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serp1 protein expression  (Proteintech)


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    Structured Review

    Proteintech serp1 protein expression
    Figure 1. Protein–protein interactions between stress-associated endoplasmic reticulum protein 1 <t>(SERP1)</t> and nonstructural protein (NS)4B. (A) NS4B interacts with SERP1, as shown in a membrane-base
    Serp1 Protein Expression, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/serp1 protein expression/product/Proteintech
    Average 93 stars, based on 5 article reviews
    serp1 protein expression - by Bioz Stars, 2026-02
    93/100 stars

    Images

    1) Product Images from "A Dengue Virus Type 2 (DENV-2) NS4B-Interacting Host Factor, SERP1, Reduces DENV-2 Production by Suppressing Viral RNA Replication."

    Article Title: A Dengue Virus Type 2 (DENV-2) NS4B-Interacting Host Factor, SERP1, Reduces DENV-2 Production by Suppressing Viral RNA Replication.

    Journal: Viruses

    doi: 10.3390/v11090787

    Figure 1. Protein–protein interactions between stress-associated endoplasmic reticulum protein 1 (SERP1) and nonstructural protein (NS)4B. (A) NS4B interacts with SERP1, as shown in a membrane-base
    Figure Legend Snippet: Figure 1. Protein–protein interactions between stress-associated endoplasmic reticulum protein 1 (SERP1) and nonstructural protein (NS)4B. (A) NS4B interacts with SERP1, as shown in a membrane-base

    Techniques Used: Protein-Protein interactions, Membrane

    Figure 2. SERP1 expressions were induced in Huh7.5 cells upon DENV-2 infection and wild-type (WT) replicon transfection. (A) The Huh7.5 cells were uninfected or infected with DENV-2 at an MOI = 1. The quantification of SERP1 transcripts was performed by RT-qPCR at 0, 1, 2, 3, 4, and 5 d.p.i. The relative quantitative values of the SERP1 gene were normalized to the level of β-actin. *, p < 0.05; ***, p < 0.001 (Student’s t-test). (B) Schematic representation of the DNA-launched DENV-2 reporter replicon pCMV-DV2Rep, which was used in a transient replicon assay. The transcriptional expression of the replicon RNA is under the control of the CMVmin promoter, and the 3′ terminus of the transcript is processed by hepatitis delta virus (HDV) ribozyme sequences. The N-terminal 102 amino acids of the C protein (C102), the Renilla luciferase gene (Rluc), the FMDV2A cleavage site, a neomycin resistance gene (Neo), an internal ribosome entry site (IRES) element, the C-terminal 24 amino acids of E (E24),
    Figure Legend Snippet: Figure 2. SERP1 expressions were induced in Huh7.5 cells upon DENV-2 infection and wild-type (WT) replicon transfection. (A) The Huh7.5 cells were uninfected or infected with DENV-2 at an MOI = 1. The quantification of SERP1 transcripts was performed by RT-qPCR at 0, 1, 2, 3, 4, and 5 d.p.i. The relative quantitative values of the SERP1 gene were normalized to the level of β-actin. *, p < 0.05; ***, p < 0.001 (Student’s t-test). (B) Schematic representation of the DNA-launched DENV-2 reporter replicon pCMV-DV2Rep, which was used in a transient replicon assay. The transcriptional expression of the replicon RNA is under the control of the CMVmin promoter, and the 3′ terminus of the transcript is processed by hepatitis delta virus (HDV) ribozyme sequences. The N-terminal 102 amino acids of the C protein (C102), the Renilla luciferase gene (Rluc), the FMDV2A cleavage site, a neomycin resistance gene (Neo), an internal ribosome entry site (IRES) element, the C-terminal 24 amino acids of E (E24),

    Techniques Used: Infection, Transfection, Quantitative RT-PCR, Expressing, Control, Virus, Luciferase

    Figure 3. The SERP1 overexpression inhibited DENV-2 infection, and SERP1 knockdown increased DENV-2 infection. (A) Western blot analysis of Flag-tagged SERP1 proteins in Huh7.5 cells expressing
    Figure Legend Snippet: Figure 3. The SERP1 overexpression inhibited DENV-2 infection, and SERP1 knockdown increased DENV-2 infection. (A) Western blot analysis of Flag-tagged SERP1 proteins in Huh7.5 cells expressing

    Techniques Used: Over Expression, Infection, Knockdown, Western Blot, Expressing

    Figure 4. Knockout of SERP1 by the II clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9 system in Huh7.5 cells decreased SERP1 mRNA levels, and viral yields were significantly enhanced in the SERP1 knockout cells. (A) SERP1 RNA expression patterns in the SERP1 knockout sublines. The products of RT-PCR performed on RNA isolated from the parental Huh7.5 cells (SERP1+/+) and SERP1 knockout sublines (SERP1+/−and SERP1−/−) using the primers in SERP1 exon 1 and exon 3, which generate a 697 bp product. The SERP1 mutant allele was amplified as a 563 bp product, where the SERP1 exon 1 region was deleted. (B) Sequencing analysis of the parental Huh7.5 cells and SERP1 knockout cell lines from the RT-PCR product. (C) Detection of SERP1 mRNA levels in the parental Huh7.5 cells and SERP1 knockout sublines by qRT-PCR. The expression values are normalized to β-actin expression. ***, p < 0.001 (Student’s t-test). (D) Kinetics of DENV-2 replication in the parental cells and SERP1 knockout sublines. The parental Huh7.5 cells and SERP1 knockout sublines were infected with DENV-2 (MOI = 1) at the indicated times. Infectious virus yield in the BHK21 clone 15 cells was quantified by plaque assay. The differences in virus yields between the parental cells (SERP1+/+) and SERP1 knockout cells (SERP1−/−) at 2 or 3 d.p.i. were analyzed using Student’s t-test. *, p < 0.05.
    Figure Legend Snippet: Figure 4. Knockout of SERP1 by the II clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9 system in Huh7.5 cells decreased SERP1 mRNA levels, and viral yields were significantly enhanced in the SERP1 knockout cells. (A) SERP1 RNA expression patterns in the SERP1 knockout sublines. The products of RT-PCR performed on RNA isolated from the parental Huh7.5 cells (SERP1+/+) and SERP1 knockout sublines (SERP1+/−and SERP1−/−) using the primers in SERP1 exon 1 and exon 3, which generate a 697 bp product. The SERP1 mutant allele was amplified as a 563 bp product, where the SERP1 exon 1 region was deleted. (B) Sequencing analysis of the parental Huh7.5 cells and SERP1 knockout cell lines from the RT-PCR product. (C) Detection of SERP1 mRNA levels in the parental Huh7.5 cells and SERP1 knockout sublines by qRT-PCR. The expression values are normalized to β-actin expression. ***, p < 0.001 (Student’s t-test). (D) Kinetics of DENV-2 replication in the parental cells and SERP1 knockout sublines. The parental Huh7.5 cells and SERP1 knockout sublines were infected with DENV-2 (MOI = 1) at the indicated times. Infectious virus yield in the BHK21 clone 15 cells was quantified by plaque assay. The differences in virus yields between the parental cells (SERP1+/+) and SERP1 knockout cells (SERP1−/−) at 2 or 3 d.p.i. were analyzed using Student’s t-test. *, p < 0.05.

    Techniques Used: Knock-Out, CRISPR, RNA Expression, Reverse Transcription Polymerase Chain Reaction, Isolation, Mutagenesis, Sequencing, Quantitative RT-PCR, Expressing, Infection, Virus, Plaque Assay

    Figure 6. Overexpression of NS4B improves the virus replication in the Huh7.5 cells overexpressing SERP1. (A) Schematic diagram of HA C-terminal fusion constructs of NS2B and NS4B. The N-terminal 2K signal peptide was deleted (△2K-NS4B-HA). (B) Immunoblot analysis of HA-tagged NS2B and NS4B proteins in the parental cells and SERP1-overexpressing Huh7.5 cells. All of the fragments represented in panel (A) were cloned in pLKO-AS2 to tag the C-terminal end of each protein. Equal amounts of lysates were incubated with anti-HA magnetic beads, and the precipitates were analyzed by Western blot using an anti-HA antibody. The parental cells (C) and SERP1-overexpressing Huh7.5 cells (D) were co-transfected with WT replicon and plasmids encoding individual viral proteins, as indicated. The cell lysates were harvested 24, 48, 72, and 96 h after transfection, and the luciferase activity of the transfected cells was measured. The replication efficiency was calculated by determining the ratio of luciferase activity obtained at 48, 72, and 96 h, to the average value obtained from all of the replicon constructs at 24 h post-transfection. The error bars represent the standard errors of the means (SEMs) from three independent experiments. *, p < 0.05; ***, p < 0.001 (Student’s t-test).
    Figure Legend Snippet: Figure 6. Overexpression of NS4B improves the virus replication in the Huh7.5 cells overexpressing SERP1. (A) Schematic diagram of HA C-terminal fusion constructs of NS2B and NS4B. The N-terminal 2K signal peptide was deleted (△2K-NS4B-HA). (B) Immunoblot analysis of HA-tagged NS2B and NS4B proteins in the parental cells and SERP1-overexpressing Huh7.5 cells. All of the fragments represented in panel (A) were cloned in pLKO-AS2 to tag the C-terminal end of each protein. Equal amounts of lysates were incubated with anti-HA magnetic beads, and the precipitates were analyzed by Western blot using an anti-HA antibody. The parental cells (C) and SERP1-overexpressing Huh7.5 cells (D) were co-transfected with WT replicon and plasmids encoding individual viral proteins, as indicated. The cell lysates were harvested 24, 48, 72, and 96 h after transfection, and the luciferase activity of the transfected cells was measured. The replication efficiency was calculated by determining the ratio of luciferase activity obtained at 48, 72, and 96 h, to the average value obtained from all of the replicon constructs at 24 h post-transfection. The error bars represent the standard errors of the means (SEMs) from three independent experiments. *, p < 0.05; ***, p < 0.001 (Student’s t-test).

    Techniques Used: Over Expression, Virus, Construct, Western Blot, Clone Assay, Incubation, Magnetic Beads, Transfection, Luciferase, Activity Assay

    Figure 7. Hypothetical model of SERP1-mediated DENV-2 infection. (A) SERP1 overexpression inhibits DENV-2 viral RNA replication and titers. (B) DENV-2 NS4B interacts with SERP1. DENV-2 NS4B may alleviate the inhibitory effect of SERP1 on DENV-2 viral replication via the interaction of NS4B with SERP1.
    Figure Legend Snippet: Figure 7. Hypothetical model of SERP1-mediated DENV-2 infection. (A) SERP1 overexpression inhibits DENV-2 viral RNA replication and titers. (B) DENV-2 NS4B interacts with SERP1. DENV-2 NS4B may alleviate the inhibitory effect of SERP1 on DENV-2 viral replication via the interaction of NS4B with SERP1.

    Techniques Used: Infection, Over Expression



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    Proteintech serp1 protein expression
    Figure 1. Protein–protein interactions between stress-associated endoplasmic reticulum protein 1 <t>(SERP1)</t> and nonstructural protein (NS)4B. (A) NS4B interacts with SERP1, as shown in a membrane-base
    Serp1 Protein Expression, 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/result/serp1 protein expression/product/Proteintech
    Average 93 stars, based on 1 article reviews
    serp1 protein expression - by Bioz Stars, 2026-02
    93/100 stars
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    Figure 1. Protein–protein interactions between stress-associated endoplasmic reticulum protein 1 (SERP1) and nonstructural protein (NS)4B. (A) NS4B interacts with SERP1, as shown in a membrane-base

    Journal: Viruses

    Article Title: A Dengue Virus Type 2 (DENV-2) NS4B-Interacting Host Factor, SERP1, Reduces DENV-2 Production by Suppressing Viral RNA Replication.

    doi: 10.3390/v11090787

    Figure Lengend Snippet: Figure 1. Protein–protein interactions between stress-associated endoplasmic reticulum protein 1 (SERP1) and nonstructural protein (NS)4B. (A) NS4B interacts with SERP1, as shown in a membrane-base

    Article Snippet: To further measure the protein level of SERP1 in the DENV-2 infected cells, we failed to detect the SERP1 protein expression in virus infected cells by either in-house mouse, rabbit, or commercial anti-SERP1 antibodies (Genetex, Abcam, Proteintech Group, Atlas antibodies), possibly because of the poor antigenicity of SERP1 (data not shown).

    Techniques: Protein-Protein interactions, Membrane

    Figure 2. SERP1 expressions were induced in Huh7.5 cells upon DENV-2 infection and wild-type (WT) replicon transfection. (A) The Huh7.5 cells were uninfected or infected with DENV-2 at an MOI = 1. The quantification of SERP1 transcripts was performed by RT-qPCR at 0, 1, 2, 3, 4, and 5 d.p.i. The relative quantitative values of the SERP1 gene were normalized to the level of β-actin. *, p < 0.05; ***, p < 0.001 (Student’s t-test). (B) Schematic representation of the DNA-launched DENV-2 reporter replicon pCMV-DV2Rep, which was used in a transient replicon assay. The transcriptional expression of the replicon RNA is under the control of the CMVmin promoter, and the 3′ terminus of the transcript is processed by hepatitis delta virus (HDV) ribozyme sequences. The N-terminal 102 amino acids of the C protein (C102), the Renilla luciferase gene (Rluc), the FMDV2A cleavage site, a neomycin resistance gene (Neo), an internal ribosome entry site (IRES) element, the C-terminal 24 amino acids of E (E24),

    Journal: Viruses

    Article Title: A Dengue Virus Type 2 (DENV-2) NS4B-Interacting Host Factor, SERP1, Reduces DENV-2 Production by Suppressing Viral RNA Replication.

    doi: 10.3390/v11090787

    Figure Lengend Snippet: Figure 2. SERP1 expressions were induced in Huh7.5 cells upon DENV-2 infection and wild-type (WT) replicon transfection. (A) The Huh7.5 cells were uninfected or infected with DENV-2 at an MOI = 1. The quantification of SERP1 transcripts was performed by RT-qPCR at 0, 1, 2, 3, 4, and 5 d.p.i. The relative quantitative values of the SERP1 gene were normalized to the level of β-actin. *, p < 0.05; ***, p < 0.001 (Student’s t-test). (B) Schematic representation of the DNA-launched DENV-2 reporter replicon pCMV-DV2Rep, which was used in a transient replicon assay. The transcriptional expression of the replicon RNA is under the control of the CMVmin promoter, and the 3′ terminus of the transcript is processed by hepatitis delta virus (HDV) ribozyme sequences. The N-terminal 102 amino acids of the C protein (C102), the Renilla luciferase gene (Rluc), the FMDV2A cleavage site, a neomycin resistance gene (Neo), an internal ribosome entry site (IRES) element, the C-terminal 24 amino acids of E (E24),

    Article Snippet: To further measure the protein level of SERP1 in the DENV-2 infected cells, we failed to detect the SERP1 protein expression in virus infected cells by either in-house mouse, rabbit, or commercial anti-SERP1 antibodies (Genetex, Abcam, Proteintech Group, Atlas antibodies), possibly because of the poor antigenicity of SERP1 (data not shown).

    Techniques: Infection, Transfection, Quantitative RT-PCR, Expressing, Control, Virus, Luciferase

    Figure 3. The SERP1 overexpression inhibited DENV-2 infection, and SERP1 knockdown increased DENV-2 infection. (A) Western blot analysis of Flag-tagged SERP1 proteins in Huh7.5 cells expressing

    Journal: Viruses

    Article Title: A Dengue Virus Type 2 (DENV-2) NS4B-Interacting Host Factor, SERP1, Reduces DENV-2 Production by Suppressing Viral RNA Replication.

    doi: 10.3390/v11090787

    Figure Lengend Snippet: Figure 3. The SERP1 overexpression inhibited DENV-2 infection, and SERP1 knockdown increased DENV-2 infection. (A) Western blot analysis of Flag-tagged SERP1 proteins in Huh7.5 cells expressing

    Article Snippet: To further measure the protein level of SERP1 in the DENV-2 infected cells, we failed to detect the SERP1 protein expression in virus infected cells by either in-house mouse, rabbit, or commercial anti-SERP1 antibodies (Genetex, Abcam, Proteintech Group, Atlas antibodies), possibly because of the poor antigenicity of SERP1 (data not shown).

    Techniques: Over Expression, Infection, Knockdown, Western Blot, Expressing

    Figure 4. Knockout of SERP1 by the II clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9 system in Huh7.5 cells decreased SERP1 mRNA levels, and viral yields were significantly enhanced in the SERP1 knockout cells. (A) SERP1 RNA expression patterns in the SERP1 knockout sublines. The products of RT-PCR performed on RNA isolated from the parental Huh7.5 cells (SERP1+/+) and SERP1 knockout sublines (SERP1+/−and SERP1−/−) using the primers in SERP1 exon 1 and exon 3, which generate a 697 bp product. The SERP1 mutant allele was amplified as a 563 bp product, where the SERP1 exon 1 region was deleted. (B) Sequencing analysis of the parental Huh7.5 cells and SERP1 knockout cell lines from the RT-PCR product. (C) Detection of SERP1 mRNA levels in the parental Huh7.5 cells and SERP1 knockout sublines by qRT-PCR. The expression values are normalized to β-actin expression. ***, p < 0.001 (Student’s t-test). (D) Kinetics of DENV-2 replication in the parental cells and SERP1 knockout sublines. The parental Huh7.5 cells and SERP1 knockout sublines were infected with DENV-2 (MOI = 1) at the indicated times. Infectious virus yield in the BHK21 clone 15 cells was quantified by plaque assay. The differences in virus yields between the parental cells (SERP1+/+) and SERP1 knockout cells (SERP1−/−) at 2 or 3 d.p.i. were analyzed using Student’s t-test. *, p < 0.05.

    Journal: Viruses

    Article Title: A Dengue Virus Type 2 (DENV-2) NS4B-Interacting Host Factor, SERP1, Reduces DENV-2 Production by Suppressing Viral RNA Replication.

    doi: 10.3390/v11090787

    Figure Lengend Snippet: Figure 4. Knockout of SERP1 by the II clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9 system in Huh7.5 cells decreased SERP1 mRNA levels, and viral yields were significantly enhanced in the SERP1 knockout cells. (A) SERP1 RNA expression patterns in the SERP1 knockout sublines. The products of RT-PCR performed on RNA isolated from the parental Huh7.5 cells (SERP1+/+) and SERP1 knockout sublines (SERP1+/−and SERP1−/−) using the primers in SERP1 exon 1 and exon 3, which generate a 697 bp product. The SERP1 mutant allele was amplified as a 563 bp product, where the SERP1 exon 1 region was deleted. (B) Sequencing analysis of the parental Huh7.5 cells and SERP1 knockout cell lines from the RT-PCR product. (C) Detection of SERP1 mRNA levels in the parental Huh7.5 cells and SERP1 knockout sublines by qRT-PCR. The expression values are normalized to β-actin expression. ***, p < 0.001 (Student’s t-test). (D) Kinetics of DENV-2 replication in the parental cells and SERP1 knockout sublines. The parental Huh7.5 cells and SERP1 knockout sublines were infected with DENV-2 (MOI = 1) at the indicated times. Infectious virus yield in the BHK21 clone 15 cells was quantified by plaque assay. The differences in virus yields between the parental cells (SERP1+/+) and SERP1 knockout cells (SERP1−/−) at 2 or 3 d.p.i. were analyzed using Student’s t-test. *, p < 0.05.

    Article Snippet: To further measure the protein level of SERP1 in the DENV-2 infected cells, we failed to detect the SERP1 protein expression in virus infected cells by either in-house mouse, rabbit, or commercial anti-SERP1 antibodies (Genetex, Abcam, Proteintech Group, Atlas antibodies), possibly because of the poor antigenicity of SERP1 (data not shown).

    Techniques: Knock-Out, CRISPR, RNA Expression, Reverse Transcription Polymerase Chain Reaction, Isolation, Mutagenesis, Sequencing, Quantitative RT-PCR, Expressing, Infection, Virus, Plaque Assay

    Figure 6. Overexpression of NS4B improves the virus replication in the Huh7.5 cells overexpressing SERP1. (A) Schematic diagram of HA C-terminal fusion constructs of NS2B and NS4B. The N-terminal 2K signal peptide was deleted (△2K-NS4B-HA). (B) Immunoblot analysis of HA-tagged NS2B and NS4B proteins in the parental cells and SERP1-overexpressing Huh7.5 cells. All of the fragments represented in panel (A) were cloned in pLKO-AS2 to tag the C-terminal end of each protein. Equal amounts of lysates were incubated with anti-HA magnetic beads, and the precipitates were analyzed by Western blot using an anti-HA antibody. The parental cells (C) and SERP1-overexpressing Huh7.5 cells (D) were co-transfected with WT replicon and plasmids encoding individual viral proteins, as indicated. The cell lysates were harvested 24, 48, 72, and 96 h after transfection, and the luciferase activity of the transfected cells was measured. The replication efficiency was calculated by determining the ratio of luciferase activity obtained at 48, 72, and 96 h, to the average value obtained from all of the replicon constructs at 24 h post-transfection. The error bars represent the standard errors of the means (SEMs) from three independent experiments. *, p < 0.05; ***, p < 0.001 (Student’s t-test).

    Journal: Viruses

    Article Title: A Dengue Virus Type 2 (DENV-2) NS4B-Interacting Host Factor, SERP1, Reduces DENV-2 Production by Suppressing Viral RNA Replication.

    doi: 10.3390/v11090787

    Figure Lengend Snippet: Figure 6. Overexpression of NS4B improves the virus replication in the Huh7.5 cells overexpressing SERP1. (A) Schematic diagram of HA C-terminal fusion constructs of NS2B and NS4B. The N-terminal 2K signal peptide was deleted (△2K-NS4B-HA). (B) Immunoblot analysis of HA-tagged NS2B and NS4B proteins in the parental cells and SERP1-overexpressing Huh7.5 cells. All of the fragments represented in panel (A) were cloned in pLKO-AS2 to tag the C-terminal end of each protein. Equal amounts of lysates were incubated with anti-HA magnetic beads, and the precipitates were analyzed by Western blot using an anti-HA antibody. The parental cells (C) and SERP1-overexpressing Huh7.5 cells (D) were co-transfected with WT replicon and plasmids encoding individual viral proteins, as indicated. The cell lysates were harvested 24, 48, 72, and 96 h after transfection, and the luciferase activity of the transfected cells was measured. The replication efficiency was calculated by determining the ratio of luciferase activity obtained at 48, 72, and 96 h, to the average value obtained from all of the replicon constructs at 24 h post-transfection. The error bars represent the standard errors of the means (SEMs) from three independent experiments. *, p < 0.05; ***, p < 0.001 (Student’s t-test).

    Article Snippet: To further measure the protein level of SERP1 in the DENV-2 infected cells, we failed to detect the SERP1 protein expression in virus infected cells by either in-house mouse, rabbit, or commercial anti-SERP1 antibodies (Genetex, Abcam, Proteintech Group, Atlas antibodies), possibly because of the poor antigenicity of SERP1 (data not shown).

    Techniques: Over Expression, Virus, Construct, Western Blot, Clone Assay, Incubation, Magnetic Beads, Transfection, Luciferase, Activity Assay

    Figure 7. Hypothetical model of SERP1-mediated DENV-2 infection. (A) SERP1 overexpression inhibits DENV-2 viral RNA replication and titers. (B) DENV-2 NS4B interacts with SERP1. DENV-2 NS4B may alleviate the inhibitory effect of SERP1 on DENV-2 viral replication via the interaction of NS4B with SERP1.

    Journal: Viruses

    Article Title: A Dengue Virus Type 2 (DENV-2) NS4B-Interacting Host Factor, SERP1, Reduces DENV-2 Production by Suppressing Viral RNA Replication.

    doi: 10.3390/v11090787

    Figure Lengend Snippet: Figure 7. Hypothetical model of SERP1-mediated DENV-2 infection. (A) SERP1 overexpression inhibits DENV-2 viral RNA replication and titers. (B) DENV-2 NS4B interacts with SERP1. DENV-2 NS4B may alleviate the inhibitory effect of SERP1 on DENV-2 viral replication via the interaction of NS4B with SERP1.

    Article Snippet: To further measure the protein level of SERP1 in the DENV-2 infected cells, we failed to detect the SERP1 protein expression in virus infected cells by either in-house mouse, rabbit, or commercial anti-SERP1 antibodies (Genetex, Abcam, Proteintech Group, Atlas antibodies), possibly because of the poor antigenicity of SERP1 (data not shown).

    Techniques: Infection, Over Expression