the cells were washed with PBS and co-cultured with HFFs for 2 days. Then, the Kasumi-3 cells were removed from the co-cultures, and the HFFs were washed with PBS and cultured for an additional 5 days for fluorescence microscopy analysis of GFP-positive plaques. (E) miR-UL148D showed robust accumulation during the establishment of experimental HCMV latency in Kasumi-3 cells. In total, 20,000 infected cells were harvested for the isolation of total RNA and DNA at each indicted time point along the 10-day time course. Viral DNA was first quantified by qPCR, and then absolute viral genomes copies were calculated by generating a standard curve. HCMV miRNAs were then assayed with a HCMV miRNA probe kit, and their levels were calculated using a standard curve. The HCMV miRNA level per virus was calculated by dividing the amount of each HCMV miRNA by the virus copy number. (F) miR-UL148D accumulated in HPCs latently infected with NR-1. HCMV miRNA levels in NR-1-infected HPCs were determined as described above. Values are shown as the mean ± SEM (n = 3). **, P<0.01.
Anti Human Igg Fc Capture Ahc Sensor, supplied by Sartorius AG, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+igg+fc+capture+biosensor/Octet+Anti-Human+Fc+Capture+(AHC)+Biosensors/10__1093_slash_abt_slash_tbag049-58-14-20
Average 97 stars, based on 1 article reviews
anti human igg fc capture ahc sensor - by Bioz Stars, 2026-10
97/100 stars
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octet anti human igg quantitation ahq biosensors  (Sartorius AG)
99
Sartorius AG octet anti human igg quantitation ahq biosensors
(A) Kasumi-3 and CD34 + HPCs were efficiently infected with the NR-1 strain of <t>HCMV.</t> Kasumi-3 and HPCs were either mock-infected or infected with a GFP-expressing NR-1 strain at the indicated multiplicities of infection (MOIs). Two days later, the cells were analyzed for GFP expression by flow cytometry. An MOI of 5 was used for the following experiment. (B) The maintenance of the NR-1 genome, the suppression of viral IE1 and the presence of latency-associated UL138 over a 10-day time course. DNA and total RNA were isolated from Kasumi-3 cells and HPCs at various time points after infection. Viral genomic DNA was assayed by PCR, and RNA molecules encoding IE1 and UL138 were assayed by RT-PCR. In both cases, gel electrophoresis was used to detect the products of the reactions. (C) Reactivation of NR-1 virus in infected Kasumi-3 cells and HPCs. Kasumi-3 cells and HPCs were latently infected along a 10-day time course. Then, a subset of each cell population was cultured for an additional 2 days under conditions favoring lytic reactivation: Kasumi-3 cells were exposed to TPA, while HPCs were grown in reactivation medium. Following this, total RNA was extracted from the cells, and the ratio of IE1 to UL138 cDNA expression was assessed by qRT-PCR in triplicate. (D) Release of infectious progeny virions in latently infected Kasumi-3 cells and HPCs following reactivation treatment. Latently infected or mock-infected Kasumi-3 cells and HPCs were cultured under conditions favoring lytic reactivation (described above) or control conditions for 6 days, after which the cells were washed with PBS and co-cultured with HFFs for 2 days. Then, the Kasumi-3 cells were removed from the co-cultures, and the HFFs were washed with PBS and cultured for an additional 5 days for fluorescence microscopy analysis of GFP-positive plaques. (E) miR-UL148D showed robust accumulation during the establishment of experimental HCMV latency in Kasumi-3 cells. In total, 20,000 infected cells were harvested for the isolation of total RNA and DNA at each indicted time point along the 10-day time course. Viral DNA was first quantified by qPCR, and then absolute viral genomes copies were calculated by generating a standard curve. HCMV miRNAs were then assayed with a HCMV miRNA probe kit, and their levels were calculated using a standard curve. The HCMV miRNA level per virus was calculated by dividing the amount of each HCMV miRNA by the virus copy number. (F) miR-UL148D accumulated in HPCs latently infected with NR-1. HCMV miRNA levels in NR-1-infected HPCs were determined as described above. Values are shown as the mean ± SEM (n = 3). **, P<0.01.
Octet Anti Human Igg Quantitation Ahq Biosensors, supplied by Sartorius AG, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+igg+fc+capture+biosensor/Octet/bio_rxiv__64898__2026__04__13__718222-41-10-16
Average 99 stars, based on 1 article reviews
octet anti human igg quantitation ahq biosensors - by Bioz Stars, 2026-10
99/100 stars
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octet anti-human igg quantitation (ahq) biosensors  (Sartorius AG)
93
Sartorius AG octet anti-human igg quantitation (ahq) biosensors
(A) Kasumi-3 and CD34 + HPCs were efficiently infected with the NR-1 strain of <t>HCMV.</t> Kasumi-3 and HPCs were either mock-infected or infected with a GFP-expressing NR-1 strain at the indicated multiplicities of infection (MOIs). Two days later, the cells were analyzed for GFP expression by flow cytometry. An MOI of 5 was used for the following experiment. (B) The maintenance of the NR-1 genome, the suppression of viral IE1 and the presence of latency-associated UL138 over a 10-day time course. DNA and total RNA were isolated from Kasumi-3 cells and HPCs at various time points after infection. Viral genomic DNA was assayed by PCR, and RNA molecules encoding IE1 and UL138 were assayed by RT-PCR. In both cases, gel electrophoresis was used to detect the products of the reactions. (C) Reactivation of NR-1 virus in infected Kasumi-3 cells and HPCs. Kasumi-3 cells and HPCs were latently infected along a 10-day time course. Then, a subset of each cell population was cultured for an additional 2 days under conditions favoring lytic reactivation: Kasumi-3 cells were exposed to TPA, while HPCs were grown in reactivation medium. Following this, total RNA was extracted from the cells, and the ratio of IE1 to UL138 cDNA expression was assessed by qRT-PCR in triplicate. (D) Release of infectious progeny virions in latently infected Kasumi-3 cells and HPCs following reactivation treatment. Latently infected or mock-infected Kasumi-3 cells and HPCs were cultured under conditions favoring lytic reactivation (described above) or control conditions for 6 days, after which the cells were washed with PBS and co-cultured with HFFs for 2 days. Then, the Kasumi-3 cells were removed from the co-cultures, and the HFFs were washed with PBS and cultured for an additional 5 days for fluorescence microscopy analysis of GFP-positive plaques. (E) miR-UL148D showed robust accumulation during the establishment of experimental HCMV latency in Kasumi-3 cells. In total, 20,000 infected cells were harvested for the isolation of total RNA and DNA at each indicted time point along the 10-day time course. Viral DNA was first quantified by qPCR, and then absolute viral genomes copies were calculated by generating a standard curve. HCMV miRNAs were then assayed with a HCMV miRNA probe kit, and their levels were calculated using a standard curve. The HCMV miRNA level per virus was calculated by dividing the amount of each HCMV miRNA by the virus copy number. (F) miR-UL148D accumulated in HPCs latently infected with NR-1. HCMV miRNA levels in NR-1-infected HPCs were determined as described above. Values are shown as the mean ± SEM (n = 3). **, P<0.01.
Octet Anti Human Igg Quantitation (Ahq) Biosensors, supplied by Sartorius AG, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+igg+fc+capture+biosensor/Octet+Anti-Human+IgG+Quantitation+(AHQ)+Biosensors/custom%40bio-layer-interferometry-ahq-biosensors%4042420197
Average 93 stars, based on 1 article reviews
octet anti-human igg quantitation (ahq) biosensors - by Bioz Stars, 2026-10
93/100 stars
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biosensor design uses fluorogen  (Proteintech)
93
Proteintech biosensor design uses fluorogen
(A) Kasumi-3 and CD34 + HPCs were efficiently infected with the NR-1 strain of <t>HCMV.</t> Kasumi-3 and HPCs were either mock-infected or infected with a GFP-expressing NR-1 strain at the indicated multiplicities of infection (MOIs). Two days later, the cells were analyzed for GFP expression by flow cytometry. An MOI of 5 was used for the following experiment. (B) The maintenance of the NR-1 genome, the suppression of viral IE1 and the presence of latency-associated UL138 over a 10-day time course. DNA and total RNA were isolated from Kasumi-3 cells and HPCs at various time points after infection. Viral genomic DNA was assayed by PCR, and RNA molecules encoding IE1 and UL138 were assayed by RT-PCR. In both cases, gel electrophoresis was used to detect the products of the reactions. (C) Reactivation of NR-1 virus in infected Kasumi-3 cells and HPCs. Kasumi-3 cells and HPCs were latently infected along a 10-day time course. Then, a subset of each cell population was cultured for an additional 2 days under conditions favoring lytic reactivation: Kasumi-3 cells were exposed to TPA, while HPCs were grown in reactivation medium. Following this, total RNA was extracted from the cells, and the ratio of IE1 to UL138 cDNA expression was assessed by qRT-PCR in triplicate. (D) Release of infectious progeny virions in latently infected Kasumi-3 cells and HPCs following reactivation treatment. Latently infected or mock-infected Kasumi-3 cells and HPCs were cultured under conditions favoring lytic reactivation (described above) or control conditions for 6 days, after which the cells were washed with PBS and co-cultured with HFFs for 2 days. Then, the Kasumi-3 cells were removed from the co-cultures, and the HFFs were washed with PBS and cultured for an additional 5 days for fluorescence microscopy analysis of GFP-positive plaques. (E) miR-UL148D showed robust accumulation during the establishment of experimental HCMV latency in Kasumi-3 cells. In total, 20,000 infected cells were harvested for the isolation of total RNA and DNA at each indicted time point along the 10-day time course. Viral DNA was first quantified by qPCR, and then absolute viral genomes copies were calculated by generating a standard curve. HCMV miRNAs were then assayed with a HCMV miRNA probe kit, and their levels were calculated using a standard curve. The HCMV miRNA level per virus was calculated by dividing the amount of each HCMV miRNA by the virus copy number. (F) miR-UL148D accumulated in HPCs latently infected with NR-1. HCMV miRNA levels in NR-1-infected HPCs were determined as described above. Values are shown as the mean ± SEM (n = 3). **, P<0.01.
Biosensor Design Uses Fluorogen, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+igg+fc+capture+biosensor/MT1-MMP+Antibody/pm29651043-3-1-5
Average 93 stars, based on 1 article reviews
biosensor design uses fluorogen - by Bioz Stars, 2026-10
93/100 stars
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anti-ebv viral capsid antigen (vca) igm  (Dia Pro Diagnostic Bioprobes Srl)
90
Dia Pro Diagnostic Bioprobes Srl anti-ebv viral capsid antigen (vca) igm
(A) Kasumi-3 and CD34 + HPCs were efficiently infected with the NR-1 strain of <t>HCMV.</t> Kasumi-3 and HPCs were either mock-infected or infected with a GFP-expressing NR-1 strain at the indicated multiplicities of infection (MOIs). Two days later, the cells were analyzed for GFP expression by flow cytometry. An MOI of 5 was used for the following experiment. (B) The maintenance of the NR-1 genome, the suppression of viral IE1 and the presence of latency-associated UL138 over a 10-day time course. DNA and total RNA were isolated from Kasumi-3 cells and HPCs at various time points after infection. Viral genomic DNA was assayed by PCR, and RNA molecules encoding IE1 and UL138 were assayed by RT-PCR. In both cases, gel electrophoresis was used to detect the products of the reactions. (C) Reactivation of NR-1 virus in infected Kasumi-3 cells and HPCs. Kasumi-3 cells and HPCs were latently infected along a 10-day time course. Then, a subset of each cell population was cultured for an additional 2 days under conditions favoring lytic reactivation: Kasumi-3 cells were exposed to TPA, while HPCs were grown in reactivation medium. Following this, total RNA was extracted from the cells, and the ratio of IE1 to UL138 cDNA expression was assessed by qRT-PCR in triplicate. (D) Release of infectious progeny virions in latently infected Kasumi-3 cells and HPCs following reactivation treatment. Latently infected or mock-infected Kasumi-3 cells and HPCs were cultured under conditions favoring lytic reactivation (described above) or control conditions for 6 days, after which the cells were washed with PBS and co-cultured with HFFs for 2 days. Then, the Kasumi-3 cells were removed from the co-cultures, and the HFFs were washed with PBS and cultured for an additional 5 days for fluorescence microscopy analysis of GFP-positive plaques. (E) miR-UL148D showed robust accumulation during the establishment of experimental HCMV latency in Kasumi-3 cells. In total, 20,000 infected cells were harvested for the isolation of total RNA and DNA at each indicted time point along the 10-day time course. Viral DNA was first quantified by qPCR, and then absolute viral genomes copies were calculated by generating a standard curve. HCMV miRNAs were then assayed with a HCMV miRNA probe kit, and their levels were calculated using a standard curve. The HCMV miRNA level per virus was calculated by dividing the amount of each HCMV miRNA by the virus copy number. (F) miR-UL148D accumulated in HPCs latently infected with NR-1. HCMV miRNA levels in NR-1-infected HPCs were determined as described above. Values are shown as the mean ± SEM (n = 3). **, P<0.01.
Anti Ebv Viral Capsid Antigen (Vca) Igm, supplied by Dia Pro Diagnostic Bioprobes Srl, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+igg+fc+capture+biosensor/anti+ebv+viral+capsid+antigen++vca++igm/pm25318810-28-6-34
Average 90 stars, based on 1 article reviews
anti-ebv viral capsid antigen (vca) igm - by Bioz Stars, 2026-10
90/100 stars
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anti human igg fc biosensors  (Sino Biological)
93
Sino Biological anti human igg fc biosensors
(A) Kasumi-3 and CD34 + HPCs were efficiently infected with the NR-1 strain of <t>HCMV.</t> Kasumi-3 and HPCs were either mock-infected or infected with a GFP-expressing NR-1 strain at the indicated multiplicities of infection (MOIs). Two days later, the cells were analyzed for GFP expression by flow cytometry. An MOI of 5 was used for the following experiment. (B) The maintenance of the NR-1 genome, the suppression of viral IE1 and the presence of latency-associated UL138 over a 10-day time course. DNA and total RNA were isolated from Kasumi-3 cells and HPCs at various time points after infection. Viral genomic DNA was assayed by PCR, and RNA molecules encoding IE1 and UL138 were assayed by RT-PCR. In both cases, gel electrophoresis was used to detect the products of the reactions. (C) Reactivation of NR-1 virus in infected Kasumi-3 cells and HPCs. Kasumi-3 cells and HPCs were latently infected along a 10-day time course. Then, a subset of each cell population was cultured for an additional 2 days under conditions favoring lytic reactivation: Kasumi-3 cells were exposed to TPA, while HPCs were grown in reactivation medium. Following this, total RNA was extracted from the cells, and the ratio of IE1 to UL138 cDNA expression was assessed by qRT-PCR in triplicate. (D) Release of infectious progeny virions in latently infected Kasumi-3 cells and HPCs following reactivation treatment. Latently infected or mock-infected Kasumi-3 cells and HPCs were cultured under conditions favoring lytic reactivation (described above) or control conditions for 6 days, after which the cells were washed with PBS and co-cultured with HFFs for 2 days. Then, the Kasumi-3 cells were removed from the co-cultures, and the HFFs were washed with PBS and cultured for an additional 5 days for fluorescence microscopy analysis of GFP-positive plaques. (E) miR-UL148D showed robust accumulation during the establishment of experimental HCMV latency in Kasumi-3 cells. In total, 20,000 infected cells were harvested for the isolation of total RNA and DNA at each indicted time point along the 10-day time course. Viral DNA was first quantified by qPCR, and then absolute viral genomes copies were calculated by generating a standard curve. HCMV miRNAs were then assayed with a HCMV miRNA probe kit, and their levels were calculated using a standard curve. The HCMV miRNA level per virus was calculated by dividing the amount of each HCMV miRNA by the virus copy number. (F) miR-UL148D accumulated in HPCs latently infected with NR-1. HCMV miRNA levels in NR-1-infected HPCs were determined as described above. Values are shown as the mean ± SEM (n = 3). **, P<0.01.
Anti Human Igg Fc Biosensors, supplied by Sino Biological, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+igg+fc+capture+biosensor/Human+IgG4-Fc+Protein/pmc08183521-62-6-24
Average 93 stars, based on 1 article reviews
anti human igg fc biosensors - by Bioz Stars, 2026-10
93/100 stars
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anti-ebv nuclear antigen (ebna) igg  (Dia Pro Diagnostic Bioprobes Srl)
90
Dia Pro Diagnostic Bioprobes Srl anti-ebv nuclear antigen (ebna) igg
(A) Kasumi-3 and CD34 + HPCs were efficiently infected with the NR-1 strain of <t>HCMV.</t> Kasumi-3 and HPCs were either mock-infected or infected with a GFP-expressing NR-1 strain at the indicated multiplicities of infection (MOIs). Two days later, the cells were analyzed for GFP expression by flow cytometry. An MOI of 5 was used for the following experiment. (B) The maintenance of the NR-1 genome, the suppression of viral IE1 and the presence of latency-associated UL138 over a 10-day time course. DNA and total RNA were isolated from Kasumi-3 cells and HPCs at various time points after infection. Viral genomic DNA was assayed by PCR, and RNA molecules encoding IE1 and UL138 were assayed by RT-PCR. In both cases, gel electrophoresis was used to detect the products of the reactions. (C) Reactivation of NR-1 virus in infected Kasumi-3 cells and HPCs. Kasumi-3 cells and HPCs were latently infected along a 10-day time course. Then, a subset of each cell population was cultured for an additional 2 days under conditions favoring lytic reactivation: Kasumi-3 cells were exposed to TPA, while HPCs were grown in reactivation medium. Following this, total RNA was extracted from the cells, and the ratio of IE1 to UL138 cDNA expression was assessed by qRT-PCR in triplicate. (D) Release of infectious progeny virions in latently infected Kasumi-3 cells and HPCs following reactivation treatment. Latently infected or mock-infected Kasumi-3 cells and HPCs were cultured under conditions favoring lytic reactivation (described above) or control conditions for 6 days, after which the cells were washed with PBS and co-cultured with HFFs for 2 days. Then, the Kasumi-3 cells were removed from the co-cultures, and the HFFs were washed with PBS and cultured for an additional 5 days for fluorescence microscopy analysis of GFP-positive plaques. (E) miR-UL148D showed robust accumulation during the establishment of experimental HCMV latency in Kasumi-3 cells. In total, 20,000 infected cells were harvested for the isolation of total RNA and DNA at each indicted time point along the 10-day time course. Viral DNA was first quantified by qPCR, and then absolute viral genomes copies were calculated by generating a standard curve. HCMV miRNAs were then assayed with a HCMV miRNA probe kit, and their levels were calculated using a standard curve. The HCMV miRNA level per virus was calculated by dividing the amount of each HCMV miRNA by the virus copy number. (F) miR-UL148D accumulated in HPCs latently infected with NR-1. HCMV miRNA levels in NR-1-infected HPCs were determined as described above. Values are shown as the mean ± SEM (n = 3). **, P<0.01.
Anti Ebv Nuclear Antigen (Ebna) Igg, supplied by Dia Pro Diagnostic Bioprobes Srl, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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bioelectronics 192 2021 113491 chrompure mouse igg  (Jackson Immuno)
94
Jackson Immuno bioelectronics 192 2021 113491 chrompure mouse igg
(A) Kasumi-3 and CD34 + HPCs were efficiently infected with the NR-1 strain of <t>HCMV.</t> Kasumi-3 and HPCs were either mock-infected or infected with a GFP-expressing NR-1 strain at the indicated multiplicities of infection (MOIs). Two days later, the cells were analyzed for GFP expression by flow cytometry. An MOI of 5 was used for the following experiment. (B) The maintenance of the NR-1 genome, the suppression of viral IE1 and the presence of latency-associated UL138 over a 10-day time course. DNA and total RNA were isolated from Kasumi-3 cells and HPCs at various time points after infection. Viral genomic DNA was assayed by PCR, and RNA molecules encoding IE1 and UL138 were assayed by RT-PCR. In both cases, gel electrophoresis was used to detect the products of the reactions. (C) Reactivation of NR-1 virus in infected Kasumi-3 cells and HPCs. Kasumi-3 cells and HPCs were latently infected along a 10-day time course. Then, a subset of each cell population was cultured for an additional 2 days under conditions favoring lytic reactivation: Kasumi-3 cells were exposed to TPA, while HPCs were grown in reactivation medium. Following this, total RNA was extracted from the cells, and the ratio of IE1 to UL138 cDNA expression was assessed by qRT-PCR in triplicate. (D) Release of infectious progeny virions in latently infected Kasumi-3 cells and HPCs following reactivation treatment. Latently infected or mock-infected Kasumi-3 cells and HPCs were cultured under conditions favoring lytic reactivation (described above) or control conditions for 6 days, after which the cells were washed with PBS and co-cultured with HFFs for 2 days. Then, the Kasumi-3 cells were removed from the co-cultures, and the HFFs were washed with PBS and cultured for an additional 5 days for fluorescence microscopy analysis of GFP-positive plaques. (E) miR-UL148D showed robust accumulation during the establishment of experimental HCMV latency in Kasumi-3 cells. In total, 20,000 infected cells were harvested for the isolation of total RNA and DNA at each indicted time point along the 10-day time course. Viral DNA was first quantified by qPCR, and then absolute viral genomes copies were calculated by generating a standard curve. HCMV miRNAs were then assayed with a HCMV miRNA probe kit, and their levels were calculated using a standard curve. The HCMV miRNA level per virus was calculated by dividing the amount of each HCMV miRNA by the virus copy number. (F) miR-UL148D accumulated in HPCs latently infected with NR-1. HCMV miRNA levels in NR-1-infected HPCs were determined as described above. Values are shown as the mean ± SEM (n = 3). **, P<0.01.
Bioelectronics 192 2021 113491 Chrompure Mouse Igg, supplied by Jackson Immuno, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+igg+fc+capture+biosensor/ChromPure+Mouse+IgG%2C+whole+molecule/pm34271399-44-51-63
Average 94 stars, based on 1 article reviews
bioelectronics 192 2021 113491 chrompure mouse igg - by Bioz Stars, 2026-10
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(A) Kasumi-3 and CD34 + HPCs were efficiently infected with the NR-1 strain of HCMV. Kasumi-3 and HPCs were either mock-infected or infected with a GFP-expressing NR-1 strain at the indicated multiplicities of infection (MOIs). Two days later, the cells were analyzed for GFP expression by flow cytometry. An MOI of 5 was used for the following experiment. (B) The maintenance of the NR-1 genome, the suppression of viral IE1 and the presence of latency-associated UL138 over a 10-day time course. DNA and total RNA were isolated from Kasumi-3 cells and HPCs at various time points after infection. Viral genomic DNA was assayed by PCR, and RNA molecules encoding IE1 and UL138 were assayed by RT-PCR. In both cases, gel electrophoresis was used to detect the products of the reactions. (C) Reactivation of NR-1 virus in infected Kasumi-3 cells and HPCs. Kasumi-3 cells and HPCs were latently infected along a 10-day time course. Then, a subset of each cell population was cultured for an additional 2 days under conditions favoring lytic reactivation: Kasumi-3 cells were exposed to TPA, while HPCs were grown in reactivation medium. Following this, total RNA was extracted from the cells, and the ratio of IE1 to UL138 cDNA expression was assessed by qRT-PCR in triplicate. (D) Release of infectious progeny virions in latently infected Kasumi-3 cells and HPCs following reactivation treatment. Latently infected or mock-infected Kasumi-3 cells and HPCs were cultured under conditions favoring lytic reactivation (described above) or control conditions for 6 days, after which the cells were washed with PBS and co-cultured with HFFs for 2 days. Then, the Kasumi-3 cells were removed from the co-cultures, and the HFFs were washed with PBS and cultured for an additional 5 days for fluorescence microscopy analysis of GFP-positive plaques. (E) miR-UL148D showed robust accumulation during the establishment of experimental HCMV latency in Kasumi-3 cells. In total, 20,000 infected cells were harvested for the isolation of total RNA and DNA at each indicted time point along the 10-day time course. Viral DNA was first quantified by qPCR, and then absolute viral genomes copies were calculated by generating a standard curve. HCMV miRNAs were then assayed with a HCMV miRNA probe kit, and their levels were calculated using a standard curve. The HCMV miRNA level per virus was calculated by dividing the amount of each HCMV miRNA by the virus copy number. (F) miR-UL148D accumulated in HPCs latently infected with NR-1. HCMV miRNA levels in NR-1-infected HPCs were determined as described above. Values are shown as the mean ± SEM (n = 3). **, P<0.01.

Journal: PLoS Pathogens

Article Title: Human Cytomegalovirus miR-UL148D Facilitates Latent Viral Infection by Targeting Host Cell Immediate Early Response Gene 5

doi: 10.1371/journal.ppat.1006007

Figure Lengend Snippet: (A) Kasumi-3 and CD34 + HPCs were efficiently infected with the NR-1 strain of HCMV. Kasumi-3 and HPCs were either mock-infected or infected with a GFP-expressing NR-1 strain at the indicated multiplicities of infection (MOIs). Two days later, the cells were analyzed for GFP expression by flow cytometry. An MOI of 5 was used for the following experiment. (B) The maintenance of the NR-1 genome, the suppression of viral IE1 and the presence of latency-associated UL138 over a 10-day time course. DNA and total RNA were isolated from Kasumi-3 cells and HPCs at various time points after infection. Viral genomic DNA was assayed by PCR, and RNA molecules encoding IE1 and UL138 were assayed by RT-PCR. In both cases, gel electrophoresis was used to detect the products of the reactions. (C) Reactivation of NR-1 virus in infected Kasumi-3 cells and HPCs. Kasumi-3 cells and HPCs were latently infected along a 10-day time course. Then, a subset of each cell population was cultured for an additional 2 days under conditions favoring lytic reactivation: Kasumi-3 cells were exposed to TPA, while HPCs were grown in reactivation medium. Following this, total RNA was extracted from the cells, and the ratio of IE1 to UL138 cDNA expression was assessed by qRT-PCR in triplicate. (D) Release of infectious progeny virions in latently infected Kasumi-3 cells and HPCs following reactivation treatment. Latently infected or mock-infected Kasumi-3 cells and HPCs were cultured under conditions favoring lytic reactivation (described above) or control conditions for 6 days, after which the cells were washed with PBS and co-cultured with HFFs for 2 days. Then, the Kasumi-3 cells were removed from the co-cultures, and the HFFs were washed with PBS and cultured for an additional 5 days for fluorescence microscopy analysis of GFP-positive plaques. (E) miR-UL148D showed robust accumulation during the establishment of experimental HCMV latency in Kasumi-3 cells. In total, 20,000 infected cells were harvested for the isolation of total RNA and DNA at each indicted time point along the 10-day time course. Viral DNA was first quantified by qPCR, and then absolute viral genomes copies were calculated by generating a standard curve. HCMV miRNAs were then assayed with a HCMV miRNA probe kit, and their levels were calculated using a standard curve. The HCMV miRNA level per virus was calculated by dividing the amount of each HCMV miRNA by the virus copy number. (F) miR-UL148D accumulated in HPCs latently infected with NR-1. HCMV miRNA levels in NR-1-infected HPCs were determined as described above. Values are shown as the mean ± SEM (n = 3). **, P<0.01.

Article Snippet: Anti-HCMV IgG and IgM antibodies in plasma were detected by ELISA using an HCMV IgG/IgM kit (DIA PRO Diagnostic Bioprobes, Milano, Italy) according to the manufacturer’s instructions.

Techniques: Infection, Expressing, Flow Cytometry, Isolation, Reverse Transcription Polymerase Chain Reaction, Nucleic Acid Electrophoresis, Virus, Cell Culture, Quantitative RT-PCR, Control, Fluorescence, Microscopy

(A, C) HCMV genome copies in Kasumi-3 cells (A) and CD34 + HPCs (C) infected with NR-1 or NR-1ΔmiR-UL148D. Total DNA was isolated from the infected cells at various time points after infection, and viral DNA was quantified by qPCR and normalized to cellular GAPDH. (B, D) Representative transcript levels from each class of viral genes in Kasumi-3 cells (B) and HPCs (D) infected with NR-1 or NR-1ΔmiR-UL148D. IE1 (immediately early), UL54 (early lytic transcript), and UL99 (late lytic transcript). Total RNA was isolated from infected cells and assayed by RT-qPCR. Samples were assayed in triplicate, and GAPDH level was used for normalization. (E, F) Restoring miR-UL148D expression via transfection with the miR-UL148D agomir reduced HCMV genome copies (E) and IE1 (F) expression in NR-1ΔmiR-UL148D-infected Kasumi-3 cells. The miR-UL148D agomir was added 24 hours before viral infection, and the culture media was replaced everyday with the addition of fresh agomir. DNA and total RNA were isolated from the Kasumi-3 cells at various time points after infection and quantified by qPCR and RT-qPCR, respectively. Samples were assayed in triplicate, and GAPDH level was used for normalization. Results derived from NR-1-infected Kasumi-3 cells are shown as a control. (G) Both NR-1ΔmiR-UL148D- and NR-1-infected Kasumi-3 cells produced infectious progeny. Infected Kasumi-3 cells harvested 10 days post-infection were stained with a monoclonal antibody against IE1 (clone 1B12, shown in red). GFP (green) and DAPI (blue) served as markers for lytic infection and nuclei, respectively. Infected Kasumi-3 cells were also co-cultured with HFFs. Viral plaque formation in the HFFs (shown by a GFP-positive status) was visualized by fluorescence microscopy. Images were collected using a 40x objective, and representative fields are shown for each infection. Values are shown as the mean ± SEM (n = 3). *, P<0.05. **, P<0.01.

Journal: PLoS Pathogens

Article Title: Human Cytomegalovirus miR-UL148D Facilitates Latent Viral Infection by Targeting Host Cell Immediate Early Response Gene 5

doi: 10.1371/journal.ppat.1006007

Figure Lengend Snippet: (A, C) HCMV genome copies in Kasumi-3 cells (A) and CD34 + HPCs (C) infected with NR-1 or NR-1ΔmiR-UL148D. Total DNA was isolated from the infected cells at various time points after infection, and viral DNA was quantified by qPCR and normalized to cellular GAPDH. (B, D) Representative transcript levels from each class of viral genes in Kasumi-3 cells (B) and HPCs (D) infected with NR-1 or NR-1ΔmiR-UL148D. IE1 (immediately early), UL54 (early lytic transcript), and UL99 (late lytic transcript). Total RNA was isolated from infected cells and assayed by RT-qPCR. Samples were assayed in triplicate, and GAPDH level was used for normalization. (E, F) Restoring miR-UL148D expression via transfection with the miR-UL148D agomir reduced HCMV genome copies (E) and IE1 (F) expression in NR-1ΔmiR-UL148D-infected Kasumi-3 cells. The miR-UL148D agomir was added 24 hours before viral infection, and the culture media was replaced everyday with the addition of fresh agomir. DNA and total RNA were isolated from the Kasumi-3 cells at various time points after infection and quantified by qPCR and RT-qPCR, respectively. Samples were assayed in triplicate, and GAPDH level was used for normalization. Results derived from NR-1-infected Kasumi-3 cells are shown as a control. (G) Both NR-1ΔmiR-UL148D- and NR-1-infected Kasumi-3 cells produced infectious progeny. Infected Kasumi-3 cells harvested 10 days post-infection were stained with a monoclonal antibody against IE1 (clone 1B12, shown in red). GFP (green) and DAPI (blue) served as markers for lytic infection and nuclei, respectively. Infected Kasumi-3 cells were also co-cultured with HFFs. Viral plaque formation in the HFFs (shown by a GFP-positive status) was visualized by fluorescence microscopy. Images were collected using a 40x objective, and representative fields are shown for each infection. Values are shown as the mean ± SEM (n = 3). *, P<0.05. **, P<0.01.

Article Snippet: Anti-HCMV IgG and IgM antibodies in plasma were detected by ELISA using an HCMV IgG/IgM kit (DIA PRO Diagnostic Bioprobes, Milano, Italy) according to the manufacturer’s instructions.

Techniques: Infection, Isolation, Quantitative RT-PCR, Expressing, Transfection, Derivative Assay, Control, Produced, Staining, Cell Culture, Fluorescence, Microscopy

(A) Schematic of miR-UL148D-binding sites on IER5, with the two seed-recognizing sites marked in red. The predicted free energy of each hybrid is indicated. (B) Downregulation of IER5 and upregulation of CDC25B protein levels in Kasumi-3 cells induced by miR-UL148D mimics. The protein levels of IER5 and CDC25B in Kasumi-3 cells 48 hours after transfection with miR-UL148D mimics were assayed with western blotting. GAPDH served as an internal control. (C) Upper panel: construction of luciferase reporter that expresses the IER5 3’UTR with or without mutation of miR-UL148D-binding sites. Mutations of the seed-recognizing sites in the IER5 3’UTR are marked in red. Lower panel: firefly luciferase activity in 293T cells that were co-transfected with various luciferase reporter constructs for the IER5 3’UTR and miR-UL148D, normalized to β-gal activity. (D) Upper panel: Construction of an expression vector harboring the ORF and 3’UTR of IER5 with or without mutation of the two miR-UL148D-binding sites. The mutations in the binding sites in the IER5 3’UTR are marked in red. Lower panel: Expression levels of IER5 and CDC25B in Kasumi-3 cells that were co-transfected with wild-type IER5 (IER5 WT) or mutated IER5 (IER5 Mut) and miR-UL148D or a scrambled oligonucleotide. Protein levels were detected by Western blot analysis after a 72-h transfection. The efficiency of transfection was monitored by assaying β-gal activity. (E) Schematic representing the hypothesis for how miR-UL148D facilitates HCMV latency. Values are shown as the mean ± SEM (n = 3). **, P<0.01.

Journal: PLoS Pathogens

Article Title: Human Cytomegalovirus miR-UL148D Facilitates Latent Viral Infection by Targeting Host Cell Immediate Early Response Gene 5

doi: 10.1371/journal.ppat.1006007

Figure Lengend Snippet: (A) Schematic of miR-UL148D-binding sites on IER5, with the two seed-recognizing sites marked in red. The predicted free energy of each hybrid is indicated. (B) Downregulation of IER5 and upregulation of CDC25B protein levels in Kasumi-3 cells induced by miR-UL148D mimics. The protein levels of IER5 and CDC25B in Kasumi-3 cells 48 hours after transfection with miR-UL148D mimics were assayed with western blotting. GAPDH served as an internal control. (C) Upper panel: construction of luciferase reporter that expresses the IER5 3’UTR with or without mutation of miR-UL148D-binding sites. Mutations of the seed-recognizing sites in the IER5 3’UTR are marked in red. Lower panel: firefly luciferase activity in 293T cells that were co-transfected with various luciferase reporter constructs for the IER5 3’UTR and miR-UL148D, normalized to β-gal activity. (D) Upper panel: Construction of an expression vector harboring the ORF and 3’UTR of IER5 with or without mutation of the two miR-UL148D-binding sites. The mutations in the binding sites in the IER5 3’UTR are marked in red. Lower panel: Expression levels of IER5 and CDC25B in Kasumi-3 cells that were co-transfected with wild-type IER5 (IER5 WT) or mutated IER5 (IER5 Mut) and miR-UL148D or a scrambled oligonucleotide. Protein levels were detected by Western blot analysis after a 72-h transfection. The efficiency of transfection was monitored by assaying β-gal activity. (E) Schematic representing the hypothesis for how miR-UL148D facilitates HCMV latency. Values are shown as the mean ± SEM (n = 3). **, P<0.01.

Article Snippet: Anti-HCMV IgG and IgM antibodies in plasma were detected by ELISA using an HCMV IgG/IgM kit (DIA PRO Diagnostic Bioprobes, Milano, Italy) according to the manufacturer’s instructions.

Techniques: Binding Assay, Transfection, Western Blot, Control, Luciferase, Mutagenesis, Activity Assay, Construct, Expressing, Plasmid Preparation