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    Thermo Fisher gene exp b2m hs00187842 m1
    Effect of tocilizumab on the expression of C5aR1, C5aR2, and C3aR in NSTEMI patients. The effect of tocilizumab, a monoclonal antibody inhibiting interleukin 6 receptor (IL-6R), on the expression of the three complement anaphylatoxin receptors [C5aR1 (A) , C5aR2 (B) , and C3aR (C) ] was investigated in patients with non-ST-elevation myocardial infarction (NSTEMI). mRNA levels were quantified by qPCR and related to the reference gene <t>beta-2-microglobulin.</t> The tocilizumab group (gray bars, n = 28) and the placebo group (white bars, n = 32) are presented at four different time-points. Baseline levels show the receptor expression at inclusion, i.e., after hospital admission, before treatment was given. Follow-up time points were day 2 and 3, and 6 months. A group of healthy individuals ( n = 15) were included as controls. The qPCR results were quantified using the 2 −ΔΔCT method, normalized to reference genes and presented as fold change with the healthy controls as calibrator. Data are given as median and 95% CI. * P
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    Images

    1) Product Images from "IL-6 Receptor Inhibition by Tocilizumab Attenuated Expression of C5a Receptor 1 and 2 in Non-ST-Elevation Myocardial Infarction"

    Article Title: IL-6 Receptor Inhibition by Tocilizumab Attenuated Expression of C5a Receptor 1 and 2 in Non-ST-Elevation Myocardial Infarction

    Journal: Frontiers in Immunology

    doi: 10.3389/fimmu.2018.02035

    Effect of tocilizumab on the expression of C5aR1, C5aR2, and C3aR in NSTEMI patients. The effect of tocilizumab, a monoclonal antibody inhibiting interleukin 6 receptor (IL-6R), on the expression of the three complement anaphylatoxin receptors [C5aR1 (A) , C5aR2 (B) , and C3aR (C) ] was investigated in patients with non-ST-elevation myocardial infarction (NSTEMI). mRNA levels were quantified by qPCR and related to the reference gene beta-2-microglobulin. The tocilizumab group (gray bars, n = 28) and the placebo group (white bars, n = 32) are presented at four different time-points. Baseline levels show the receptor expression at inclusion, i.e., after hospital admission, before treatment was given. Follow-up time points were day 2 and 3, and 6 months. A group of healthy individuals ( n = 15) were included as controls. The qPCR results were quantified using the 2 −ΔΔCT method, normalized to reference genes and presented as fold change with the healthy controls as calibrator. Data are given as median and 95% CI. * P
    Figure Legend Snippet: Effect of tocilizumab on the expression of C5aR1, C5aR2, and C3aR in NSTEMI patients. The effect of tocilizumab, a monoclonal antibody inhibiting interleukin 6 receptor (IL-6R), on the expression of the three complement anaphylatoxin receptors [C5aR1 (A) , C5aR2 (B) , and C3aR (C) ] was investigated in patients with non-ST-elevation myocardial infarction (NSTEMI). mRNA levels were quantified by qPCR and related to the reference gene beta-2-microglobulin. The tocilizumab group (gray bars, n = 28) and the placebo group (white bars, n = 32) are presented at four different time-points. Baseline levels show the receptor expression at inclusion, i.e., after hospital admission, before treatment was given. Follow-up time points were day 2 and 3, and 6 months. A group of healthy individuals ( n = 15) were included as controls. The qPCR results were quantified using the 2 −ΔΔCT method, normalized to reference genes and presented as fold change with the healthy controls as calibrator. Data are given as median and 95% CI. * P

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction

    2) Product Images from "p53-dependent and p53-independent anticancer effects of different histone deacetylase inhibitors"

    Article Title: p53-dependent and p53-independent anticancer effects of different histone deacetylase inhibitors

    Journal: British Journal of Cancer

    doi: 10.1038/bjc.2013.742

    Antineoplastic effects of vorinostat in combination with TRAIL in HCT-116 p53+ and p53− cells. Four hours after administration of vorinostat, cells were exposed to TRAIL for 48 h. Cell death and Δ ψ m were determined by flow-cytometric analyses of PI uptake or DiOC 6 (3) staining, respectively. Cells in sub-G1 phase were determined by flow-cytometric cell-cycle analysis. Means ±s.e.m. of each three separate measurements are shown.
    Figure Legend Snippet: Antineoplastic effects of vorinostat in combination with TRAIL in HCT-116 p53+ and p53− cells. Four hours after administration of vorinostat, cells were exposed to TRAIL for 48 h. Cell death and Δ ψ m were determined by flow-cytometric analyses of PI uptake or DiOC 6 (3) staining, respectively. Cells in sub-G1 phase were determined by flow-cytometric cell-cycle analysis. Means ±s.e.m. of each three separate measurements are shown.

    Techniques Used: Flow Cytometry, Staining, Cell Cycle Assay

    Antineoplastic effects of vorinostat in combination with bortezomib or CAPE in HCT-116 p53+ and p53− cells. ( A ) Four hours after administration of vorinostat, cells were exposed to bortezomib for 48 h. ( B ) One hour after administration of CAPE, cells were exposed to vorinostat for 48 h. Cell death and Δ ψ m were determined by flow-cytometric analyses of PI uptake or DiOC 6 (3) staining, respectively. Means ±s.e.m. of each three separate measurements are shown.
    Figure Legend Snippet: Antineoplastic effects of vorinostat in combination with bortezomib or CAPE in HCT-116 p53+ and p53− cells. ( A ) Four hours after administration of vorinostat, cells were exposed to bortezomib for 48 h. ( B ) One hour after administration of CAPE, cells were exposed to vorinostat for 48 h. Cell death and Δ ψ m were determined by flow-cytometric analyses of PI uptake or DiOC 6 (3) staining, respectively. Means ±s.e.m. of each three separate measurements are shown.

    Techniques Used: Flow Cytometry, Staining

    Antineoplastic effects of tenovin-1 in HCT-116 p53+ and p53− cells. Cells were exposed to tenovin-1 for 24 h (caspase-3 activity) or 48 h (other read-outs). z-VAD-fmk was applied 1 h before treatment with tenovin-1 ( A , C ). ( A ) Cell death and Δ ψ m were determined by flow-cytometric analyses of PI uptake or DiOC 6 (3) staining, respectively; caspase-3 activity was determined using the fluorogenic substrate Ac-DEVD-AMC, relative caspase-3 activities are the ratio of treated cells to untreated cells. ( B ) Pifithrin- α was applied 1 h before treatment with tenovin-1 or vorinostat; cell death was determined by flow-cytometric analysis of PI uptake. ( C ) Cell-cycle profiles were determined by flow cytometry. Means ±s.e.m. of each three separate measurements are shown. * P
    Figure Legend Snippet: Antineoplastic effects of tenovin-1 in HCT-116 p53+ and p53− cells. Cells were exposed to tenovin-1 for 24 h (caspase-3 activity) or 48 h (other read-outs). z-VAD-fmk was applied 1 h before treatment with tenovin-1 ( A , C ). ( A ) Cell death and Δ ψ m were determined by flow-cytometric analyses of PI uptake or DiOC 6 (3) staining, respectively; caspase-3 activity was determined using the fluorogenic substrate Ac-DEVD-AMC, relative caspase-3 activities are the ratio of treated cells to untreated cells. ( B ) Pifithrin- α was applied 1 h before treatment with tenovin-1 or vorinostat; cell death was determined by flow-cytometric analysis of PI uptake. ( C ) Cell-cycle profiles were determined by flow cytometry. Means ±s.e.m. of each three separate measurements are shown. * P

    Techniques Used: Activity Assay, Flow Cytometry, Staining, Cytometry

    Effects of HDACi and tenovin-1 on gene expression in HCT-116 p53+ and p53− cells. Cells were exposed to drugs for 24 h. ( A ) mRNA expression levels were determined by real-time RT–PCR and normalised to β -2-microglobulin mRNA levels. Means±s.e.m. of each two separate measurements are shown. ( B ) Cells were treated with 2 μ M HDACi or 10 μ M tenovin-1. Protein expression levels were determined by western blotting.
    Figure Legend Snippet: Effects of HDACi and tenovin-1 on gene expression in HCT-116 p53+ and p53− cells. Cells were exposed to drugs for 24 h. ( A ) mRNA expression levels were determined by real-time RT–PCR and normalised to β -2-microglobulin mRNA levels. Means±s.e.m. of each two separate measurements are shown. ( B ) Cells were treated with 2 μ M HDACi or 10 μ M tenovin-1. Protein expression levels were determined by western blotting.

    Techniques Used: Expressing, Quantitative RT-PCR, Western Blot

    Antineoplastic effects of HDACi in HCT-116 p53+ and p53− cells. Cells were exposed to HDACi or etoposide for 24 h ( E ) or 48 h ( A–D , F ); in the time-course experiments ( A , C ), cells were exposed to 5 μ M of vorinostat, entinostat and apicidin, 5 m M VPA or 100 μ M etoposide. z-VAD-fmk was applied 1 h before treatment with HDACi ( D , F ). ( A , D ) Cell death was determined by flow-cytometric analysis of PI uptake. ( B ) Cell viability was determined by MTT assay. ( C , D ) Δ ψ m was determined by flow-cytometric analysis of DiOC 6 (3) staining. ( E ) Caspase-3 activity was determined using the fluorogenic substrate Ac-DEVD-AMC, relative caspase-3 activities are the ratio of treated cells to untreated cells. ( F ) Cell-cycle profiles were determined by flow cytometry. Means ±s.e.m. of each three separate measurements are shown.
    Figure Legend Snippet: Antineoplastic effects of HDACi in HCT-116 p53+ and p53− cells. Cells were exposed to HDACi or etoposide for 24 h ( E ) or 48 h ( A–D , F ); in the time-course experiments ( A , C ), cells were exposed to 5 μ M of vorinostat, entinostat and apicidin, 5 m M VPA or 100 μ M etoposide. z-VAD-fmk was applied 1 h before treatment with HDACi ( D , F ). ( A , D ) Cell death was determined by flow-cytometric analysis of PI uptake. ( B ) Cell viability was determined by MTT assay. ( C , D ) Δ ψ m was determined by flow-cytometric analysis of DiOC 6 (3) staining. ( E ) Caspase-3 activity was determined using the fluorogenic substrate Ac-DEVD-AMC, relative caspase-3 activities are the ratio of treated cells to untreated cells. ( F ) Cell-cycle profiles were determined by flow cytometry. Means ±s.e.m. of each three separate measurements are shown.

    Techniques Used: Flow Cytometry, MTT Assay, Staining, Activity Assay, Cytometry

    Antineoplastic effects of vorinostat in combination with obatoclax in HCT-116 p53+ and p53− cells. One hour after administration of obatoclax, cells were exposed to vorinostat for 48 h. Cell death and Δ ψ m were determined by flow-cytometric analyses of PI uptake or DiOC 6 (3) staining, respectively. Means ±s.e.m. of each three separate measurements are shown.
    Figure Legend Snippet: Antineoplastic effects of vorinostat in combination with obatoclax in HCT-116 p53+ and p53− cells. One hour after administration of obatoclax, cells were exposed to vorinostat for 48 h. Cell death and Δ ψ m were determined by flow-cytometric analyses of PI uptake or DiOC 6 (3) staining, respectively. Means ±s.e.m. of each three separate measurements are shown.

    Techniques Used: Flow Cytometry, Staining

    3) Product Images from "Gene expression profile of muscle adaptation to high-intensity intermittent exercise training in young men"

    Article Title: Gene expression profile of muscle adaptation to high-intensity intermittent exercise training in young men

    Journal: Scientific Reports

    doi: 10.1038/s41598-018-35115-x

    The expression of CARNS1 ( a ), FGF6 ( b ), MYLK4 ( c) , PGK1 ( d ), PPP1R3C ( e ), and SGK1 ( f ) genes in the skeletal muscle before and after HIIT (n = 11). The mRNA levels of the six genes were determined by quantitative PCR and significantly increased after the HIIT. The bars represent means and SDs. The B2M mRNA was used as an internal control. * P
    Figure Legend Snippet: The expression of CARNS1 ( a ), FGF6 ( b ), MYLK4 ( c) , PGK1 ( d ), PPP1R3C ( e ), and SGK1 ( f ) genes in the skeletal muscle before and after HIIT (n = 11). The mRNA levels of the six genes were determined by quantitative PCR and significantly increased after the HIIT. The bars represent means and SDs. The B2M mRNA was used as an internal control. * P

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction

    4) Product Images from "CXCR3 Identifies Human Naive CD8+ T Cells with Enhanced Effector Differentiation Potential"

    Article Title: CXCR3 Identifies Human Naive CD8+ T Cells with Enhanced Effector Differentiation Potential

    Journal: The Journal of Immunology Author Choice

    doi: 10.4049/jimmunol.1901072

    CXCR3 identifies two subsets of T N cells in humans. ( A ) Representative flow cytometric analysis of CXCR3 expression on the surface of T N cells (CD45RO − CCR7 + CD27 + CD95 − ). Numbers indicate the percentage of cells in each gate. ( B ) Expression of CXCR3 relative to B2M mRNA in flow-sorted T N R3 − and T N R3 + cells ( n = 5). Each color indicates a different donor. Data are shown as mean ± SEM. n.d., not detected. ( C ) Frequency analysis of T cell subsets in PB samples from healthy individuals ( n = 26). Data are shown as mean ± SEM. T SCM (CD45RO − CCR7 + CD27 + CD95 + ); T CM , central T MEM (CD45RO + CCR7 + ); T EM , effector T MEM (CD45RO + CCR7 − ); and T TE , terminal effector T (CD45RO − CCR7 − ) cells. ( D ) tSNE map displaying the surface immunophenotypes of circulating T N R3 − , T N R3 + , and T MEM cells overlaid on the total CD8 + T cell population. Left, T N R3 − (red); right, T N R3 + (blue). Data were obtained using CyTOF. Individual markers are shown in ( E ). (E) Heatmap showing percent expression of the indicated markers among CD8 + T cell subsets identified in PB. Data were obtained using CyTOF. Subsets were defined as in (C). ( F ) Frequency analysis of T N R3 − and T N R3 + cells among total CD8 + T cells isolated from human tonsils ( n = 5), spleen ( n = 3), liver ( n = 3), gut ( n = 6), skin ( n = 5), and lungs ( n = 4). Data are shown as mean ± SEM. * p
    Figure Legend Snippet: CXCR3 identifies two subsets of T N cells in humans. ( A ) Representative flow cytometric analysis of CXCR3 expression on the surface of T N cells (CD45RO − CCR7 + CD27 + CD95 − ). Numbers indicate the percentage of cells in each gate. ( B ) Expression of CXCR3 relative to B2M mRNA in flow-sorted T N R3 − and T N R3 + cells ( n = 5). Each color indicates a different donor. Data are shown as mean ± SEM. n.d., not detected. ( C ) Frequency analysis of T cell subsets in PB samples from healthy individuals ( n = 26). Data are shown as mean ± SEM. T SCM (CD45RO − CCR7 + CD27 + CD95 + ); T CM , central T MEM (CD45RO + CCR7 + ); T EM , effector T MEM (CD45RO + CCR7 − ); and T TE , terminal effector T (CD45RO − CCR7 − ) cells. ( D ) tSNE map displaying the surface immunophenotypes of circulating T N R3 − , T N R3 + , and T MEM cells overlaid on the total CD8 + T cell population. Left, T N R3 − (red); right, T N R3 + (blue). Data were obtained using CyTOF. Individual markers are shown in ( E ). (E) Heatmap showing percent expression of the indicated markers among CD8 + T cell subsets identified in PB. Data were obtained using CyTOF. Subsets were defined as in (C). ( F ) Frequency analysis of T N R3 − and T N R3 + cells among total CD8 + T cells isolated from human tonsils ( n = 5), spleen ( n = 3), liver ( n = 3), gut ( n = 6), skin ( n = 5), and lungs ( n = 4). Data are shown as mean ± SEM. * p

    Techniques Used: Flow Cytometry, Expressing, Isolation

    5) Product Images from "Transcriptional Regulation of 15-Lipoxygenase Expression by Histone H3 Lysine 4 Methylation/Demethylation"

    Article Title: Transcriptional Regulation of 15-Lipoxygenase Expression by Histone H3 Lysine 4 Methylation/Demethylation

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0052703

    SMYD3 and SMCX regulate 15-LOX-1 expression in cultured HL-derived cells cells and prostate cancer cells. (A) Real-time PCR assay of 15-LOX-1 mRNA expression in L1236 and LNCaP cells treated with SMYD3 siRNAs or control siRNA (n = 4). The results were normalized to the mRNA level of beta-2 microglobulin. The efficiency of SMYD3 siRNA knocking down was evaluated using Western blots. Bar, SD; * p
    Figure Legend Snippet: SMYD3 and SMCX regulate 15-LOX-1 expression in cultured HL-derived cells cells and prostate cancer cells. (A) Real-time PCR assay of 15-LOX-1 mRNA expression in L1236 and LNCaP cells treated with SMYD3 siRNAs or control siRNA (n = 4). The results were normalized to the mRNA level of beta-2 microglobulin. The efficiency of SMYD3 siRNA knocking down was evaluated using Western blots. Bar, SD; * p

    Techniques Used: Expressing, Cell Culture, Derivative Assay, Real-time Polymerase Chain Reaction, Western Blot

    6) Product Images from "Species-Specific Differences in the Expression of the HNF1A, HNF1B and HNF4A Genes"

    Article Title: Species-Specific Differences in the Expression of the HNF1A, HNF1B and HNF4A Genes

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0007855

    The expression profile of the HNF1A gene in human, mouse and rat. The expression profile of the HNF1A gene in human, mouse and rat is given. The species is given on the X-axis and the relative quantification of each isoform relative to the B2M gene is given on the Y-axis. Each transcript is normalized to the levels of human HNF1A(A) in each tissue. HNF1A(A) is given by black bars, HNF1A(B) by grey bars and HNF1A(C) by white bars. Error bars indicate the upper and lower limits of transcript expression. a. islet, b. pancreas, c. liver, d. kidney.
    Figure Legend Snippet: The expression profile of the HNF1A gene in human, mouse and rat. The expression profile of the HNF1A gene in human, mouse and rat is given. The species is given on the X-axis and the relative quantification of each isoform relative to the B2M gene is given on the Y-axis. Each transcript is normalized to the levels of human HNF1A(A) in each tissue. HNF1A(A) is given by black bars, HNF1A(B) by grey bars and HNF1A(C) by white bars. Error bars indicate the upper and lower limits of transcript expression. a. islet, b. pancreas, c. liver, d. kidney.

    Techniques Used: Expressing

    The expression profile of the HNF4A gene in human, mouse and rat. The expression profile of the HNF4A gene in human, mouse and rat is given. The species and transcript identity is given on the X-axis and the relative quantification of each isoform relative to the B2M gene is given on the Y-axis. Each transcript is normalized to the levels of human HNF1A(A) in each tissue. Error bars indicate the upper and lower limits of transcript expression. a. islet, b. pancreas, c. liver, d. kidney.
    Figure Legend Snippet: The expression profile of the HNF4A gene in human, mouse and rat. The expression profile of the HNF4A gene in human, mouse and rat is given. The species and transcript identity is given on the X-axis and the relative quantification of each isoform relative to the B2M gene is given on the Y-axis. Each transcript is normalized to the levels of human HNF1A(A) in each tissue. Error bars indicate the upper and lower limits of transcript expression. a. islet, b. pancreas, c. liver, d. kidney.

    Techniques Used: Expressing

    The expression profile of the HNF1B gene in human, mouse and rat. The expression profile of the HNF1B gene in human, mouse and rat is given. The species and transcript identity identity is given on the X-axis and the relative quantification of each isoform relative to the B2M gene is given on the Y-axis. Each transcript is normalized to the levels of human HNF1A(A) in each tissue. Error bars indicate the upper and lower limits of transcript expression. a. islet, b. pancreas, c. liver, d. kidney.
    Figure Legend Snippet: The expression profile of the HNF1B gene in human, mouse and rat. The expression profile of the HNF1B gene in human, mouse and rat is given. The species and transcript identity identity is given on the X-axis and the relative quantification of each isoform relative to the B2M gene is given on the Y-axis. Each transcript is normalized to the levels of human HNF1A(A) in each tissue. Error bars indicate the upper and lower limits of transcript expression. a. islet, b. pancreas, c. liver, d. kidney.

    Techniques Used: Expressing

    7) Product Images from "Low level DUX4 expression disrupts myogenesis through deregulation of myogenic gene expression"

    Article Title: Low level DUX4 expression disrupts myogenesis through deregulation of myogenic gene expression

    Journal: Scientific Reports

    doi: 10.1038/s41598-018-35150-8

    Effects of DUX4 expression on the MYF5 −118 enhancer. ( A ) Map of the MYF5 upstream region is shown above, with three defined upstream enhancers (−136 kb, −118 kb, and −68 kb, determined by LiftOver of the corresponding mouse −130 kb, −111 kb, and −57 kb enhancers, respectively) highlighted in red outline. Sequence conservation (score of the phastCons algorithm using alignment of 20 mammals) is shown below the gene model. ChIP- and RNA-seq blowups are shown below, zooming in on two areas: the left contains the −118 enhancer region, which has a DUX4 ChIP-seq peak and evidence of DUX4-induced reverse transcription; the right is a control region, lacking DUX4 binding, and showing only transcription in the forward direction (of the PTPRQ gene). DUX4 ChIP-seq reads 14 are shown in green. ENCODE project RNA-seq in LHCN-M2 cells is shown in red (forward transcription above; reverse transcription below). Transcription of the exons of PTPRQ are apparent in the forward strand on the right panel. Below the ENCODE data is shown RNA-seq performed on LHCN-M2-iDUX4 cells in the absence of doxycycline, which shows a similar pattern to the parent LHCN-M2 cells. The last set of transcription tracks show LHCN-M2-iDUX4 cells exposed to doxycycline to induce DUX4. The forward strand expression of PTPRQ is still present, but the cells now show a new transcript adjacent to the −118 enhancer on the reverse strand, which we name DIME (DUX4-Induced MYF5 Enhancer), with two prominent exons. Gene models for PTPRQ and DIME are shown below, with qPCR primers designed for detecting spliced DIME transcript at bottom. ( B ) Expression of DIME transcript in LHCN-M2-iDUX4 cells induced with various concentrations of doxycycline for 14 hours. ( C ) Expression of the canonical DUX4 target genes, ZSCAN4 and MBD3L2 , in LHCN-M2-iDUX4 cells induced with various concentrations of doxycycline for 14 hours. ( D ) Luciferase assay in iC2C12-DUX4 and 293T-iDUX4 cells transfected with −118 kb or −136 kb MYF5 enhancer reporter constructs. Luciferase signal was measured 24 hours post induction (500 ng/mL doxycycline). Data are presented as mean ± SEM; *p
    Figure Legend Snippet: Effects of DUX4 expression on the MYF5 −118 enhancer. ( A ) Map of the MYF5 upstream region is shown above, with three defined upstream enhancers (−136 kb, −118 kb, and −68 kb, determined by LiftOver of the corresponding mouse −130 kb, −111 kb, and −57 kb enhancers, respectively) highlighted in red outline. Sequence conservation (score of the phastCons algorithm using alignment of 20 mammals) is shown below the gene model. ChIP- and RNA-seq blowups are shown below, zooming in on two areas: the left contains the −118 enhancer region, which has a DUX4 ChIP-seq peak and evidence of DUX4-induced reverse transcription; the right is a control region, lacking DUX4 binding, and showing only transcription in the forward direction (of the PTPRQ gene). DUX4 ChIP-seq reads 14 are shown in green. ENCODE project RNA-seq in LHCN-M2 cells is shown in red (forward transcription above; reverse transcription below). Transcription of the exons of PTPRQ are apparent in the forward strand on the right panel. Below the ENCODE data is shown RNA-seq performed on LHCN-M2-iDUX4 cells in the absence of doxycycline, which shows a similar pattern to the parent LHCN-M2 cells. The last set of transcription tracks show LHCN-M2-iDUX4 cells exposed to doxycycline to induce DUX4. The forward strand expression of PTPRQ is still present, but the cells now show a new transcript adjacent to the −118 enhancer on the reverse strand, which we name DIME (DUX4-Induced MYF5 Enhancer), with two prominent exons. Gene models for PTPRQ and DIME are shown below, with qPCR primers designed for detecting spliced DIME transcript at bottom. ( B ) Expression of DIME transcript in LHCN-M2-iDUX4 cells induced with various concentrations of doxycycline for 14 hours. ( C ) Expression of the canonical DUX4 target genes, ZSCAN4 and MBD3L2 , in LHCN-M2-iDUX4 cells induced with various concentrations of doxycycline for 14 hours. ( D ) Luciferase assay in iC2C12-DUX4 and 293T-iDUX4 cells transfected with −118 kb or −136 kb MYF5 enhancer reporter constructs. Luciferase signal was measured 24 hours post induction (500 ng/mL doxycycline). Data are presented as mean ± SEM; *p

    Techniques Used: Expressing, Sequencing, Chromatin Immunoprecipitation, RNA Sequencing Assay, Binding Assay, Real-time Polymerase Chain Reaction, Luciferase, Transfection, Construct

    8) Product Images from "Human Cytomegalovirus Downregulates Expression of Receptors for Platelet-Derived Growth Factor by Smooth Muscle Cells ▿"

    Article Title: Human Cytomegalovirus Downregulates Expression of Receptors for Platelet-Derived Growth Factor by Smooth Muscle Cells ▿

    Journal:

    doi: 10.1128/JVI.02197-06

    Downregulation of PDGFR expression in HCMV (AD169)-infected SMCs is dependent on the expression of IE and/or E viral genes. (A and B) Expression of PDGFR-α (A) and -β (B) following infection of SMCs with HCMV, HCMV inactivated by UV irradiation
    Figure Legend Snippet: Downregulation of PDGFR expression in HCMV (AD169)-infected SMCs is dependent on the expression of IE and/or E viral genes. (A and B) Expression of PDGFR-α (A) and -β (B) following infection of SMCs with HCMV, HCMV inactivated by UV irradiation

    Techniques Used: Expressing, Infection, Irradiation

    Time dependency of the reduction in PDGFR-α and -β expression in HCMV-infected SMCs. The expression of PDGFR-α (A) and PDGFR-β (B) on uninfected and HCMV-infected SMCs was analyzed at 1, 3, and 6 dpi by flow cytometry.
    Figure Legend Snippet: Time dependency of the reduction in PDGFR-α and -β expression in HCMV-infected SMCs. The expression of PDGFR-α (A) and PDGFR-β (B) on uninfected and HCMV-infected SMCs was analyzed at 1, 3, and 6 dpi by flow cytometry.

    Techniques Used: Expressing, Infection, Flow Cytometry, Cytometry

    Infection with HCMV results in downregulation of the expression of PDGFR-α and -β on the surface of SMCs. (A and B) The dose-dependent effects of infection with AD169 (at an MOI of 0.01 to 10) on SMC expression of PDGFR-α (A) and
    Figure Legend Snippet: Infection with HCMV results in downregulation of the expression of PDGFR-α and -β on the surface of SMCs. (A and B) The dose-dependent effects of infection with AD169 (at an MOI of 0.01 to 10) on SMC expression of PDGFR-α (A) and

    Techniques Used: Infection, Expressing

    HCMV reduces the total levels of expression of PDGFR-α and -β by SMCs and fibroblasts. (A to D) Following infection with HCMV at an MOI of 1, total cellular protein was extracted and Western blotting was performed at 3 dpi with polyclonal
    Figure Legend Snippet: HCMV reduces the total levels of expression of PDGFR-α and -β by SMCs and fibroblasts. (A to D) Following infection with HCMV at an MOI of 1, total cellular protein was extracted and Western blotting was performed at 3 dpi with polyclonal

    Techniques Used: Expressing, Infection, Western Blot

    HCMV apparently inhibits transcription of the genes encoding PDGFR-α and -β in SMCs. PDGFR-α and PDGFR-β mRNA levels were determined by analysis of total cellular mRNA by real-time PCR, and the data are presented as means
    Figure Legend Snippet: HCMV apparently inhibits transcription of the genes encoding PDGFR-α and -β in SMCs. PDGFR-α and PDGFR-β mRNA levels were determined by analysis of total cellular mRNA by real-time PCR, and the data are presented as means

    Techniques Used: Real-time Polymerase Chain Reaction

    9) Product Images from "Low level DUX4 expression disrupts myogenesis through deregulation of myogenic gene expression"

    Article Title: Low level DUX4 expression disrupts myogenesis through deregulation of myogenic gene expression

    Journal: Scientific Reports

    doi: 10.1038/s41598-018-35150-8

    Effects of DUX4 expression on the MYF5 −118 enhancer. ( A ) Map of the MYF5 upstream region is shown above, with three defined upstream enhancers (−136 kb, −118 kb, and −68 kb, determined by LiftOver of the corresponding mouse −130 kb, −111 kb, and −57 kb enhancers, respectively) highlighted in red outline. Sequence conservation (score of the phastCons algorithm using alignment of 20 mammals) is shown below the gene model. ChIP- and RNA-seq blowups are shown below, zooming in on two areas: the left contains the −118 enhancer region, which has a DUX4 ChIP-seq peak and evidence of DUX4-induced reverse transcription; the right is a control region, lacking DUX4 binding, and showing only transcription in the forward direction (of the PTPRQ are shown in green. ENCODE project RNA-seq in LHCN-M2 cells is shown in red (forward transcription above; reverse transcription below). Transcription of the exons of PTPRQ are apparent in the forward strand on the right panel. Below the ENCODE data is shown RNA-seq performed on LHCN-M2-iDUX4 cells in the absence of doxycycline, which shows a similar pattern to the parent LHCN-M2 cells. The last set of transcription tracks show LHCN-M2-iDUX4 cells exposed to doxycycline to induce DUX4. The forward strand expression of PTPRQ is still present, but the cells now show a new transcript adjacent to the −118 enhancer on the reverse strand, which we name DIME (DUX4-Induced MYF5 Enhancer), with two prominent exons. Gene models for PTPRQ and DIME are shown below, with qPCR primers designed for detecting spliced DIME transcript at bottom. ( B ) Expression of DIME transcript in LHCN-M2-iDUX4 cells induced with various concentrations of doxycycline for 14 hours. ( C ) Expression of the canonical DUX4 target genes, ZSCAN4 and MBD3L2 , in LHCN-M2-iDUX4 cells induced with various concentrations of doxycycline for 14 hours. ( D ) Luciferase assay in iC2C12-DUX4 and 293T-iDUX4 cells transfected with −118 kb or −136 kb MYF5 enhancer reporter constructs. Luciferase signal was measured 24 hours post induction (500 ng/mL doxycycline). Data are presented as mean ± SEM; *p
    Figure Legend Snippet: Effects of DUX4 expression on the MYF5 −118 enhancer. ( A ) Map of the MYF5 upstream region is shown above, with three defined upstream enhancers (−136 kb, −118 kb, and −68 kb, determined by LiftOver of the corresponding mouse −130 kb, −111 kb, and −57 kb enhancers, respectively) highlighted in red outline. Sequence conservation (score of the phastCons algorithm using alignment of 20 mammals) is shown below the gene model. ChIP- and RNA-seq blowups are shown below, zooming in on two areas: the left contains the −118 enhancer region, which has a DUX4 ChIP-seq peak and evidence of DUX4-induced reverse transcription; the right is a control region, lacking DUX4 binding, and showing only transcription in the forward direction (of the PTPRQ are shown in green. ENCODE project RNA-seq in LHCN-M2 cells is shown in red (forward transcription above; reverse transcription below). Transcription of the exons of PTPRQ are apparent in the forward strand on the right panel. Below the ENCODE data is shown RNA-seq performed on LHCN-M2-iDUX4 cells in the absence of doxycycline, which shows a similar pattern to the parent LHCN-M2 cells. The last set of transcription tracks show LHCN-M2-iDUX4 cells exposed to doxycycline to induce DUX4. The forward strand expression of PTPRQ is still present, but the cells now show a new transcript adjacent to the −118 enhancer on the reverse strand, which we name DIME (DUX4-Induced MYF5 Enhancer), with two prominent exons. Gene models for PTPRQ and DIME are shown below, with qPCR primers designed for detecting spliced DIME transcript at bottom. ( B ) Expression of DIME transcript in LHCN-M2-iDUX4 cells induced with various concentrations of doxycycline for 14 hours. ( C ) Expression of the canonical DUX4 target genes, ZSCAN4 and MBD3L2 , in LHCN-M2-iDUX4 cells induced with various concentrations of doxycycline for 14 hours. ( D ) Luciferase assay in iC2C12-DUX4 and 293T-iDUX4 cells transfected with −118 kb or −136 kb MYF5 enhancer reporter constructs. Luciferase signal was measured 24 hours post induction (500 ng/mL doxycycline). Data are presented as mean ± SEM; *p

    Techniques Used: Expressing, Sequencing, Chromatin Immunoprecipitation, RNA Sequencing Assay, Binding Assay, Real-time Polymerase Chain Reaction, Luciferase, Transfection, Construct

    Myogenic genes perturbed by DUX4 within 6 hours. Triplicate RNA-seq profiles are rendered as a heat map. LHCN-M2-iDUX4 cells were induced for 6 hours with 250 ng/mL doxycycline. Downregulated targets are shown above; upregulated targets shown below. This rapid alteration in key myogenic regulators demonstrates that the myogenic program is deeply perturbed within 6 hours of DUX4 expression. The green box to the right of the heat map indicates genes with DUX4-binding sites identified by ChIP-seq within 10 kb of their TSS.
    Figure Legend Snippet: Myogenic genes perturbed by DUX4 within 6 hours. Triplicate RNA-seq profiles are rendered as a heat map. LHCN-M2-iDUX4 cells were induced for 6 hours with 250 ng/mL doxycycline. Downregulated targets are shown above; upregulated targets shown below. This rapid alteration in key myogenic regulators demonstrates that the myogenic program is deeply perturbed within 6 hours of DUX4 expression. The green box to the right of the heat map indicates genes with DUX4-binding sites identified by ChIP-seq within 10 kb of their TSS.

    Techniques Used: RNA Sequencing Assay, Expressing, Binding Assay, Chromatin Immunoprecipitation

    10) Product Images from "Mapping of the UGT1A locus identifies an uncommon coding variant that affects mRNA expression and protects from bladder cancer"

    Article Title: Mapping of the UGT1A locus identifies an uncommon coding variant that affects mRNA expression and protects from bladder cancer

    Journal: Human Molecular Genetics

    doi: 10.1093/hmg/ddr619

    Expression of the UGT1A6 protein and UGT1A6.1 splicing form in normal human tissues. ( A ). ( B ) mRNA expression in a panel of normal human tissues. Expression values were normalized by two endogenous controls, beta-2-microglobulin ( B2M ) and cyclophilin ( PPIA ). Expression values are presented on log2 scale in relation to the the expression level in the liver. ( C ) mRNA expression in 88 normal liver tissue samples from healthy controls. Expression values of the total set passed the normally test and were analyzed with the unpaired two-sided t -test. The results are presented on the log2 scale in relation to the mean of the GG group.
    Figure Legend Snippet: Expression of the UGT1A6 protein and UGT1A6.1 splicing form in normal human tissues. ( A ). ( B ) mRNA expression in a panel of normal human tissues. Expression values were normalized by two endogenous controls, beta-2-microglobulin ( B2M ) and cyclophilin ( PPIA ). Expression values are presented on log2 scale in relation to the the expression level in the liver. ( C ) mRNA expression in 88 normal liver tissue samples from healthy controls. Expression values of the total set passed the normally test and were analyzed with the unpaired two-sided t -test. The results are presented on the log2 scale in relation to the mean of the GG group.

    Techniques Used: Expressing

    11) Product Images from "A Role for Iodide and Thyroglobulin in Modulating the Function of Human Immune Cells"

    Article Title: A Role for Iodide and Thyroglobulin in Modulating the Function of Human Immune Cells

    Journal: Frontiers in Immunology

    doi: 10.3389/fimmu.2017.01573

    Human immune cells express and regulate iodide transporters, thyroglobulin, and thyroid peroxidase. (A) Leukocytes were left unstimulated (US) (−) or activated (+) with PMA and ionomycin for 18 h, total RNA was extracted, and then the cDNA from samples was amplified with PCR. Shown is DNA gel electrophoresis image of two representative donors. (B) Leukocytes mRNA was amplified using real-time quantitative PCR, and then each gene was normalized to internal B2M control. Fold increase over US controls was graphed ± SEM of nine independent donors. (C) Leukocytes were stained with no antibody (control), NIS, or PENDRIN antibodies. The cells were then stained with secondary Alexa-647 and primary-conjugated CD45 Krome-orange antibodies. Leukocyte subsets (granulocytes, monocytes, and lymphocytes) were gated on based on CD45 and side-scatter characteristics. The gated subset histograms are shown as cell counts and antibody staining intensity representative of six donors. (D) Median fluorescent intensity (MFI) values from panel (C) were subtracted from background staining and then graphed ± SEM of six to seven independent donors.
    Figure Legend Snippet: Human immune cells express and regulate iodide transporters, thyroglobulin, and thyroid peroxidase. (A) Leukocytes were left unstimulated (US) (−) or activated (+) with PMA and ionomycin for 18 h, total RNA was extracted, and then the cDNA from samples was amplified with PCR. Shown is DNA gel electrophoresis image of two representative donors. (B) Leukocytes mRNA was amplified using real-time quantitative PCR, and then each gene was normalized to internal B2M control. Fold increase over US controls was graphed ± SEM of nine independent donors. (C) Leukocytes were stained with no antibody (control), NIS, or PENDRIN antibodies. The cells were then stained with secondary Alexa-647 and primary-conjugated CD45 Krome-orange antibodies. Leukocyte subsets (granulocytes, monocytes, and lymphocytes) were gated on based on CD45 and side-scatter characteristics. The gated subset histograms are shown as cell counts and antibody staining intensity representative of six donors. (D) Median fluorescent intensity (MFI) values from panel (C) were subtracted from background staining and then graphed ± SEM of six to seven independent donors.

    Techniques Used: Amplification, Polymerase Chain Reaction, DNA Gel Electrophoresis, Real-time Polymerase Chain Reaction, Staining

    12) Product Images from "Gene expression profile of muscle adaptation to high-intensity intermittent exercise training in young men"

    Article Title: Gene expression profile of muscle adaptation to high-intensity intermittent exercise training in young men

    Journal: Scientific Reports

    doi: 10.1038/s41598-018-35115-x

    The expression of CARNS1 ( a ), FGF6 ( b ), MYLK4 ( c) , PGK1 ( d ), PPP1R3C ( e ), and SGK1 ( f ) genes in the skeletal muscle before and after HIIT (n = 11). The mRNA levels of the six genes were determined by quantitative PCR and significantly increased after the HIIT. The bars represent means and SDs. The B2M mRNA was used as an internal control. * P
    Figure Legend Snippet: The expression of CARNS1 ( a ), FGF6 ( b ), MYLK4 ( c) , PGK1 ( d ), PPP1R3C ( e ), and SGK1 ( f ) genes in the skeletal muscle before and after HIIT (n = 11). The mRNA levels of the six genes were determined by quantitative PCR and significantly increased after the HIIT. The bars represent means and SDs. The B2M mRNA was used as an internal control. * P

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction

    13) Product Images from "IL-6 Receptor Inhibition by Tocilizumab Attenuated Expression of C5a Receptor 1 and 2 in Non-ST-Elevation Myocardial Infarction"

    Article Title: IL-6 Receptor Inhibition by Tocilizumab Attenuated Expression of C5a Receptor 1 and 2 in Non-ST-Elevation Myocardial Infarction

    Journal: Frontiers in Immunology

    doi: 10.3389/fimmu.2018.02035

    Effect of tocilizumab on the expression of C5aR1, C5aR2, and C3aR in NSTEMI patients. The effect of tocilizumab, a monoclonal antibody inhibiting interleukin 6 receptor (IL-6R), on the expression of the three complement anaphylatoxin receptors [C5aR1 (A) , C5aR2 (B) , and C3aR (C) ] was investigated in patients with non-ST-elevation myocardial infarction (NSTEMI). mRNA levels were quantified by qPCR and related to the reference gene beta-2-microglobulin. The tocilizumab group (gray bars, n = 28) and the placebo group (white bars, n = 32) are presented at four different time-points. Baseline levels show the receptor expression at inclusion, i.e., after hospital admission, before treatment was given. Follow-up time points were day 2 and 3, and 6 months. A group of healthy individuals ( n = 15) were included as controls. The qPCR results were quantified using the 2 −ΔΔCT method, normalized to reference genes and presented as fold change with the healthy controls as calibrator. Data are given as median and 95% CI. * P
    Figure Legend Snippet: Effect of tocilizumab on the expression of C5aR1, C5aR2, and C3aR in NSTEMI patients. The effect of tocilizumab, a monoclonal antibody inhibiting interleukin 6 receptor (IL-6R), on the expression of the three complement anaphylatoxin receptors [C5aR1 (A) , C5aR2 (B) , and C3aR (C) ] was investigated in patients with non-ST-elevation myocardial infarction (NSTEMI). mRNA levels were quantified by qPCR and related to the reference gene beta-2-microglobulin. The tocilizumab group (gray bars, n = 28) and the placebo group (white bars, n = 32) are presented at four different time-points. Baseline levels show the receptor expression at inclusion, i.e., after hospital admission, before treatment was given. Follow-up time points were day 2 and 3, and 6 months. A group of healthy individuals ( n = 15) were included as controls. The qPCR results were quantified using the 2 −ΔΔCT method, normalized to reference genes and presented as fold change with the healthy controls as calibrator. Data are given as median and 95% CI. * P

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction

    14) Product Images from "Age-related changes in expression and function of Toll-like receptors in human skin"

    Article Title: Age-related changes in expression and function of Toll-like receptors in human skin

    Journal: Development (Cambridge, England)

    doi: 10.1242/dev.083477

    TLR expression profile of human skin before and after birth. ( A ) Embryonic (9-11 weeks EGA), fetal (12-13 weeks EGA) and adult (18-45 years) skin specimens were investigated ( n =6-9 donors/group) for the indicated TLR expression levels using quantitative RT-PCR. Reactions were executed in duplicates and data were normalized to the housekeeping gene B2M. ( B ) Epidermis was separated from the dermis of skin samples from infants (3-10 months), children (5-12 years) and adults (18-31 years) ( n =4-8 donors/group) using ammonium thiocyanate. Indicated TLR expression levels were determined using quantitative RT-PCR. Reactions were executed in duplicates and data were normalized to the housekeeping gene GAPDH. Bars represent the mean of investigated groups. The x - and y -axis indicate selected age groups and relative mRNA expression, respectively. * P
    Figure Legend Snippet: TLR expression profile of human skin before and after birth. ( A ) Embryonic (9-11 weeks EGA), fetal (12-13 weeks EGA) and adult (18-45 years) skin specimens were investigated ( n =6-9 donors/group) for the indicated TLR expression levels using quantitative RT-PCR. Reactions were executed in duplicates and data were normalized to the housekeeping gene B2M. ( B ) Epidermis was separated from the dermis of skin samples from infants (3-10 months), children (5-12 years) and adults (18-31 years) ( n =4-8 donors/group) using ammonium thiocyanate. Indicated TLR expression levels were determined using quantitative RT-PCR. Reactions were executed in duplicates and data were normalized to the housekeeping gene GAPDH. Bars represent the mean of investigated groups. The x - and y -axis indicate selected age groups and relative mRNA expression, respectively. * P

    Techniques Used: Expressing, Quantitative RT-PCR

    Related Articles

    Amplification:

    Article Title: Regulator of Cell Cycle (RGCC) Expression during the Progression of Alzheimer's Disease
    Article Snippet: .. Samples were assayed on a real-time (RT)-PCR cycler (ABI 7500; Applied Biosystems, Foster City, CA, USA) in 96-well optical plates as described previously , . qPCR was performed using TaqMan hydrolysis probe primer sets (Applied Biosystems) specific for amplification of the following human transcripts: rgcc (probe set Hs00204129_m1), tumor protein p53 ( tp53 ; Hs01034249_m1), and cdk1 (Hs00938777_m1). .. A primer set specific for human glyceraldehyde 3-phosphate dehydrogenase ( gapdh ) (Hs02758991_g1) was used as a control housekeeping transcript.

    Quantitative RT-PCR:

    Article Title: Regulator of Cell Cycle (RGCC) Expression during the Progression of Alzheimer's Disease
    Article Snippet: .. Samples were assayed on a real-time (RT)-PCR cycler (ABI 7500; Applied Biosystems, Foster City, CA, USA) in 96-well optical plates as described previously , . qPCR was performed using TaqMan hydrolysis probe primer sets (Applied Biosystems) specific for amplification of the following human transcripts: rgcc (probe set Hs00204129_m1), tumor protein p53 ( tp53 ; Hs01034249_m1), and cdk1 (Hs00938777_m1). .. A primer set specific for human glyceraldehyde 3-phosphate dehydrogenase ( gapdh ) (Hs02758991_g1) was used as a control housekeeping transcript.

    Real-time Polymerase Chain Reaction:

    Article Title: MicroRNA expression analysis identifies a subset of downregulated miRNAs in ALS motor neuron progenitors
    Article Snippet: .. We assayed the gene expression of STX1A (Hs00270282_m1), SIRT1 (Hs01009006_m1), TP53 (Hs01034249_m1), SYT1 (Hs00194572_m1), XIAP (Hs00745222_s1), MDM2 (Hs00540450_s1) and ATF3 (Hs00231069_m1) by quantitative real-time PCR analysis by means of the ΔΔCt method. .. The expression levels of each gene were normalized to the average levels of the housekeeping gene 18S (Hs99999901_s1) and referred to the relevant control samples.

    Article Title: LRH-1 drives colon cancer cell growth by repressing the expression of the CDKN1A gene in a p53-dependent manner
    Article Snippet: .. Gene expression analyses were carried out using an Applied Biosystems 7900HT Fast Real-Time PCR System with TaqMan® gene expression assays (Applied Biosystems, UK) for LRH-1 (Hs00892377_m1), CDKN1A (Hs00355782_m1), TP53 (Hs01034249_m1) and GAPDH (Hs99999905_m1). .. Electrophoretic mobility shift assay (EMSA) In vitro transcription of LRH-1 and LRH-1 G95W expression plasmids was performed with the T7 RNA polymerase kit (Invitrogen).

    Article Title: Regulator of Cell Cycle (RGCC) Expression during the Progression of Alzheimer's Disease
    Article Snippet: .. Samples were assayed on a real-time (RT)-PCR cycler (ABI 7500; Applied Biosystems, Foster City, CA, USA) in 96-well optical plates as described previously , . qPCR was performed using TaqMan hydrolysis probe primer sets (Applied Biosystems) specific for amplification of the following human transcripts: rgcc (probe set Hs00204129_m1), tumor protein p53 ( tp53 ; Hs01034249_m1), and cdk1 (Hs00938777_m1). .. A primer set specific for human glyceraldehyde 3-phosphate dehydrogenase ( gapdh ) (Hs02758991_g1) was used as a control housekeeping transcript.

    other:

    Article Title: Chemical Library Screening and Structure-Function Relationship Studies Identify Bisacodyl as a Potent and Selective Cytotoxic Agent Towards Quiescent Human Glioblastoma Tumor Stem-Like Cells
    Article Snippet: Individual assay IDs are as follows: p53: Hs 01034249-m1; BAX: Hs00180269-m1; p21: Hs 00355782-m1.

    Article Title: Identification of DJ-1/PARK-7 as a determinant of stroma-dependent and TNF-?-induced apoptosis in MDS using mass spectrometry and phosphopeptide analysis
    Article Snippet: ABI part numbers for the assays were as follows: DJ-1, Hs00697109_m1; p53, Hs01034249_m1; β-actin, Hs00607939.

    Expressing:

    Article Title: MicroRNA expression analysis identifies a subset of downregulated miRNAs in ALS motor neuron progenitors
    Article Snippet: .. We assayed the gene expression of STX1A (Hs00270282_m1), SIRT1 (Hs01009006_m1), TP53 (Hs01034249_m1), SYT1 (Hs00194572_m1), XIAP (Hs00745222_s1), MDM2 (Hs00540450_s1) and ATF3 (Hs00231069_m1) by quantitative real-time PCR analysis by means of the ΔΔCt method. .. The expression levels of each gene were normalized to the average levels of the housekeeping gene 18S (Hs99999901_s1) and referred to the relevant control samples.

    Article Title: LRH-1 drives colon cancer cell growth by repressing the expression of the CDKN1A gene in a p53-dependent manner
    Article Snippet: .. Gene expression analyses were carried out using an Applied Biosystems 7900HT Fast Real-Time PCR System with TaqMan® gene expression assays (Applied Biosystems, UK) for LRH-1 (Hs00892377_m1), CDKN1A (Hs00355782_m1), TP53 (Hs01034249_m1) and GAPDH (Hs99999905_m1). .. Electrophoretic mobility shift assay (EMSA) In vitro transcription of LRH-1 and LRH-1 G95W expression plasmids was performed with the T7 RNA polymerase kit (Invitrogen).

    Article Title: MiR-21, miR-34a, miR-125b, miR-181d and miR-648 levels inversely correlate with MGMT and TP53 expression in primary glioblastoma patients
    Article Snippet: .. The cDNA samples were kept frozen at –20°C. mRNA expression levels were measured using standard TaqMan Gene Expression Assays (Applied Biosystems, Foster City, CA, USA): tumor protein TP53 (TP53 , Hs01034249_m1), methylguanine-DNA methyltransferase (MGMT , Hs01037698_m1), and glyceraldehydes-3-phosphate dehydrogenase (GAPDH , Hs99999905_m1) as the endogenous control. .. TaqMan PCR assays were performed in 10-μl reactions using 50 ng cDNA, 5 μl KAPA PROBE FAST qPCR Kit Master Mix ABI Prism (Kapa Biosystems), and 0.5 μl of the appropriate TaqMan Gene Expression Assay.

    Reverse Transcription Polymerase Chain Reaction:

    Article Title: Single CpG hypermethylation, allele methylation errors, and decreased expression of multiple tumor suppressor genes in normal body cells of mutation‐negative early‐onset and high‐risk breast cancer patients
    Article Snippet: .. RT PCR was performed with TaqMan Fast Advanced Master Mix (ThermoScientific), 50 ng cDNA per reaction, and pre‐validated TaqMan assays for BRCA1 (HS01556193_m1), BRCA2 (Hs00609073_m1), RAD51C (Hs00427442_m1), ATM (Hs00175892_m1), PTEN (Hs02621230_s1), TP53 (Hs01034249_m1), MLH1 (Hs00979919_m1), and RB1 (Hs01078066_m1), according to the manufacturer's protocol. .. RT PCR reactions were run on ABI Viia7 System (Applied Biosystems, Massachusetts, USA).

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    Thermo Fisher gene exp b2m hs00187842 m1
    Effect of tocilizumab on the expression of C5aR1, C5aR2, and C3aR in NSTEMI patients. The effect of tocilizumab, a monoclonal antibody inhibiting interleukin 6 receptor (IL-6R), on the expression of the three complement anaphylatoxin receptors [C5aR1 (A) , C5aR2 (B) , and C3aR (C) ] was investigated in patients with non-ST-elevation myocardial infarction (NSTEMI). mRNA levels were quantified by qPCR and related to the reference gene <t>beta-2-microglobulin.</t> The tocilizumab group (gray bars, n = 28) and the placebo group (white bars, n = 32) are presented at four different time-points. Baseline levels show the receptor expression at inclusion, i.e., after hospital admission, before treatment was given. Follow-up time points were day 2 and 3, and 6 months. A group of healthy individuals ( n = 15) were included as controls. The qPCR results were quantified using the 2 −ΔΔCT method, normalized to reference genes and presented as fold change with the healthy controls as calibrator. Data are given as median and 95% CI. * P
    Gene Exp B2m Hs00187842 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 32 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Effect of tocilizumab on the expression of C5aR1, C5aR2, and C3aR in NSTEMI patients. The effect of tocilizumab, a monoclonal antibody inhibiting interleukin 6 receptor (IL-6R), on the expression of the three complement anaphylatoxin receptors [C5aR1 (A) , C5aR2 (B) , and C3aR (C) ] was investigated in patients with non-ST-elevation myocardial infarction (NSTEMI). mRNA levels were quantified by qPCR and related to the reference gene beta-2-microglobulin. The tocilizumab group (gray bars, n = 28) and the placebo group (white bars, n = 32) are presented at four different time-points. Baseline levels show the receptor expression at inclusion, i.e., after hospital admission, before treatment was given. Follow-up time points were day 2 and 3, and 6 months. A group of healthy individuals ( n = 15) were included as controls. The qPCR results were quantified using the 2 −ΔΔCT method, normalized to reference genes and presented as fold change with the healthy controls as calibrator. Data are given as median and 95% CI. * P

    Journal: Frontiers in Immunology

    Article Title: IL-6 Receptor Inhibition by Tocilizumab Attenuated Expression of C5a Receptor 1 and 2 in Non-ST-Elevation Myocardial Infarction

    doi: 10.3389/fimmu.2018.02035

    Figure Lengend Snippet: Effect of tocilizumab on the expression of C5aR1, C5aR2, and C3aR in NSTEMI patients. The effect of tocilizumab, a monoclonal antibody inhibiting interleukin 6 receptor (IL-6R), on the expression of the three complement anaphylatoxin receptors [C5aR1 (A) , C5aR2 (B) , and C3aR (C) ] was investigated in patients with non-ST-elevation myocardial infarction (NSTEMI). mRNA levels were quantified by qPCR and related to the reference gene beta-2-microglobulin. The tocilizumab group (gray bars, n = 28) and the placebo group (white bars, n = 32) are presented at four different time-points. Baseline levels show the receptor expression at inclusion, i.e., after hospital admission, before treatment was given. Follow-up time points were day 2 and 3, and 6 months. A group of healthy individuals ( n = 15) were included as controls. The qPCR results were quantified using the 2 −ΔΔCT method, normalized to reference genes and presented as fold change with the healthy controls as calibrator. Data are given as median and 95% CI. * P

    Article Snippet: Beta-2-microglobulin (HS 00187842) was stably expressed and used as endogenous control.

    Techniques: Expressing, Real-time Polymerase Chain Reaction

    Antineoplastic effects of vorinostat in combination with TRAIL in HCT-116 p53+ and p53− cells. Four hours after administration of vorinostat, cells were exposed to TRAIL for 48 h. Cell death and Δ ψ m were determined by flow-cytometric analyses of PI uptake or DiOC 6 (3) staining, respectively. Cells in sub-G1 phase were determined by flow-cytometric cell-cycle analysis. Means ±s.e.m. of each three separate measurements are shown.

    Journal: British Journal of Cancer

    Article Title: p53-dependent and p53-independent anticancer effects of different histone deacetylase inhibitors

    doi: 10.1038/bjc.2013.742

    Figure Lengend Snippet: Antineoplastic effects of vorinostat in combination with TRAIL in HCT-116 p53+ and p53− cells. Four hours after administration of vorinostat, cells were exposed to TRAIL for 48 h. Cell death and Δ ψ m were determined by flow-cytometric analyses of PI uptake or DiOC 6 (3) staining, respectively. Cells in sub-G1 phase were determined by flow-cytometric cell-cycle analysis. Means ±s.e.m. of each three separate measurements are shown.

    Article Snippet: Reactions were done in duplicate using Applied Biosystems Gene Expression Assays (p53: Hs01034249_m1; MDM2: Hs99999008_m1; MDM4: Hs00159092_m1; p21: Hs00355782_m1; β -2-microglobulin: Hs00187842_m1) and Universal PCR Master Mix.

    Techniques: Flow Cytometry, Staining, Cell Cycle Assay

    Antineoplastic effects of vorinostat in combination with bortezomib or CAPE in HCT-116 p53+ and p53− cells. ( A ) Four hours after administration of vorinostat, cells were exposed to bortezomib for 48 h. ( B ) One hour after administration of CAPE, cells were exposed to vorinostat for 48 h. Cell death and Δ ψ m were determined by flow-cytometric analyses of PI uptake or DiOC 6 (3) staining, respectively. Means ±s.e.m. of each three separate measurements are shown.

    Journal: British Journal of Cancer

    Article Title: p53-dependent and p53-independent anticancer effects of different histone deacetylase inhibitors

    doi: 10.1038/bjc.2013.742

    Figure Lengend Snippet: Antineoplastic effects of vorinostat in combination with bortezomib or CAPE in HCT-116 p53+ and p53− cells. ( A ) Four hours after administration of vorinostat, cells were exposed to bortezomib for 48 h. ( B ) One hour after administration of CAPE, cells were exposed to vorinostat for 48 h. Cell death and Δ ψ m were determined by flow-cytometric analyses of PI uptake or DiOC 6 (3) staining, respectively. Means ±s.e.m. of each three separate measurements are shown.

    Article Snippet: Reactions were done in duplicate using Applied Biosystems Gene Expression Assays (p53: Hs01034249_m1; MDM2: Hs99999008_m1; MDM4: Hs00159092_m1; p21: Hs00355782_m1; β -2-microglobulin: Hs00187842_m1) and Universal PCR Master Mix.

    Techniques: Flow Cytometry, Staining

    Antineoplastic effects of tenovin-1 in HCT-116 p53+ and p53− cells. Cells were exposed to tenovin-1 for 24 h (caspase-3 activity) or 48 h (other read-outs). z-VAD-fmk was applied 1 h before treatment with tenovin-1 ( A , C ). ( A ) Cell death and Δ ψ m were determined by flow-cytometric analyses of PI uptake or DiOC 6 (3) staining, respectively; caspase-3 activity was determined using the fluorogenic substrate Ac-DEVD-AMC, relative caspase-3 activities are the ratio of treated cells to untreated cells. ( B ) Pifithrin- α was applied 1 h before treatment with tenovin-1 or vorinostat; cell death was determined by flow-cytometric analysis of PI uptake. ( C ) Cell-cycle profiles were determined by flow cytometry. Means ±s.e.m. of each three separate measurements are shown. * P

    Journal: British Journal of Cancer

    Article Title: p53-dependent and p53-independent anticancer effects of different histone deacetylase inhibitors

    doi: 10.1038/bjc.2013.742

    Figure Lengend Snippet: Antineoplastic effects of tenovin-1 in HCT-116 p53+ and p53− cells. Cells were exposed to tenovin-1 for 24 h (caspase-3 activity) or 48 h (other read-outs). z-VAD-fmk was applied 1 h before treatment with tenovin-1 ( A , C ). ( A ) Cell death and Δ ψ m were determined by flow-cytometric analyses of PI uptake or DiOC 6 (3) staining, respectively; caspase-3 activity was determined using the fluorogenic substrate Ac-DEVD-AMC, relative caspase-3 activities are the ratio of treated cells to untreated cells. ( B ) Pifithrin- α was applied 1 h before treatment with tenovin-1 or vorinostat; cell death was determined by flow-cytometric analysis of PI uptake. ( C ) Cell-cycle profiles were determined by flow cytometry. Means ±s.e.m. of each three separate measurements are shown. * P

    Article Snippet: Reactions were done in duplicate using Applied Biosystems Gene Expression Assays (p53: Hs01034249_m1; MDM2: Hs99999008_m1; MDM4: Hs00159092_m1; p21: Hs00355782_m1; β -2-microglobulin: Hs00187842_m1) and Universal PCR Master Mix.

    Techniques: Activity Assay, Flow Cytometry, Staining, Cytometry

    Effects of HDACi and tenovin-1 on gene expression in HCT-116 p53+ and p53− cells. Cells were exposed to drugs for 24 h. ( A ) mRNA expression levels were determined by real-time RT–PCR and normalised to β -2-microglobulin mRNA levels. Means±s.e.m. of each two separate measurements are shown. ( B ) Cells were treated with 2 μ M HDACi or 10 μ M tenovin-1. Protein expression levels were determined by western blotting.

    Journal: British Journal of Cancer

    Article Title: p53-dependent and p53-independent anticancer effects of different histone deacetylase inhibitors

    doi: 10.1038/bjc.2013.742

    Figure Lengend Snippet: Effects of HDACi and tenovin-1 on gene expression in HCT-116 p53+ and p53− cells. Cells were exposed to drugs for 24 h. ( A ) mRNA expression levels were determined by real-time RT–PCR and normalised to β -2-microglobulin mRNA levels. Means±s.e.m. of each two separate measurements are shown. ( B ) Cells were treated with 2 μ M HDACi or 10 μ M tenovin-1. Protein expression levels were determined by western blotting.

    Article Snippet: Reactions were done in duplicate using Applied Biosystems Gene Expression Assays (p53: Hs01034249_m1; MDM2: Hs99999008_m1; MDM4: Hs00159092_m1; p21: Hs00355782_m1; β -2-microglobulin: Hs00187842_m1) and Universal PCR Master Mix.

    Techniques: Expressing, Quantitative RT-PCR, Western Blot

    Antineoplastic effects of HDACi in HCT-116 p53+ and p53− cells. Cells were exposed to HDACi or etoposide for 24 h ( E ) or 48 h ( A–D , F ); in the time-course experiments ( A , C ), cells were exposed to 5 μ M of vorinostat, entinostat and apicidin, 5 m M VPA or 100 μ M etoposide. z-VAD-fmk was applied 1 h before treatment with HDACi ( D , F ). ( A , D ) Cell death was determined by flow-cytometric analysis of PI uptake. ( B ) Cell viability was determined by MTT assay. ( C , D ) Δ ψ m was determined by flow-cytometric analysis of DiOC 6 (3) staining. ( E ) Caspase-3 activity was determined using the fluorogenic substrate Ac-DEVD-AMC, relative caspase-3 activities are the ratio of treated cells to untreated cells. ( F ) Cell-cycle profiles were determined by flow cytometry. Means ±s.e.m. of each three separate measurements are shown.

    Journal: British Journal of Cancer

    Article Title: p53-dependent and p53-independent anticancer effects of different histone deacetylase inhibitors

    doi: 10.1038/bjc.2013.742

    Figure Lengend Snippet: Antineoplastic effects of HDACi in HCT-116 p53+ and p53− cells. Cells were exposed to HDACi or etoposide for 24 h ( E ) or 48 h ( A–D , F ); in the time-course experiments ( A , C ), cells were exposed to 5 μ M of vorinostat, entinostat and apicidin, 5 m M VPA or 100 μ M etoposide. z-VAD-fmk was applied 1 h before treatment with HDACi ( D , F ). ( A , D ) Cell death was determined by flow-cytometric analysis of PI uptake. ( B ) Cell viability was determined by MTT assay. ( C , D ) Δ ψ m was determined by flow-cytometric analysis of DiOC 6 (3) staining. ( E ) Caspase-3 activity was determined using the fluorogenic substrate Ac-DEVD-AMC, relative caspase-3 activities are the ratio of treated cells to untreated cells. ( F ) Cell-cycle profiles were determined by flow cytometry. Means ±s.e.m. of each three separate measurements are shown.

    Article Snippet: Reactions were done in duplicate using Applied Biosystems Gene Expression Assays (p53: Hs01034249_m1; MDM2: Hs99999008_m1; MDM4: Hs00159092_m1; p21: Hs00355782_m1; β -2-microglobulin: Hs00187842_m1) and Universal PCR Master Mix.

    Techniques: Flow Cytometry, MTT Assay, Staining, Activity Assay, Cytometry

    Antineoplastic effects of vorinostat in combination with obatoclax in HCT-116 p53+ and p53− cells. One hour after administration of obatoclax, cells were exposed to vorinostat for 48 h. Cell death and Δ ψ m were determined by flow-cytometric analyses of PI uptake or DiOC 6 (3) staining, respectively. Means ±s.e.m. of each three separate measurements are shown.

    Journal: British Journal of Cancer

    Article Title: p53-dependent and p53-independent anticancer effects of different histone deacetylase inhibitors

    doi: 10.1038/bjc.2013.742

    Figure Lengend Snippet: Antineoplastic effects of vorinostat in combination with obatoclax in HCT-116 p53+ and p53− cells. One hour after administration of obatoclax, cells were exposed to vorinostat for 48 h. Cell death and Δ ψ m were determined by flow-cytometric analyses of PI uptake or DiOC 6 (3) staining, respectively. Means ±s.e.m. of each three separate measurements are shown.

    Article Snippet: Reactions were done in duplicate using Applied Biosystems Gene Expression Assays (p53: Hs01034249_m1; MDM2: Hs99999008_m1; MDM4: Hs00159092_m1; p21: Hs00355782_m1; β -2-microglobulin: Hs00187842_m1) and Universal PCR Master Mix.

    Techniques: Flow Cytometry, Staining

    The expression of CARNS1 ( a ), FGF6 ( b ), MYLK4 ( c) , PGK1 ( d ), PPP1R3C ( e ), and SGK1 ( f ) genes in the skeletal muscle before and after HIIT (n = 11). The mRNA levels of the six genes were determined by quantitative PCR and significantly increased after the HIIT. The bars represent means and SDs. The B2M mRNA was used as an internal control. * P

    Journal: Scientific Reports

    Article Title: Gene expression profile of muscle adaptation to high-intensity intermittent exercise training in young men

    doi: 10.1038/s41598-018-35115-x

    Figure Lengend Snippet: The expression of CARNS1 ( a ), FGF6 ( b ), MYLK4 ( c) , PGK1 ( d ), PPP1R3C ( e ), and SGK1 ( f ) genes in the skeletal muscle before and after HIIT (n = 11). The mRNA levels of the six genes were determined by quantitative PCR and significantly increased after the HIIT. The bars represent means and SDs. The B2M mRNA was used as an internal control. * P

    Article Snippet: Beta-2 microglobulin ( B2M : Hs00187842-m1) was used as an internal expression control , .

    Techniques: Expressing, Real-time Polymerase Chain Reaction

    CXCR3 identifies two subsets of T N cells in humans. ( A ) Representative flow cytometric analysis of CXCR3 expression on the surface of T N cells (CD45RO − CCR7 + CD27 + CD95 − ). Numbers indicate the percentage of cells in each gate. ( B ) Expression of CXCR3 relative to B2M mRNA in flow-sorted T N R3 − and T N R3 + cells ( n = 5). Each color indicates a different donor. Data are shown as mean ± SEM. n.d., not detected. ( C ) Frequency analysis of T cell subsets in PB samples from healthy individuals ( n = 26). Data are shown as mean ± SEM. T SCM (CD45RO − CCR7 + CD27 + CD95 + ); T CM , central T MEM (CD45RO + CCR7 + ); T EM , effector T MEM (CD45RO + CCR7 − ); and T TE , terminal effector T (CD45RO − CCR7 − ) cells. ( D ) tSNE map displaying the surface immunophenotypes of circulating T N R3 − , T N R3 + , and T MEM cells overlaid on the total CD8 + T cell population. Left, T N R3 − (red); right, T N R3 + (blue). Data were obtained using CyTOF. Individual markers are shown in ( E ). (E) Heatmap showing percent expression of the indicated markers among CD8 + T cell subsets identified in PB. Data were obtained using CyTOF. Subsets were defined as in (C). ( F ) Frequency analysis of T N R3 − and T N R3 + cells among total CD8 + T cells isolated from human tonsils ( n = 5), spleen ( n = 3), liver ( n = 3), gut ( n = 6), skin ( n = 5), and lungs ( n = 4). Data are shown as mean ± SEM. * p

    Journal: The Journal of Immunology Author Choice

    Article Title: CXCR3 Identifies Human Naive CD8+ T Cells with Enhanced Effector Differentiation Potential

    doi: 10.4049/jimmunol.1901072

    Figure Lengend Snippet: CXCR3 identifies two subsets of T N cells in humans. ( A ) Representative flow cytometric analysis of CXCR3 expression on the surface of T N cells (CD45RO − CCR7 + CD27 + CD95 − ). Numbers indicate the percentage of cells in each gate. ( B ) Expression of CXCR3 relative to B2M mRNA in flow-sorted T N R3 − and T N R3 + cells ( n = 5). Each color indicates a different donor. Data are shown as mean ± SEM. n.d., not detected. ( C ) Frequency analysis of T cell subsets in PB samples from healthy individuals ( n = 26). Data are shown as mean ± SEM. T SCM (CD45RO − CCR7 + CD27 + CD95 + ); T CM , central T MEM (CD45RO + CCR7 + ); T EM , effector T MEM (CD45RO + CCR7 − ); and T TE , terminal effector T (CD45RO − CCR7 − ) cells. ( D ) tSNE map displaying the surface immunophenotypes of circulating T N R3 − , T N R3 + , and T MEM cells overlaid on the total CD8 + T cell population. Left, T N R3 − (red); right, T N R3 + (blue). Data were obtained using CyTOF. Individual markers are shown in ( E ). (E) Heatmap showing percent expression of the indicated markers among CD8 + T cell subsets identified in PB. Data were obtained using CyTOF. Subsets were defined as in (C). ( F ) Frequency analysis of T N R3 − and T N R3 + cells among total CD8 + T cells isolated from human tonsils ( n = 5), spleen ( n = 3), liver ( n = 3), gut ( n = 6), skin ( n = 5), and lungs ( n = 4). Data are shown as mean ± SEM. * p

    Article Snippet: Expression levels were normalized (Δcycle threshold [Ct]) to the reference gene B2M (Hs00187842_m1) using the equation 2− (Ct CXCR3 – Ct B2M ) .

    Techniques: Flow Cytometry, Expressing, Isolation