non targeting control sirna  (Santa Cruz Biotechnology)

 
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    Name:
    Control siRNA A
    Description:
    resuspend to 66 µl 10 µM sufficient for 10 20 transfections suitable as a negative control for experiments using targeted siRNA transfection consists of a scrambled sequence that will not lead to the specific degradation of any cellular message aliquot and store at 20°C
    Catalog Number:
    SC-37007
    Price:
    None
    Category:
    Gene Editing Control siRNA A
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    Structured Review

    Santa Cruz Biotechnology non targeting control sirna
    <t>RelB</t> regulates Cox-2 transcription in human lung fibroblasts. (A) RelB <t>siRNA:</t> knockdown of RelB in Normal (non-smoker) human lung fibroblasts was approximately 50%. Representative western blot is shown. (B) RelB siRNA- Cox-2 mRNA: There was a significant reduction in the relative level of Cox-2 mRNA induction by IL-1β in RelB knock-down cells (** p
    resuspend to 66 µl 10 µM sufficient for 10 20 transfections suitable as a negative control for experiments using targeted siRNA transfection consists of a scrambled sequence that will not lead to the specific degradation of any cellular message aliquot and store at 20°C
    https://www.bioz.com/result/non targeting control sirna/product/Santa Cruz Biotechnology
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    Images

    1) Product Images from "Low levels of the AhR in chronic obstructive pulmonary disease (COPD)-derived lung cells increases COX-2 protein by altering mRNA stability"

    Article Title: Low levels of the AhR in chronic obstructive pulmonary disease (COPD)-derived lung cells increases COX-2 protein by altering mRNA stability

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0180881

    RelB regulates Cox-2 transcription in human lung fibroblasts. (A) RelB siRNA: knockdown of RelB in Normal (non-smoker) human lung fibroblasts was approximately 50%. Representative western blot is shown. (B) RelB siRNA- Cox-2 mRNA: There was a significant reduction in the relative level of Cox-2 mRNA induction by IL-1β in RelB knock-down cells (** p
    Figure Legend Snippet: RelB regulates Cox-2 transcription in human lung fibroblasts. (A) RelB siRNA: knockdown of RelB in Normal (non-smoker) human lung fibroblasts was approximately 50%. Representative western blot is shown. (B) RelB siRNA- Cox-2 mRNA: There was a significant reduction in the relative level of Cox-2 mRNA induction by IL-1β in RelB knock-down cells (** p

    Techniques Used: Western Blot

    2) Product Images from "AKAP6 inhibition impairs myoblast differentiation and muscle regeneration: Positive loop between AKAP6 and myogenin"

    Article Title: AKAP6 inhibition impairs myoblast differentiation and muscle regeneration: Positive loop between AKAP6 and myogenin

    Journal: Scientific Reports

    doi: 10.1038/srep16523

    AKAP6 depletion decreases myogenin and MyHC levels and impairs myotube formation. ( A ) Inhibition of AKAP6 expression by using an AKAP6 siRNA was confirmed with RT-PCR and western blotting. C2C12 cells were transfected with a specific siRNA against AKAP6 and further incubated under differentiation conditions for 3 days. Quantification graphs for western blotting are shown. The expression was normalized to that of the proliferation group and shown as fold changes (n = 3 each, right). # p
    Figure Legend Snippet: AKAP6 depletion decreases myogenin and MyHC levels and impairs myotube formation. ( A ) Inhibition of AKAP6 expression by using an AKAP6 siRNA was confirmed with RT-PCR and western blotting. C2C12 cells were transfected with a specific siRNA against AKAP6 and further incubated under differentiation conditions for 3 days. Quantification graphs for western blotting are shown. The expression was normalized to that of the proliferation group and shown as fold changes (n = 3 each, right). # p

    Techniques Used: Inhibition, Expressing, Reverse Transcription Polymerase Chain Reaction, Western Blot, Transfection, Incubation

    MEF2A, not MEF2C or MEF2D, mediates myogenin up-regulation by AKAP6. ( A ) C2C12 cells transfected with AKAP6 siRNA were harvested on day 3 after differentiation and western blot was performed. MEF2A was decreased by AKAP6 siRNA. Results presented in the quantification graph are expressed as a fold change from values under proliferation conditions (bottom, n = 4). ## p
    Figure Legend Snippet: MEF2A, not MEF2C or MEF2D, mediates myogenin up-regulation by AKAP6. ( A ) C2C12 cells transfected with AKAP6 siRNA were harvested on day 3 after differentiation and western blot was performed. MEF2A was decreased by AKAP6 siRNA. Results presented in the quantification graph are expressed as a fold change from values under proliferation conditions (bottom, n = 4). ## p

    Techniques Used: Transfection, Western Blot

    3) Product Images from "Possible reparative effect of low-intensity pulsed ultrasound (LIPUS) on injured meniscus"

    Article Title: Possible reparative effect of low-intensity pulsed ultrasound (LIPUS) on injured meniscus

    Journal: Journal of Cell Communication and Signaling

    doi: 10.1007/s12079-018-0496-9

    Effect of LIPUS on gene expression of cartilage markers in CCN2 knocked-down meniscus cells. Human meniscus inner cells were seeded into 35 mm dish at a density of 1.5 × 10 5 /dish (at 80–90% of confluence) and were transfected with 10 nM of siRNA against CCN2 or siRNA with non-targeting scramble sequence as a negative control after 24 h. Twenty-four hours after transfection, LIPUS treatment was performed. Total cellular RNA was harvested 40 min after LIPUS treatment and evaluated for the expression of CCN2 , SOX9 and ACAN using quantitative real-time RT-PCR analysis. Approximately 90% inhibition of CCN2 expression was achieved. Induced expressions of SOX9 and ACAN by LIPUS treatment were suppressed in CCN2 knocked-down human meniscus inner cells ( p > 0.05, Welch’s t test). ** p
    Figure Legend Snippet: Effect of LIPUS on gene expression of cartilage markers in CCN2 knocked-down meniscus cells. Human meniscus inner cells were seeded into 35 mm dish at a density of 1.5 × 10 5 /dish (at 80–90% of confluence) and were transfected with 10 nM of siRNA against CCN2 or siRNA with non-targeting scramble sequence as a negative control after 24 h. Twenty-four hours after transfection, LIPUS treatment was performed. Total cellular RNA was harvested 40 min after LIPUS treatment and evaluated for the expression of CCN2 , SOX9 and ACAN using quantitative real-time RT-PCR analysis. Approximately 90% inhibition of CCN2 expression was achieved. Induced expressions of SOX9 and ACAN by LIPUS treatment were suppressed in CCN2 knocked-down human meniscus inner cells ( p > 0.05, Welch’s t test). ** p

    Techniques Used: Expressing, Transfection, Sequencing, Negative Control, Quantitative RT-PCR, Inhibition

    4) Product Images from "MACROPHAGES PRODUCE TGFBI (BIGH3) FOLLOWING INGESTION OF APOPTOTIC CELLS AND REGULATE MMP14 LEVELS AND COLLAGEN TURNOVER IN FIBROBLASTS"

    Article Title: MACROPHAGES PRODUCE TGFBI (BIGH3) FOLLOWING INGESTION OF APOPTOTIC CELLS AND REGULATE MMP14 LEVELS AND COLLAGEN TURNOVER IN FIBROBLASTS

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    doi:

    DNA binding by p53 (A) and effects of MMP14 or p53 overexpression, or MMP14 or PU.1 siRNA inhibition on the expression levels of MMP14 and collagen (B,C). In Panel A , electromobility shift assays were used, on two independent occasions, to validate the results of the protein-DNA array experiments. The p53-specific 32 P-labeled probe was incubated with nuclear lysates from non-stimulated control or TGFBI-activated fibroblasts, as indicated, or in the presence of 10-fold excess of the mutant (scrambled) or unlabeled (cold) specific probe, as indicated. The cold but not the scrambled probe inhibited p53 binding (arrows), suggesting that the binding is specific. In Panels B and C , fibroblast cultures were transfected with MMP14-encoding or p53-encoding plasmid, or with MMP14 or PU.1 siRNA as indicated. Western blotting assays were performed using antibodies against MMP14 or collagen. At least three independent experiments were conducted for each panel shown, with consistent results.
    Figure Legend Snippet: DNA binding by p53 (A) and effects of MMP14 or p53 overexpression, or MMP14 or PU.1 siRNA inhibition on the expression levels of MMP14 and collagen (B,C). In Panel A , electromobility shift assays were used, on two independent occasions, to validate the results of the protein-DNA array experiments. The p53-specific 32 P-labeled probe was incubated with nuclear lysates from non-stimulated control or TGFBI-activated fibroblasts, as indicated, or in the presence of 10-fold excess of the mutant (scrambled) or unlabeled (cold) specific probe, as indicated. The cold but not the scrambled probe inhibited p53 binding (arrows), suggesting that the binding is specific. In Panels B and C , fibroblast cultures were transfected with MMP14-encoding or p53-encoding plasmid, or with MMP14 or PU.1 siRNA as indicated. Western blotting assays were performed using antibodies against MMP14 or collagen. At least three independent experiments were conducted for each panel shown, with consistent results.

    Techniques Used: Binding Assay, Over Expression, Inhibition, Expressing, DNA Array, Labeling, Incubation, Mutagenesis, Transfection, Plasmid Preparation, Western Blot

    5) Product Images from "Gadd45b is an epigenetic regulator of juvenile social behavior and alters local pro-inflammatory cytokine production in the rodent amygdala"

    Article Title: Gadd45b is an epigenetic regulator of juvenile social behavior and alters local pro-inflammatory cytokine production in the rodent amygdala

    Journal: Brain, behavior, and immunity

    doi: 10.1016/j.bbi.2015.02.018

    Neonatal Gadd45b siRNA treatment epigenetically alters Adra2a promoter DNA methylation near a CREB binding site at P2 (control: 0.175 ± 0.0175, N = 5 vs. Gadd45b: 0.371 ± 0.0764, N = 6; p = 0.0489) and P33 (control: 0.249 ± 0.0310,
    Figure Legend Snippet: Neonatal Gadd45b siRNA treatment epigenetically alters Adra2a promoter DNA methylation near a CREB binding site at P2 (control: 0.175 ± 0.0175, N = 5 vs. Gadd45b: 0.371 ± 0.0764, N = 6; p = 0.0489) and P33 (control: 0.249 ± 0.0310,

    Techniques Used: DNA Methylation Assay, Binding Assay

    Gadd45b siRNA specificity in the amygdala. Two days of Gadd45b siRNA gives approximately 20% knockdown of mRNA (control: 0.4861 ± 0.0276, N = 5; Gadd45b: 0.3967 ± 0.0130, N = 5); * p = 0.0191. Gadd45b siRNA does not significantly decrease
    Figure Legend Snippet: Gadd45b siRNA specificity in the amygdala. Two days of Gadd45b siRNA gives approximately 20% knockdown of mRNA (control: 0.4861 ± 0.0276, N = 5; Gadd45b: 0.3967 ± 0.0130, N = 5); * p = 0.0191. Gadd45b siRNA does not significantly decrease

    Techniques Used:

    Neonatal Gadd45b siRNA infusion increases the initiation of play fighting. (A) Transient neonatal disruption of Gadd45b expression in the amygdala more than doubles the frequency of juvenile social play (control siRNA males: 2.064 ± 0.5007, N
    Figure Legend Snippet: Neonatal Gadd45b siRNA infusion increases the initiation of play fighting. (A) Transient neonatal disruption of Gadd45b expression in the amygdala more than doubles the frequency of juvenile social play (control siRNA males: 2.064 ± 0.5007, N

    Techniques Used: Expressing

    Gadd45b siRNA infused males exhibit abnormal social behavior, with no preference for the social chamber. Repeated measures ANOVA analysis reveals a strong preference for the social chamber in control siRNA males ( F = 15.23, p
    Figure Legend Snippet: Gadd45b siRNA infused males exhibit abnormal social behavior, with no preference for the social chamber. Repeated measures ANOVA analysis reveals a strong preference for the social chamber in control siRNA males ( F = 15.23, p

    Techniques Used:

    3.7. Gadd45b siRNA epigenetically alters methylation of the Adra2a promoter in the amygdala
    Figure Legend Snippet: 3.7. Gadd45b siRNA epigenetically alters methylation of the Adra2a promoter in the amygdala

    Techniques Used: Methylation

    6) Product Images from "The Role of NF-?B Signaling in the Maintenance of Pluripotency of Human Induced Pluripotent Stem Cells"

    Article Title: The Role of NF-?B Signaling in the Maintenance of Pluripotency of Human Induced Pluripotent Stem Cells

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0056399

    Downregulation of Oct3/4 and Nanog by knockdown of NF-κB. Western blot analysis of actin, NF-κB p65, IκBα, Oct3/4, Nanog, WT-1, and Pax-2 in human iPS cells treated with siRNA (A). Immunohistochemical staining for NF-κB p65 (B–D) and Oct3/4 (E–G) in human iPS cells treated with siRNA. No treatment (B and E), treatment with control siRNA (C and F), and treatment with p65 siRNA (D and G). Negative control staining without a primary antibody is shown (H) (Original magnification, x200).
    Figure Legend Snippet: Downregulation of Oct3/4 and Nanog by knockdown of NF-κB. Western blot analysis of actin, NF-κB p65, IκBα, Oct3/4, Nanog, WT-1, and Pax-2 in human iPS cells treated with siRNA (A). Immunohistochemical staining for NF-κB p65 (B–D) and Oct3/4 (E–G) in human iPS cells treated with siRNA. No treatment (B and E), treatment with control siRNA (C and F), and treatment with p65 siRNA (D and G). Negative control staining without a primary antibody is shown (H) (Original magnification, x200).

    Techniques Used: Western Blot, Immunohistochemistry, Staining, Negative Control

    Specific knockdown of NF-κB activity by treatment with p65 siRNA. Representative photomicrographs of human iPS cells: no treatment (A–D), treatment with control siRNA (E–H), treatment wirth p65 siRNA (I–L) (original magnification, x200). A representative EMSA shows NF-κB and AP-1 binding activity in human iPS cells treated with siRNA (M). Representative photographs of alkaline phosphatase staining of human iPS cells treated with siRNA (N–P) (original magnification, x200). No treatment (N), treatment with control siRNA (O), treatment with p65 siRNA (P).
    Figure Legend Snippet: Specific knockdown of NF-κB activity by treatment with p65 siRNA. Representative photomicrographs of human iPS cells: no treatment (A–D), treatment with control siRNA (E–H), treatment wirth p65 siRNA (I–L) (original magnification, x200). A representative EMSA shows NF-κB and AP-1 binding activity in human iPS cells treated with siRNA (M). Representative photographs of alkaline phosphatase staining of human iPS cells treated with siRNA (N–P) (original magnification, x200). No treatment (N), treatment with control siRNA (O), treatment with p65 siRNA (P).

    Techniques Used: Activity Assay, Binding Assay, Staining

    7) Product Images from "Decreased expression of the NF-κB family member RelB in lung fibroblasts from Smokers with and without COPD potentiates cigarette smoke-induced COX-2 expression"

    Article Title: Decreased expression of the NF-κB family member RelB in lung fibroblasts from Smokers with and without COPD potentiates cigarette smoke-induced COX-2 expression

    Journal: Respiratory Research

    doi: 10.1186/s12931-015-0214-6

    siRNA-mediated knock-down of RelB potentiates CSE-induced Cox-2 mRNA and protein expression in Normal lung fibroblasts. (A) RelB siRNA: Lung fibroblasts derived from Normal subjects were transfected with siRNA against RelB (siRelB). RelB protein levels were decreased by approximately 40% compared to Ctrl-transfected (siCtrl; relative-change: 0.59 ± 0.065). Results are expressed as the mean ± SEM, n = 4 independent experiments . (B) Cox-2 mRNA: Normal fibroblasts transfected with RelB siRNA were exposed to 2% CSE for 6 hours and Cox-2 mRNA expression evaluated by qRT-PCR. There was a significant increase in Cox-2 mRNA expression only when RelB expression is reduced (siRelB; fold-induction 15 ± 8; *p
    Figure Legend Snippet: siRNA-mediated knock-down of RelB potentiates CSE-induced Cox-2 mRNA and protein expression in Normal lung fibroblasts. (A) RelB siRNA: Lung fibroblasts derived from Normal subjects were transfected with siRNA against RelB (siRelB). RelB protein levels were decreased by approximately 40% compared to Ctrl-transfected (siCtrl; relative-change: 0.59 ± 0.065). Results are expressed as the mean ± SEM, n = 4 independent experiments . (B) Cox-2 mRNA: Normal fibroblasts transfected with RelB siRNA were exposed to 2% CSE for 6 hours and Cox-2 mRNA expression evaluated by qRT-PCR. There was a significant increase in Cox-2 mRNA expression only when RelB expression is reduced (siRelB; fold-induction 15 ± 8; *p

    Techniques Used: Expressing, Derivative Assay, Transfection, Quantitative RT-PCR

    8) Product Images from "Transient receptor potential channel TRPM8 is over-expressed and required for cellular proliferation in pancreatic adenocarcinoma"

    Article Title: Transient receptor potential channel TRPM8 is over-expressed and required for cellular proliferation in pancreatic adenocarcinoma

    Journal: Cancer letters

    doi: 10.1016/j.canlet.2010.04.023

    TRPM8-deficient pancreatic adenocarcinoma cells have impaired ability to progress through the cell division cycle. Serum-deprived PANC-1 and BxPC-3 cells were transfected with anti- TRPM8 siRNA or non-targeting control siRNA. Forty-eight hours later, the cells were analyzed for DNA content by flow cytometry. The proportion of cells in each phase of the cell cycle is indicated. Non-specific sub-G 0 /G 1 events were gated out for accurate analysis of cell cycle distribution curves in the viable cells. This experiment was repeated with similar results.
    Figure Legend Snippet: TRPM8-deficient pancreatic adenocarcinoma cells have impaired ability to progress through the cell division cycle. Serum-deprived PANC-1 and BxPC-3 cells were transfected with anti- TRPM8 siRNA or non-targeting control siRNA. Forty-eight hours later, the cells were analyzed for DNA content by flow cytometry. The proportion of cells in each phase of the cell cycle is indicated. Non-specific sub-G 0 /G 1 events were gated out for accurate analysis of cell cycle distribution curves in the viable cells. This experiment was repeated with similar results.

    Techniques Used: Transfection, Flow Cytometry, Cytometry

    RNA interference-mediated silencing of TRPM8 induces alterations of cellular and nuclear morphology suggestive of proliferative arrest. PANC-1 and BxPC-3 cells transfected with siRNA directed against TR PM8 or non-targeting control siRNA. A. Phase contrast micrographs of TRPM8-deficient cells with multiple micronuclei (red arrowheads). B. Fluorescent micrographs of DAPI-stained TRPM8-deficient cells with abnormal nuclear morphology (white arrows). These experiments were repeated two times with essentially the same results.
    Figure Legend Snippet: RNA interference-mediated silencing of TRPM8 induces alterations of cellular and nuclear morphology suggestive of proliferative arrest. PANC-1 and BxPC-3 cells transfected with siRNA directed against TR PM8 or non-targeting control siRNA. A. Phase contrast micrographs of TRPM8-deficient cells with multiple micronuclei (red arrowheads). B. Fluorescent micrographs of DAPI-stained TRPM8-deficient cells with abnormal nuclear morphology (white arrows). These experiments were repeated two times with essentially the same results.

    Techniques Used: Transfection, Staining

    Anti- TRPM8 siRNA up-regulates expression of p21 CDKN1A and p27 CDKN1B . Total RNA extracted from PANC-1 and BxPC-3 cells 72 h following transfection with siRNA directed against TR PM8 or non-targeting control siRNA was analyzed for p21 CDKN1A and p27 CDKN1B mRNA levels by quantitative real-time PCR. Each value represents the relative p21 CDKN1A or p27 CDKN1B mRNA level in the anti- TRPM8 siRNA transfected cells as compared to that in control siRNA transfected cells. This experiment was independently performed twice, and the same pattern of changes in p21 CDKN1A and p27 CDKN1B mRNA was observed.
    Figure Legend Snippet: Anti- TRPM8 siRNA up-regulates expression of p21 CDKN1A and p27 CDKN1B . Total RNA extracted from PANC-1 and BxPC-3 cells 72 h following transfection with siRNA directed against TR PM8 or non-targeting control siRNA was analyzed for p21 CDKN1A and p27 CDKN1B mRNA levels by quantitative real-time PCR. Each value represents the relative p21 CDKN1A or p27 CDKN1B mRNA level in the anti- TRPM8 siRNA transfected cells as compared to that in control siRNA transfected cells. This experiment was independently performed twice, and the same pattern of changes in p21 CDKN1A and p27 CDKN1B mRNA was observed.

    Techniques Used: Expressing, Transfection, Real-time Polymerase Chain Reaction

    SiRNA-induced knock down of TRPM8 reduces the ability ofpan creatic adenocarcinoma cells to proliferate. PANC-1 and BxPC-3 cells treated with siRNA anti- TRPM8 were analyzed by the MTS assay and by counting cells. Proliferation of the TRPM8-deficient cells is expressed as a percentage of that in control siRNA transfected cells. Each value represents the mean of 6 independent cell samples +/− standard deviation. * P
    Figure Legend Snippet: SiRNA-induced knock down of TRPM8 reduces the ability ofpan creatic adenocarcinoma cells to proliferate. PANC-1 and BxPC-3 cells treated with siRNA anti- TRPM8 were analyzed by the MTS assay and by counting cells. Proliferation of the TRPM8-deficient cells is expressed as a percentage of that in control siRNA transfected cells. Each value represents the mean of 6 independent cell samples +/− standard deviation. * P

    Techniques Used: MTS Assay, Transfection, Standard Deviation

    9) Product Images from "Bacterial lipoproteins induce distinct IL-8 inductions relying on their lipid moieties in pulmonary epithelial cells"

    Article Title: Bacterial lipoproteins induce distinct IL-8 inductions relying on their lipid moieties in pulmonary epithelial cells

    Journal: bioRxiv

    doi: 10.1101/2020.04.03.024471

    Lipopeptides induce IL-8 expression via intracellular TLR2 in A549 cells. (A) TLR2 knockdown effect on IL-8 production induced by lipopeptides in A549 cells. siRNA-transfected cells were treated with either pam2CSK4 or pam3CSK4 for additional 24 h. (B) Blocking antibodies for TLR2, TLR4, and CD14 had no effect on lipopeptide-induced IL-8 production. Cells were treated with blocking antibodies for 1 h prior to the lipopeptide stimulation for 24 h. Mouse IgG2aκ (for TLR2 and TLR4 antibodies) and IgG1aκ (for CD14 antibody) were used as isotype controls. Bars indicate means ± S.D. (n=3). (C) Intracellular localization of TLR2 in A549 cells was determined by immunostaining and FACS. Grey areas indicate isotype control. Dotted lines indicate fixed cells for surface staining and closed lines indicate permeabilized cells for intracellular staining of TLR.
    Figure Legend Snippet: Lipopeptides induce IL-8 expression via intracellular TLR2 in A549 cells. (A) TLR2 knockdown effect on IL-8 production induced by lipopeptides in A549 cells. siRNA-transfected cells were treated with either pam2CSK4 or pam3CSK4 for additional 24 h. (B) Blocking antibodies for TLR2, TLR4, and CD14 had no effect on lipopeptide-induced IL-8 production. Cells were treated with blocking antibodies for 1 h prior to the lipopeptide stimulation for 24 h. Mouse IgG2aκ (for TLR2 and TLR4 antibodies) and IgG1aκ (for CD14 antibody) were used as isotype controls. Bars indicate means ± S.D. (n=3). (C) Intracellular localization of TLR2 in A549 cells was determined by immunostaining and FACS. Grey areas indicate isotype control. Dotted lines indicate fixed cells for surface staining and closed lines indicate permeabilized cells for intracellular staining of TLR.

    Techniques Used: Expressing, Transfection, Blocking Assay, Immunostaining, FACS, Staining

    TLR2 knockdown efficiency. A549 cells were transfected with either control or TLR2 siRNA for 6 h and then treated with either pam2CSK4 or pam3CSK4 for additional 24 h to determine IL-8 secretion. The cells were collected and TLR2 mRNA expression was determined by quantitative RT-PCR from total RNA. Bars indicate means ± S.D. (n=3).
    Figure Legend Snippet: TLR2 knockdown efficiency. A549 cells were transfected with either control or TLR2 siRNA for 6 h and then treated with either pam2CSK4 or pam3CSK4 for additional 24 h to determine IL-8 secretion. The cells were collected and TLR2 mRNA expression was determined by quantitative RT-PCR from total RNA. Bars indicate means ± S.D. (n=3).

    Techniques Used: Transfection, Expressing, Quantitative RT-PCR

    10) Product Images from "Suxiao Jiuxin pill promotes exosome secretion from mouse cardiac mesenchymal stem cells in vitro"

    Article Title: Suxiao Jiuxin pill promotes exosome secretion from mouse cardiac mesenchymal stem cells in vitro

    Journal: Acta Pharmacologica Sinica

    doi: 10.1038/aps.2018.19

    Knockdown of Rab27a or Rab27b inhibits SJP-mediated exosome release in C-MSCs. (A, B) qRT-PCR quantification of Rab27a and Rab27b mRNA levels (normalized to GADPH levels) in C-MSCs transfected with Rab27a siRNA, Rab27b siRNA, or non-targeting (NT) siRNA ( * P
    Figure Legend Snippet: Knockdown of Rab27a or Rab27b inhibits SJP-mediated exosome release in C-MSCs. (A, B) qRT-PCR quantification of Rab27a and Rab27b mRNA levels (normalized to GADPH levels) in C-MSCs transfected with Rab27a siRNA, Rab27b siRNA, or non-targeting (NT) siRNA ( * P

    Techniques Used: Quantitative RT-PCR, Transfection

    11) Product Images from "Tumor suppressor FOXO3 regulates ribonucleotide reductase subunit RRM2B and impacts on survival of cancer patients"

    Article Title: Tumor suppressor FOXO3 regulates ribonucleotide reductase subunit RRM2B and impacts on survival of cancer patients

    Journal: Oncotarget

    doi:

    FOXO3 activates RRM2B transcriptional activity a) The graph shows three putative FHREs on the RRM2B promoter, where FOXO3 could potentially bind to and activate RRM2B transcription. b) Cells were co-transfected with different FHRE of RRM2B-Luc and either control, WT, or FOXO3(A)3 plasmids as indicated, and then reporter assays were carried out. (means ± SEM, n = 2). c) Cells were co-transfected with WT or RRM2B-Luc (-964) mutants and either control or FOXO3(A)3 plasmids as indicated, and reporter assays were performed. (means ± SEM, n = 2). d) Cells were co-transfected with WT RRM2B-Luc and either control or FOXO3(A)3 plasmids as well as treated with control or FOXO3 siRNA and analyzed by reporter assay 48 hours later. (means ± SEM, n = 3).
    Figure Legend Snippet: FOXO3 activates RRM2B transcriptional activity a) The graph shows three putative FHREs on the RRM2B promoter, where FOXO3 could potentially bind to and activate RRM2B transcription. b) Cells were co-transfected with different FHRE of RRM2B-Luc and either control, WT, or FOXO3(A)3 plasmids as indicated, and then reporter assays were carried out. (means ± SEM, n = 2). c) Cells were co-transfected with WT or RRM2B-Luc (-964) mutants and either control or FOXO3(A)3 plasmids as indicated, and reporter assays were performed. (means ± SEM, n = 2). d) Cells were co-transfected with WT RRM2B-Luc and either control or FOXO3(A)3 plasmids as well as treated with control or FOXO3 siRNA and analyzed by reporter assay 48 hours later. (means ± SEM, n = 3).

    Techniques Used: Activity Assay, Transfection, Reporter Assay

    FOXO3 and RRM2B expression correlate in cancer cells a) HeLa, H1299, and MDA-231 cells were treated with either control siRNA (C) or FOXO3 siRNA (F) for 72 hours, and harvested for Western blot analysis with antibodies anti-FOXO3, anti-RRM2B, anti-p53, and anti-β-ACTIN (as loading control). b) Cells were treated with control or FOXO3 siRNA for 72 hours. Samples from U2OS, MDA-231 and HeLa cells were analyzed by qPCR. H1299 cells were analyzed by PCR, and then relative expression was analyzed by image J software. c) H1299 cells were seeded onto the coverslips in culture dishes. Cells were treated with siRNA for 72 hours, fixed and then immunoflourescence assay was performed. DAPI served as nuclear marker. d) H1299 cells were transfected with indicated plasmids, and then harvested for Western blots and RNA expression analysis 48 hours later.
    Figure Legend Snippet: FOXO3 and RRM2B expression correlate in cancer cells a) HeLa, H1299, and MDA-231 cells were treated with either control siRNA (C) or FOXO3 siRNA (F) for 72 hours, and harvested for Western blot analysis with antibodies anti-FOXO3, anti-RRM2B, anti-p53, and anti-β-ACTIN (as loading control). b) Cells were treated with control or FOXO3 siRNA for 72 hours. Samples from U2OS, MDA-231 and HeLa cells were analyzed by qPCR. H1299 cells were analyzed by PCR, and then relative expression was analyzed by image J software. c) H1299 cells were seeded onto the coverslips in culture dishes. Cells were treated with siRNA for 72 hours, fixed and then immunoflourescence assay was performed. DAPI served as nuclear marker. d) H1299 cells were transfected with indicated plasmids, and then harvested for Western blots and RNA expression analysis 48 hours later.

    Techniques Used: Expressing, Multiple Displacement Amplification, Western Blot, Real-time Polymerase Chain Reaction, Polymerase Chain Reaction, Software, Marker, Transfection, RNA Expression

    12) Product Images from "Targeted silencing of TRPM7 ion channel induces replicative senescence and produces enhanced cytotoxicity with gemcitabine in pancreatic adenocarcinoma"

    Article Title: Targeted silencing of TRPM7 ion channel induces replicative senescence and produces enhanced cytotoxicity with gemcitabine in pancreatic adenocarcinoma

    Journal: Cancer Letters

    doi: 10.1016/j.canlet.2011.12.007

    Combination of anti- TRPM7 siRNA with gemcitabine produced enhanced cytotoxicity. PANC-1 cells transfected with anti- TRPM7 siRNA or non-targeting control siRNA were incubated in the presence or absence of gemcitabine at 1 µM or 5 µM and
    Figure Legend Snippet: Combination of anti- TRPM7 siRNA with gemcitabine produced enhanced cytotoxicity. PANC-1 cells transfected with anti- TRPM7 siRNA or non-targeting control siRNA were incubated in the presence or absence of gemcitabine at 1 µM or 5 µM and

    Techniques Used: Produced, Transfection, Incubation

    RNA interference-mediated silencing of TRPM7 did not induce apoptotic cell death. BxPC-3 and PANC-1 cells transfected with anti- TRPM7 siRNA or non-targeting control siRNA were incubated with FITC-conjugated annexin V and PI, and then analyzed for apoptosis
    Figure Legend Snippet: RNA interference-mediated silencing of TRPM7 did not induce apoptotic cell death. BxPC-3 and PANC-1 cells transfected with anti- TRPM7 siRNA or non-targeting control siRNA were incubated with FITC-conjugated annexin V and PI, and then analyzed for apoptosis

    Techniques Used: Transfection, Incubation

    SiRNA-mediated repression of TRPM7 induced cellular morphology indicative of a senescent phenotype. BxPC-3 and PANC-1 cells transfected with anti- TRPM7 siRNA or non-targeting control siRNA were stained with hematoxylin and eosin, and examined under a
    Figure Legend Snippet: SiRNA-mediated repression of TRPM7 induced cellular morphology indicative of a senescent phenotype. BxPC-3 and PANC-1 cells transfected with anti- TRPM7 siRNA or non-targeting control siRNA were stained with hematoxylin and eosin, and examined under a

    Techniques Used: Transfection, Staining

    TRPM7-deficient cells contained multiple nuclei suggesting mitotic arrest. BxPC-3 and PANC-1 cells transfected with anti- TRPM7 siRNA or non-targeting control siRNA were stained with DAPI, and examined under a compound light microscope with fluorescence.
    Figure Legend Snippet: TRPM7-deficient cells contained multiple nuclei suggesting mitotic arrest. BxPC-3 and PANC-1 cells transfected with anti- TRPM7 siRNA or non-targeting control siRNA were stained with DAPI, and examined under a compound light microscope with fluorescence.

    Techniques Used: Transfection, Staining, Light Microscopy, Fluorescence

    TRPM7-deficient cells underwent replicative senescence. BxPC-3 and PANC-1 cells transfected with anti- TRPM7 siRNA or non-targeting control siRNA were analyzed for SA β-gal activity. Images were acquired under an inverted light microscope with
    Figure Legend Snippet: TRPM7-deficient cells underwent replicative senescence. BxPC-3 and PANC-1 cells transfected with anti- TRPM7 siRNA or non-targeting control siRNA were analyzed for SA β-gal activity. Images were acquired under an inverted light microscope with

    Techniques Used: Transfection, Activity Assay, Light Microscopy

    No enhanced cytotoxicity by anti- TRPM7 siRNA in combination with SAHA. PANC-1 cells transfected with anti- TRPM7 siRNA or non-targeting control siRNA were incubated in the presence or absence of SAHA at 1 µM or 5 µM and then analyzed for
    Figure Legend Snippet: No enhanced cytotoxicity by anti- TRPM7 siRNA in combination with SAHA. PANC-1 cells transfected with anti- TRPM7 siRNA or non-targeting control siRNA were incubated in the presence or absence of SAHA at 1 µM or 5 µM and then analyzed for

    Techniques Used: Transfection, Incubation

    13) Product Images from "AhR and Arnt differentially regulate NF-κB signaling and chemokine responses in human bronchial epithelial cells"

    Article Title: AhR and Arnt differentially regulate NF-κB signaling and chemokine responses in human bronchial epithelial cells

    Journal: Cell Communication and Signaling : CCS

    doi: 10.1186/s12964-014-0048-8

    AhR and Arnt differentially regulate CXCL8 and CCL5 responses as well as p65 phosphorylation in Poly I: C- exposed BEAS- 2B cells. Cells were transfected with siRNA against p65 (siP65), AhR (siAHR), Arnt (siARNT) or non-targeting control siRNA (siNT), and exposed to 10 μg/ml Poly I:C. Intracellular protein levels of total and phospho-p65 (Ser536) as well as AhR and Arnt were detected by Western blotting after 2 and 4 h exposure, as described under “Materials and methods”. The figure displays representative blots (A) , as well as relative changes in phospho-p65 compared to total p65 quantified by densitometric analysis of the Western blots (B) . CXCL8 (C and E) and CCL5 (D and F) protein levels in the medium were measured by ELISA after 18 h exposure, as described under “Materials and methods”. The results are expressed as mean ± SEM (n ≥ 3). *Significantly different from unexposed controls; †Significantly different from cells transfected with non-targeting siRNA.
    Figure Legend Snippet: AhR and Arnt differentially regulate CXCL8 and CCL5 responses as well as p65 phosphorylation in Poly I: C- exposed BEAS- 2B cells. Cells were transfected with siRNA against p65 (siP65), AhR (siAHR), Arnt (siARNT) or non-targeting control siRNA (siNT), and exposed to 10 μg/ml Poly I:C. Intracellular protein levels of total and phospho-p65 (Ser536) as well as AhR and Arnt were detected by Western blotting after 2 and 4 h exposure, as described under “Materials and methods”. The figure displays representative blots (A) , as well as relative changes in phospho-p65 compared to total p65 quantified by densitometric analysis of the Western blots (B) . CXCL8 (C and E) and CCL5 (D and F) protein levels in the medium were measured by ELISA after 18 h exposure, as described under “Materials and methods”. The results are expressed as mean ± SEM (n ≥ 3). *Significantly different from unexposed controls; †Significantly different from cells transfected with non-targeting siRNA.

    Techniques Used: Transfection, Western Blot, Enzyme-linked Immunosorbent Assay

    RelB suppresses CXCL8, but not CCL5, in BEAS- 2B cells. Cells were transfected with siRNA against RelB (siRELB) or non-targeting control siRNA (siNT). Transfected cells were exposed to 20 μM 1-NP, 1-AP, or vehicle (DMSO) alone (A-D) or 10 μg/ml Poly I:C or vehicle (water) alone (E and F) . CXCL8 (A) and CCL5 (B) gene expression were measured after 6 h by real-time PCR. CXCL8 (C and E) and CCL5 (D and F) protein levels in the medium were measured by ELISA after 18 h exposure as described under “Materials and methods”. Efficiency of transfection was assessed by Western blotting (G) . The results are expressed as mean ± SEM (A/B: n = 1 (triplicate determinations); C-F : n ≥ 3; G: representative blot, n = 3) *Significantly different from unexposed controls; †Significantly different from cells transfected with non-targeting siRNA.
    Figure Legend Snippet: RelB suppresses CXCL8, but not CCL5, in BEAS- 2B cells. Cells were transfected with siRNA against RelB (siRELB) or non-targeting control siRNA (siNT). Transfected cells were exposed to 20 μM 1-NP, 1-AP, or vehicle (DMSO) alone (A-D) or 10 μg/ml Poly I:C or vehicle (water) alone (E and F) . CXCL8 (A) and CCL5 (B) gene expression were measured after 6 h by real-time PCR. CXCL8 (C and E) and CCL5 (D and F) protein levels in the medium were measured by ELISA after 18 h exposure as described under “Materials and methods”. Efficiency of transfection was assessed by Western blotting (G) . The results are expressed as mean ± SEM (A/B: n = 1 (triplicate determinations); C-F : n ≥ 3; G: representative blot, n = 3) *Significantly different from unexposed controls; †Significantly different from cells transfected with non-targeting siRNA.

    Techniques Used: Transfection, Expressing, Real-time Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay, Western Blot

    Depletion of AhR and Arnt increases RelB levels in Poly I: C - exposed BEAS- 2B cells. Cells were transfected with siRNA against AhR (siAHR), Arnt (siARNT) or non-targeting control siRNA (siNT), and exposed to 10 μg/ml Poly I:C for 2 and 4 h. Intracellular protein levels of RelB and β-actin were detected by Western blotting as described under “Materials and methods”. The figure displays representative blots of RelB levels in unexposed cells (A) and Poly I:C-exposed cells (B) . The graph depicts relative changes in RelB (B) compared to β-actin quantified by densitometric analysis of the Western blots. The results are expressed as mean ± SEM (n = 3). *Significantly different from unexposed controls; †Significantly different from cells transfected with non-targeting siRNA.
    Figure Legend Snippet: Depletion of AhR and Arnt increases RelB levels in Poly I: C - exposed BEAS- 2B cells. Cells were transfected with siRNA against AhR (siAHR), Arnt (siARNT) or non-targeting control siRNA (siNT), and exposed to 10 μg/ml Poly I:C for 2 and 4 h. Intracellular protein levels of RelB and β-actin were detected by Western blotting as described under “Materials and methods”. The figure displays representative blots of RelB levels in unexposed cells (A) and Poly I:C-exposed cells (B) . The graph depicts relative changes in RelB (B) compared to β-actin quantified by densitometric analysis of the Western blots. The results are expressed as mean ± SEM (n = 3). *Significantly different from unexposed controls; †Significantly different from cells transfected with non-targeting siRNA.

    Techniques Used: Transfection, Western Blot

    AhR and Arnt differentially regulate CXCL8 and CCL5 responses in 1- NP- or 1- AP- exposed BEAS- 2B cells. Cells were transfected with siRNA against AhR (siAHR) and Arnt (siARNT) or non-targeting control siRNA (siNT), and exposed to 20 μM 1-NP, 1-AP or vehicle (DMSO) alone. CXCL8 (A) and CCL5 (B) gene expression were measured after 6 h by real-time PCR. CXCL8 (C) and CCL5 (D) protein levels in the medium were measured by ELISA after 18 h exposure as described under “Materials and methods”. Efficiency of transfection was assessed by Western blotting (E) as well as expression of CYP1A1 after 6 h exposure to 20 μM B[a]P, 1-NP and 1-AP, by real-time PCR (F) . The results are expressed as mean ± SEM (A/B/F: n = 1 (triplicate determinations); C/D: n ≥ 3; E: representative blots, n ≥ 3). *Significantly different from unexposed controls; †Significantly different from cells transfected with non-targeting siRNA.
    Figure Legend Snippet: AhR and Arnt differentially regulate CXCL8 and CCL5 responses in 1- NP- or 1- AP- exposed BEAS- 2B cells. Cells were transfected with siRNA against AhR (siAHR) and Arnt (siARNT) or non-targeting control siRNA (siNT), and exposed to 20 μM 1-NP, 1-AP or vehicle (DMSO) alone. CXCL8 (A) and CCL5 (B) gene expression were measured after 6 h by real-time PCR. CXCL8 (C) and CCL5 (D) protein levels in the medium were measured by ELISA after 18 h exposure as described under “Materials and methods”. Efficiency of transfection was assessed by Western blotting (E) as well as expression of CYP1A1 after 6 h exposure to 20 μM B[a]P, 1-NP and 1-AP, by real-time PCR (F) . The results are expressed as mean ± SEM (A/B/F: n = 1 (triplicate determinations); C/D: n ≥ 3; E: representative blots, n ≥ 3). *Significantly different from unexposed controls; †Significantly different from cells transfected with non-targeting siRNA.

    Techniques Used: Transfection, Expressing, Real-time Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay, Western Blot

    AhR silencing increased TNF- α-, but not 1- NP- induced p50/ p65 reporter gene expression in BEAS- 2B cells. Cells were transfected with a NF-κB-luciferase (p50/p65) reporter gene, and exposed to 1-NP or TNF-α for 6 or 16 h (A) , and assayed for luciferase activity as described under “Materials and methods”. Cells transfected siRNAs against AhR (siAHR), Arnt (siARNT) or non-targeting control siRNA (siNT) were further transfected with NF-κB-luciferase promoter and assayed for luciferase activity after a 16 h exposure to 1-NP (20 μM) or TNF-α (50 ng/ml) (B) . The results are expressed as mean ± SEM (A: n = 2; B: n = 5). *Significantly different from unexposed controls; †Significantly different from cells transfected with non-targeting siRNA.
    Figure Legend Snippet: AhR silencing increased TNF- α-, but not 1- NP- induced p50/ p65 reporter gene expression in BEAS- 2B cells. Cells were transfected with a NF-κB-luciferase (p50/p65) reporter gene, and exposed to 1-NP or TNF-α for 6 or 16 h (A) , and assayed for luciferase activity as described under “Materials and methods”. Cells transfected siRNAs against AhR (siAHR), Arnt (siARNT) or non-targeting control siRNA (siNT) were further transfected with NF-κB-luciferase promoter and assayed for luciferase activity after a 16 h exposure to 1-NP (20 μM) or TNF-α (50 ng/ml) (B) . The results are expressed as mean ± SEM (A: n = 2; B: n = 5). *Significantly different from unexposed controls; †Significantly different from cells transfected with non-targeting siRNA.

    Techniques Used: Expressing, Transfection, Luciferase, Activity Assay

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    Endogenous immunofluorescence of LC3 after PKCε downregulation. a Cells were <t>transfected</t> with PKCε <t>siRNA</t> (PKCε siRNA) and non-targeting siRNA (Control siRNA) and then were treated with rapamycin (300 nM) for 24 h, as described in Autophagosome visualization section. Representative images from HeLaPKCεA/E, U-138 MG, and U-118 MG cells are shown. Scale bars equate to 10 μm. b AUTOCOUNTER analysis in imaging of U-138 MG and U-118 MG cells after siRNA silencing of PKCε (72 h) and Rapamycin (300 nM) treatment (24 h). The ratio between vesicle area and cell area (Aves/Acell), number of vesicles (#ves), and number of vesicles grouped, according to their area, into three defined classes (small: 0
    Non Targeting Sirna Control Sirna, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Transcription factor activities involved in mediating NaCl-induced expression of the c-Fos gene in RPE cells. mRNA levels were determined with real-time reverse transcription (RT)–PCR analysis in cells cultured for 2 h in iso- (control) and hyperosmotic (+ 100 mM NaCl) media, and are expressed as folds of the unstimulated control. A : The level of c-Fos mRNA was determined in cells cultured in the presence of the following inhibitory compounds: the AP-1 inhibitor SR11302 (5 µM), the cAMP response element-binding protein (CREB) inhibitor 666–15 (250 nM), a HIF inhibitor (HIF-Inh; 5 µM), the STAT3 inhibitor Stattic (1 µM), and the nuclear factor (NF)-κB inhibitor CAPE (5 µM). B, C : mRNA levels were determined in cells transfected with nuclear factor of activated T cell 5 <t>(NFAT5)</t> <t>siRNA</t> (siNFAT5; 5 nM) and non-targeted siRNA (siNon; 5 nM), respectively. B : Transfection of RPE cells with NFAT5 siRNA for 48 h resulted in a reduction of the NFAT5 mRNA level in cells cultured for 2 h in iso- and hyperosmotic media. Non-targeted siRNA had no effects. As negative control, transfection reagent (TR) without siRNA was tested. C : Knocking down NFAT5 with siRNA reduced the level of c-Fos mRNA under hyperosmotic conditions. Each bar represents data obtained in three to nine independent experiments using cell lines from different donors. Significant difference versus unstimulated control: *p
    Non Targeted Control Sirna, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Depletion of Epac1 attenuates adenosine-induced increase in TER and Rac1 activation in pulmonary endothelial cells. A. <t>HPAEC</t> were treated with Epac1 specific <t>siRNA</t> or non-targeting siRNA and then challenged with 50 μM adenosine in TER measurement assay. Depletion of Epac1 significantly attenuated adenosine-induced endothelial barrier enhancement. n=3; mean +/− SEM; * p
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    Endogenous immunofluorescence of LC3 after PKCε downregulation. a Cells were transfected with PKCε siRNA (PKCε siRNA) and non-targeting siRNA (Control siRNA) and then were treated with rapamycin (300 nM) for 24 h, as described in Autophagosome visualization section. Representative images from HeLaPKCεA/E, U-138 MG, and U-118 MG cells are shown. Scale bars equate to 10 μm. b AUTOCOUNTER analysis in imaging of U-138 MG and U-118 MG cells after siRNA silencing of PKCε (72 h) and Rapamycin (300 nM) treatment (24 h). The ratio between vesicle area and cell area (Aves/Acell), number of vesicles (#ves), and number of vesicles grouped, according to their area, into three defined classes (small: 0

    Journal: BMC Cancer

    Article Title: Impact of PKCε downregulation on autophagy in glioblastoma cells

    doi: 10.1186/s12885-018-4095-1

    Figure Lengend Snippet: Endogenous immunofluorescence of LC3 after PKCε downregulation. a Cells were transfected with PKCε siRNA (PKCε siRNA) and non-targeting siRNA (Control siRNA) and then were treated with rapamycin (300 nM) for 24 h, as described in Autophagosome visualization section. Representative images from HeLaPKCεA/E, U-138 MG, and U-118 MG cells are shown. Scale bars equate to 10 μm. b AUTOCOUNTER analysis in imaging of U-138 MG and U-118 MG cells after siRNA silencing of PKCε (72 h) and Rapamycin (300 nM) treatment (24 h). The ratio between vesicle area and cell area (Aves/Acell), number of vesicles (#ves), and number of vesicles grouped, according to their area, into three defined classes (small: 0

    Article Snippet: siRNA transfection Two glioblastoma cell lines (U-138 MG and U-118 MG) were transfected with small interfering RNA against PKCε (PKCε siRNA) and non-targeting siRNA (Control-siRNA) (Santa Cruz Biotechnology, CA, USA).

    Techniques: Immunofluorescence, Transfection, Imaging

    Knockdown of PKCɛ diminishes the level and phosphorylation of Akt in glioma cells. a U-138 MG and b U-118 MG were transfected for 72 h with PKCε siRNA and Control siRNA and then were treated for 24 h with rapamycin (300 nM) or 3-MA (5 mM). GAPDH was used as a loading control and as an internal standard. Representative blots are shown. The densitometric analysis represents means ±SD of three independent experiments

    Journal: BMC Cancer

    Article Title: Impact of PKCε downregulation on autophagy in glioblastoma cells

    doi: 10.1186/s12885-018-4095-1

    Figure Lengend Snippet: Knockdown of PKCɛ diminishes the level and phosphorylation of Akt in glioma cells. a U-138 MG and b U-118 MG were transfected for 72 h with PKCε siRNA and Control siRNA and then were treated for 24 h with rapamycin (300 nM) or 3-MA (5 mM). GAPDH was used as a loading control and as an internal standard. Representative blots are shown. The densitometric analysis represents means ±SD of three independent experiments

    Article Snippet: siRNA transfection Two glioblastoma cell lines (U-138 MG and U-118 MG) were transfected with small interfering RNA against PKCε (PKCε siRNA) and non-targeting siRNA (Control-siRNA) (Santa Cruz Biotechnology, CA, USA).

    Techniques: Transfection

    Changes in autophagy gene expression in U-138 MG cells after PKCε downregulation and rapamycin or 3-MA treatment. The heat map shows the relative expression of human autophagy genes in U-138 MG cells transfected for 72 h with PKCε siRNA (PKCε siRNA) and in cells transfected and then treated for 24 h with rapamycin (PKCε siRNA + Rap) or 3-MA (PKCε siRNA + 3-MA). Each row represents an average gene expression normalized to the expression of the indicated gene in cells transfected with non-targeting siRNA (Control siRNA). Red color indicates genes that were upregulated, and blue color indicates genes that were downregulated. White indicates genes whose expression is unchanged in analyzed cells as compared to Control siRNA. Experiments were performed three times in duplicates

    Journal: BMC Cancer

    Article Title: Impact of PKCε downregulation on autophagy in glioblastoma cells

    doi: 10.1186/s12885-018-4095-1

    Figure Lengend Snippet: Changes in autophagy gene expression in U-138 MG cells after PKCε downregulation and rapamycin or 3-MA treatment. The heat map shows the relative expression of human autophagy genes in U-138 MG cells transfected for 72 h with PKCε siRNA (PKCε siRNA) and in cells transfected and then treated for 24 h with rapamycin (PKCε siRNA + Rap) or 3-MA (PKCε siRNA + 3-MA). Each row represents an average gene expression normalized to the expression of the indicated gene in cells transfected with non-targeting siRNA (Control siRNA). Red color indicates genes that were upregulated, and blue color indicates genes that were downregulated. White indicates genes whose expression is unchanged in analyzed cells as compared to Control siRNA. Experiments were performed three times in duplicates

    Article Snippet: siRNA transfection Two glioblastoma cell lines (U-138 MG and U-118 MG) were transfected with small interfering RNA against PKCε (PKCε siRNA) and non-targeting siRNA (Control-siRNA) (Santa Cruz Biotechnology, CA, USA).

    Techniques: Expressing, Transfection

    Influence of PKCε downregulation and rapamycin or 3-MA treatment on protein level directly involved in autophagy activation (mTOR, PI3K, Beclin1). a U-138 MG and b U-118 MG cells were transfected for 72 h with PKCε siRNA (PKCε siRNA) and non-targeting siRNA (Control siRNA) and then were treated for 24 h with rapamycin (300 nM) (PKCε siRNA + Rap) or 3-MA (5 mM) (PKCε siRNA + 3-MA). GAPDH was used as a loading control and as an internal standard. Representative blots are shown. In case of mTOR the order of bands has been changing, due to a different final construct of probe layout. The densitometric analysis represents means ±SD of three independent experiments. * P

    Journal: BMC Cancer

    Article Title: Impact of PKCε downregulation on autophagy in glioblastoma cells

    doi: 10.1186/s12885-018-4095-1

    Figure Lengend Snippet: Influence of PKCε downregulation and rapamycin or 3-MA treatment on protein level directly involved in autophagy activation (mTOR, PI3K, Beclin1). a U-138 MG and b U-118 MG cells were transfected for 72 h with PKCε siRNA (PKCε siRNA) and non-targeting siRNA (Control siRNA) and then were treated for 24 h with rapamycin (300 nM) (PKCε siRNA + Rap) or 3-MA (5 mM) (PKCε siRNA + 3-MA). GAPDH was used as a loading control and as an internal standard. Representative blots are shown. In case of mTOR the order of bands has been changing, due to a different final construct of probe layout. The densitometric analysis represents means ±SD of three independent experiments. * P

    Article Snippet: siRNA transfection Two glioblastoma cell lines (U-138 MG and U-118 MG) were transfected with small interfering RNA against PKCε (PKCε siRNA) and non-targeting siRNA (Control-siRNA) (Santa Cruz Biotechnology, CA, USA).

    Techniques: Activation Assay, Transfection, Construct

    Effect of PKCε downregulation and rapamycin or 3-MA treatment on proteins engaged in the formation of a double-membrane structure known as autophagosome (Atg5, LC3-II). a U-138 MG and b U-118 MG cells were transfected for 72 h with PKCε siRNA (PKCε siRNA) and non-targeting siRNA (Control siRNA) and then were treated for 24 h with rapamycin (300 nM) (PKCε siRNA + Rap) or 3-MA (5 mM) (PKCε siRNA + 3-MA). GAPDH was used as a loading control and as an internal standard. Representative blots are shown. The densitometric analysis represents means ±SD of three independent experiments. * P

    Journal: BMC Cancer

    Article Title: Impact of PKCε downregulation on autophagy in glioblastoma cells

    doi: 10.1186/s12885-018-4095-1

    Figure Lengend Snippet: Effect of PKCε downregulation and rapamycin or 3-MA treatment on proteins engaged in the formation of a double-membrane structure known as autophagosome (Atg5, LC3-II). a U-138 MG and b U-118 MG cells were transfected for 72 h with PKCε siRNA (PKCε siRNA) and non-targeting siRNA (Control siRNA) and then were treated for 24 h with rapamycin (300 nM) (PKCε siRNA + Rap) or 3-MA (5 mM) (PKCε siRNA + 3-MA). GAPDH was used as a loading control and as an internal standard. Representative blots are shown. The densitometric analysis represents means ±SD of three independent experiments. * P

    Article Snippet: siRNA transfection Two glioblastoma cell lines (U-138 MG and U-118 MG) were transfected with small interfering RNA against PKCε (PKCε siRNA) and non-targeting siRNA (Control-siRNA) (Santa Cruz Biotechnology, CA, USA).

    Techniques: Transfection

    Effect of PKCε downregulation and rapamycin or 3-MA treatment on Bcl-2, a protein that regulates autophagy process. a U-138 MG and b U-118 MG cells were transfected for 72 h with PKCε siRNA (PKCε siRNA) and non-targeting siRNA (Control siRNA) and then were treated for 24 h with rapamycin (300 nM) (PKCε siRNA + Rap) or 3-MA (5 mM) (PKCε siRNA + 3-MA). GAPDH was used as a loading control and as an internal standard. Representative blots are shown. The densitometric analysis represents means ±SD of three independent experiments. * P

    Journal: BMC Cancer

    Article Title: Impact of PKCε downregulation on autophagy in glioblastoma cells

    doi: 10.1186/s12885-018-4095-1

    Figure Lengend Snippet: Effect of PKCε downregulation and rapamycin or 3-MA treatment on Bcl-2, a protein that regulates autophagy process. a U-138 MG and b U-118 MG cells were transfected for 72 h with PKCε siRNA (PKCε siRNA) and non-targeting siRNA (Control siRNA) and then were treated for 24 h with rapamycin (300 nM) (PKCε siRNA + Rap) or 3-MA (5 mM) (PKCε siRNA + 3-MA). GAPDH was used as a loading control and as an internal standard. Representative blots are shown. The densitometric analysis represents means ±SD of three independent experiments. * P

    Article Snippet: siRNA transfection Two glioblastoma cell lines (U-138 MG and U-118 MG) were transfected with small interfering RNA against PKCε (PKCε siRNA) and non-targeting siRNA (Control-siRNA) (Santa Cruz Biotechnology, CA, USA).

    Techniques: Transfection

    Changes in autophagy gene expression in U-118 MG cells after PKCε downregulation and rapamycin or 3-MA treatment. The heat map shows the relative expression of human autophagy genes in U-118 MG cells transfected for 72 h with PKCε siRNA (PKCε siRNA) and in cells transfected and then treated for 24 h with rapamycin (PKCε siRNA + Rap) or 3-MA (PKCε siRNA + 3-MA). Each row represents an average gene expression normalized to the expression of the indicated gene in cells transfected with non-targeting siRNA (Control siRNA). Red color indicates genes that were upregulated, and blue color indicates genes that were downregulated. White indicates genes whose expression is unchanged in analyzed cells as compared to Control siRNA. Experiments were performed three times in duplicates

    Journal: BMC Cancer

    Article Title: Impact of PKCε downregulation on autophagy in glioblastoma cells

    doi: 10.1186/s12885-018-4095-1

    Figure Lengend Snippet: Changes in autophagy gene expression in U-118 MG cells after PKCε downregulation and rapamycin or 3-MA treatment. The heat map shows the relative expression of human autophagy genes in U-118 MG cells transfected for 72 h with PKCε siRNA (PKCε siRNA) and in cells transfected and then treated for 24 h with rapamycin (PKCε siRNA + Rap) or 3-MA (PKCε siRNA + 3-MA). Each row represents an average gene expression normalized to the expression of the indicated gene in cells transfected with non-targeting siRNA (Control siRNA). Red color indicates genes that were upregulated, and blue color indicates genes that were downregulated. White indicates genes whose expression is unchanged in analyzed cells as compared to Control siRNA. Experiments were performed three times in duplicates

    Article Snippet: siRNA transfection Two glioblastoma cell lines (U-138 MG and U-118 MG) were transfected with small interfering RNA against PKCε (PKCε siRNA) and non-targeting siRNA (Control-siRNA) (Santa Cruz Biotechnology, CA, USA).

    Techniques: Expressing, Transfection

    Effect of PKCε downregulation on the adhesion of glioblastoma cells. a . U-138 MG and b U-118 MG cells were transfected for 72 h with PKCε siRNA (PKCε siRNA) and Control siRNA and then were seeded in culture plates coated with Matrigel (Corning Life Sciences, NY, USA). The photos represent cell adhesion under the microscope at 100 x magnification field. c Evaluation of FAK expression in U-138 MG and U-118 MG cells with knockdown PKCε. Total protein expression and FAK phosphorylation at Tyr-397/Tyr-576/577 were assessed. GAPDH was used as a loading control and as an internal standard. Representative blots are shown. The densitometric analysis represents means ±SD of three independent experiments. * P

    Journal: BMC Cancer

    Article Title: Impact of PKCε downregulation on autophagy in glioblastoma cells

    doi: 10.1186/s12885-018-4095-1

    Figure Lengend Snippet: Effect of PKCε downregulation on the adhesion of glioblastoma cells. a . U-138 MG and b U-118 MG cells were transfected for 72 h with PKCε siRNA (PKCε siRNA) and Control siRNA and then were seeded in culture plates coated with Matrigel (Corning Life Sciences, NY, USA). The photos represent cell adhesion under the microscope at 100 x magnification field. c Evaluation of FAK expression in U-138 MG and U-118 MG cells with knockdown PKCε. Total protein expression and FAK phosphorylation at Tyr-397/Tyr-576/577 were assessed. GAPDH was used as a loading control and as an internal standard. Representative blots are shown. The densitometric analysis represents means ±SD of three independent experiments. * P

    Article Snippet: siRNA transfection Two glioblastoma cell lines (U-138 MG and U-118 MG) were transfected with small interfering RNA against PKCε (PKCε siRNA) and non-targeting siRNA (Control-siRNA) (Santa Cruz Biotechnology, CA, USA).

    Techniques: Transfection, Microscopy, Expressing

    Modulation SQSTM1/p62 after PRKCE silencing and rapamycin treatment. a U-138 MG and b U-118 MG cells were transfected for 72 h with PKCε siRNA (PKCε siRNA) and non-targeting siRNA (Control siRNA) and then were treated for 24 h with rapamycin (300 nM). GAPDH was used as a loading control and as an internal standard. Representative blots are shown. The densitometric analysis represents means ±SD of three independent experiments. * P

    Journal: BMC Cancer

    Article Title: Impact of PKCε downregulation on autophagy in glioblastoma cells

    doi: 10.1186/s12885-018-4095-1

    Figure Lengend Snippet: Modulation SQSTM1/p62 after PRKCE silencing and rapamycin treatment. a U-138 MG and b U-118 MG cells were transfected for 72 h with PKCε siRNA (PKCε siRNA) and non-targeting siRNA (Control siRNA) and then were treated for 24 h with rapamycin (300 nM). GAPDH was used as a loading control and as an internal standard. Representative blots are shown. The densitometric analysis represents means ±SD of three independent experiments. * P

    Article Snippet: siRNA transfection Two glioblastoma cell lines (U-138 MG and U-118 MG) were transfected with small interfering RNA against PKCε (PKCε siRNA) and non-targeting siRNA (Control-siRNA) (Santa Cruz Biotechnology, CA, USA).

    Techniques: Transfection

    The effect of PRKCE silencing on U-138 MG and U-118 MG cells. Cells were harvested 72 h after transfection with non-targeting siRNA (Control siRNA) or PKCε siRNA. The downregulation of PRKCE mRNA expression ( a ) and PKCε protein level ( b ) are shown. The bar graphs present average values of three independent experiments. ** P

    Journal: BMC Cancer

    Article Title: Impact of PKCε downregulation on autophagy in glioblastoma cells

    doi: 10.1186/s12885-018-4095-1

    Figure Lengend Snippet: The effect of PRKCE silencing on U-138 MG and U-118 MG cells. Cells were harvested 72 h after transfection with non-targeting siRNA (Control siRNA) or PKCε siRNA. The downregulation of PRKCE mRNA expression ( a ) and PKCε protein level ( b ) are shown. The bar graphs present average values of three independent experiments. ** P

    Article Snippet: siRNA transfection Two glioblastoma cell lines (U-138 MG and U-118 MG) were transfected with small interfering RNA against PKCε (PKCε siRNA) and non-targeting siRNA (Control-siRNA) (Santa Cruz Biotechnology, CA, USA).

    Techniques: Transfection, Expressing

    Transcription factor activities involved in mediating NaCl-induced expression of the c-Fos gene in RPE cells. mRNA levels were determined with real-time reverse transcription (RT)–PCR analysis in cells cultured for 2 h in iso- (control) and hyperosmotic (+ 100 mM NaCl) media, and are expressed as folds of the unstimulated control. A : The level of c-Fos mRNA was determined in cells cultured in the presence of the following inhibitory compounds: the AP-1 inhibitor SR11302 (5 µM), the cAMP response element-binding protein (CREB) inhibitor 666–15 (250 nM), a HIF inhibitor (HIF-Inh; 5 µM), the STAT3 inhibitor Stattic (1 µM), and the nuclear factor (NF)-κB inhibitor CAPE (5 µM). B, C : mRNA levels were determined in cells transfected with nuclear factor of activated T cell 5 (NFAT5) siRNA (siNFAT5; 5 nM) and non-targeted siRNA (siNon; 5 nM), respectively. B : Transfection of RPE cells with NFAT5 siRNA for 48 h resulted in a reduction of the NFAT5 mRNA level in cells cultured for 2 h in iso- and hyperosmotic media. Non-targeted siRNA had no effects. As negative control, transfection reagent (TR) without siRNA was tested. C : Knocking down NFAT5 with siRNA reduced the level of c-Fos mRNA under hyperosmotic conditions. Each bar represents data obtained in three to nine independent experiments using cell lines from different donors. Significant difference versus unstimulated control: *p

    Journal: Molecular Vision

    Article Title: Activator protein-1 contributes to the NaCl-induced expression of VEGF and PlGF in RPE cells

    doi:

    Figure Lengend Snippet: Transcription factor activities involved in mediating NaCl-induced expression of the c-Fos gene in RPE cells. mRNA levels were determined with real-time reverse transcription (RT)–PCR analysis in cells cultured for 2 h in iso- (control) and hyperosmotic (+ 100 mM NaCl) media, and are expressed as folds of the unstimulated control. A : The level of c-Fos mRNA was determined in cells cultured in the presence of the following inhibitory compounds: the AP-1 inhibitor SR11302 (5 µM), the cAMP response element-binding protein (CREB) inhibitor 666–15 (250 nM), a HIF inhibitor (HIF-Inh; 5 µM), the STAT3 inhibitor Stattic (1 µM), and the nuclear factor (NF)-κB inhibitor CAPE (5 µM). B, C : mRNA levels were determined in cells transfected with nuclear factor of activated T cell 5 (NFAT5) siRNA (siNFAT5; 5 nM) and non-targeted siRNA (siNon; 5 nM), respectively. B : Transfection of RPE cells with NFAT5 siRNA for 48 h resulted in a reduction of the NFAT5 mRNA level in cells cultured for 2 h in iso- and hyperosmotic media. Non-targeted siRNA had no effects. As negative control, transfection reagent (TR) without siRNA was tested. C : Knocking down NFAT5 with siRNA reduced the level of c-Fos mRNA under hyperosmotic conditions. Each bar represents data obtained in three to nine independent experiments using cell lines from different donors. Significant difference versus unstimulated control: *p

    Article Snippet: Human-specific siRNA against NFAT5 and non-targeted control siRNA were obtained from Santa Cruz Biotechnology (Heidelberg, Germany).

    Techniques: Expressing, Reverse Transcription Polymerase Chain Reaction, Cell Culture, Binding Assay, Transfection, Negative Control

    Depletion of Epac1 attenuates adenosine-induced increase in TER and Rac1 activation in pulmonary endothelial cells. A. HPAEC were treated with Epac1 specific siRNA or non-targeting siRNA and then challenged with 50 μM adenosine in TER measurement assay. Depletion of Epac1 significantly attenuated adenosine-induced endothelial barrier enhancement. n=3; mean +/− SEM; * p

    Journal: Journal of cellular physiology

    Article Title: Extracellular adenosine-induced Rac1 activation in pulmonary endothelium: molecular mechanisms and barrier-protective role

    doi: 10.1002/jcp.26281

    Figure Lengend Snippet: Depletion of Epac1 attenuates adenosine-induced increase in TER and Rac1 activation in pulmonary endothelial cells. A. HPAEC were treated with Epac1 specific siRNA or non-targeting siRNA and then challenged with 50 μM adenosine in TER measurement assay. Depletion of Epac1 significantly attenuated adenosine-induced endothelial barrier enhancement. n=3; mean +/− SEM; * p

    Article Snippet: Briefly, HPAEC were transfected either with control, non-targeting siRNA or with siRNAs specific for protein of interest (listed above).

    Techniques: Activation Assay

    Depletion of Vav2 attenuates adenosine-induced increase in TER and Rac1 activation in pulmonary endothelial cells. A. HPAEC were treated with Vav2, specific siRNA or non-specific siRNA and then challenged with 50 μM adenosine in the TER measurement assay. Depletion of Vav2 significantly attenuated adenosine-induced endothelial barrier enhancement. Arrow indicates the time point when adenosine was added. n=4; mean +/− SEM;*** p

    Journal: Journal of cellular physiology

    Article Title: Extracellular adenosine-induced Rac1 activation in pulmonary endothelium: molecular mechanisms and barrier-protective role

    doi: 10.1002/jcp.26281

    Figure Lengend Snippet: Depletion of Vav2 attenuates adenosine-induced increase in TER and Rac1 activation in pulmonary endothelial cells. A. HPAEC were treated with Vav2, specific siRNA or non-specific siRNA and then challenged with 50 μM adenosine in the TER measurement assay. Depletion of Vav2 significantly attenuated adenosine-induced endothelial barrier enhancement. Arrow indicates the time point when adenosine was added. n=4; mean +/− SEM;*** p

    Article Snippet: Briefly, HPAEC were transfected either with control, non-targeting siRNA or with siRNAs specific for protein of interest (listed above).

    Techniques: Activation Assay

    Depletion of Rap1b modestly affects adenosine-induced increase in TER while substantially decreases Rac1 activation in pulmonary endothelial cells. A. HPAEC were treated with Rap1b specific siRNA or non-specific siRNA and then challenged with 50 μM adenosine in TER measurement assay. Depletion of Rap1b modestly affected maximal adenosine-induced endothelial barrier enhancement. Arrow indicates the time point when adenosine was added. n=4; mean +/− SEM; B. Effect of adenosine in Rac1 activation in Rap1b depleted cells. HPAEC were transfected with Rap1b specific siRNA or non-specific siRNA and then 72 hours later challenged with 50 μM adenosine at different time points in Rac1 activity assay. Cells were serum starved for 2 hours before adenosine treatment and Rac1 activity was measured according to the manufacturer’s protocol. n=4; mean +/− SEM; **p

    Journal: Journal of cellular physiology

    Article Title: Extracellular adenosine-induced Rac1 activation in pulmonary endothelium: molecular mechanisms and barrier-protective role

    doi: 10.1002/jcp.26281

    Figure Lengend Snippet: Depletion of Rap1b modestly affects adenosine-induced increase in TER while substantially decreases Rac1 activation in pulmonary endothelial cells. A. HPAEC were treated with Rap1b specific siRNA or non-specific siRNA and then challenged with 50 μM adenosine in TER measurement assay. Depletion of Rap1b modestly affected maximal adenosine-induced endothelial barrier enhancement. Arrow indicates the time point when adenosine was added. n=4; mean +/− SEM; B. Effect of adenosine in Rac1 activation in Rap1b depleted cells. HPAEC were transfected with Rap1b specific siRNA or non-specific siRNA and then 72 hours later challenged with 50 μM adenosine at different time points in Rac1 activity assay. Cells were serum starved for 2 hours before adenosine treatment and Rac1 activity was measured according to the manufacturer’s protocol. n=4; mean +/− SEM; **p

    Article Snippet: Briefly, HPAEC were transfected either with control, non-targeting siRNA or with siRNAs specific for protein of interest (listed above).

    Techniques: Activation Assay, Transfection, Activity Assay

    Tiam1 depletion has no effect on adenosine-induced increase in TER and Rac1 activation in pulmonary endothelial cells. A. HPAEC were treated with Tiam1 specific siRNA or non-specific siRNA and then challenged with 50 μM adenosine in TER measurement assay. Depletion of Tiam1 did not affect adenosine-induced endothelial barrier enhancement. Arrow indicates the time point when adenosine was added. n=4; mean +/− SEM; B. Effect of adenosine on Rac1 activation in Tiam1 depleted cells. HPAEC were transfected with Tiam1 specific siRNA or non-specific siRNA and then 72 hours later challenged with 50 μM adenosine at different time points in Rac1 activity assay. Cells were serum starved for 2 hours before adenosine treatment and Rac1 activity was measured according to the manufacturer’s protocol. n=4; mean +/− SEM; **P

    Journal: Journal of cellular physiology

    Article Title: Extracellular adenosine-induced Rac1 activation in pulmonary endothelium: molecular mechanisms and barrier-protective role

    doi: 10.1002/jcp.26281

    Figure Lengend Snippet: Tiam1 depletion has no effect on adenosine-induced increase in TER and Rac1 activation in pulmonary endothelial cells. A. HPAEC were treated with Tiam1 specific siRNA or non-specific siRNA and then challenged with 50 μM adenosine in TER measurement assay. Depletion of Tiam1 did not affect adenosine-induced endothelial barrier enhancement. Arrow indicates the time point when adenosine was added. n=4; mean +/− SEM; B. Effect of adenosine on Rac1 activation in Tiam1 depleted cells. HPAEC were transfected with Tiam1 specific siRNA or non-specific siRNA and then 72 hours later challenged with 50 μM adenosine at different time points in Rac1 activity assay. Cells were serum starved for 2 hours before adenosine treatment and Rac1 activity was measured according to the manufacturer’s protocol. n=4; mean +/− SEM; **P

    Article Snippet: Briefly, HPAEC were transfected either with control, non-targeting siRNA or with siRNAs specific for protein of interest (listed above).

    Techniques: Activation Assay, Transfection, Activity Assay

    Depletion of Rap1a attenuates adenosine-induced increase in TER and Rac1 activation in pulmonary endothelial cells. A. HPAEC were treated with Rap1a specific siRNA or non-specific siRNA and then challenged with 50 μM adenosine in TER measurement assay. Depletion of Rap1a significantly attenuated adenosine-induced endothelial barrier enhancement. Arrow indicates the time point when adenosine was added. n=4; mean +/− SEM; **p

    Journal: Journal of cellular physiology

    Article Title: Extracellular adenosine-induced Rac1 activation in pulmonary endothelium: molecular mechanisms and barrier-protective role

    doi: 10.1002/jcp.26281

    Figure Lengend Snippet: Depletion of Rap1a attenuates adenosine-induced increase in TER and Rac1 activation in pulmonary endothelial cells. A. HPAEC were treated with Rap1a specific siRNA or non-specific siRNA and then challenged with 50 μM adenosine in TER measurement assay. Depletion of Rap1a significantly attenuated adenosine-induced endothelial barrier enhancement. Arrow indicates the time point when adenosine was added. n=4; mean +/− SEM; **p

    Article Snippet: Briefly, HPAEC were transfected either with control, non-targeting siRNA or with siRNAs specific for protein of interest (listed above).

    Techniques: Activation Assay