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Cell Signaling Technology Inc control pbs
<t>WPF-induced</t> activation of EGFR-ERK pathway. Human gastric epithelial cell line (GES-1) cells were treated with control <t>(PBS)</t> or WPF (1.3 mg/mL) for 12 h before protein was extracted by cell lysis buffer and analyzed using Western blot. GAPDH was used as a loading control. ( A ) Representative blots of p-ERK, ERK, p-EGFR and EGFR; ( B ) Changes of p-ERK/ERK; ( C ) Changes of p-EGFR/EGFR. Data are presented as mean ± SD. * p
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1) Product Images from "A Novel Combination of Wheat Peptides and Fucoidan Attenuates Ethanol-Induced Gastric Mucosal Damage through Anti-Oxidant, Anti-Inflammatory, and Pro-Survival Mechanisms"

Article Title: A Novel Combination of Wheat Peptides and Fucoidan Attenuates Ethanol-Induced Gastric Mucosal Damage through Anti-Oxidant, Anti-Inflammatory, and Pro-Survival Mechanisms

Journal: Nutrients

doi: 10.3390/nu9090978

WPF-induced activation of EGFR-ERK pathway. Human gastric epithelial cell line (GES-1) cells were treated with control (PBS) or WPF (1.3 mg/mL) for 12 h before protein was extracted by cell lysis buffer and analyzed using Western blot. GAPDH was used as a loading control. ( A ) Representative blots of p-ERK, ERK, p-EGFR and EGFR; ( B ) Changes of p-ERK/ERK; ( C ) Changes of p-EGFR/EGFR. Data are presented as mean ± SD. * p
Figure Legend Snippet: WPF-induced activation of EGFR-ERK pathway. Human gastric epithelial cell line (GES-1) cells were treated with control (PBS) or WPF (1.3 mg/mL) for 12 h before protein was extracted by cell lysis buffer and analyzed using Western blot. GAPDH was used as a loading control. ( A ) Representative blots of p-ERK, ERK, p-EGFR and EGFR; ( B ) Changes of p-ERK/ERK; ( C ) Changes of p-EGFR/EGFR. Data are presented as mean ± SD. * p

Techniques Used: Activation Assay, Lysis, Western Blot

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Immunohistochemistry:

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Expressing:

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Western Blot:

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Article Snippet: .. For western blotting, IPEC-J2 cells were immediately washed with ice-cold PBS two times, and the cell pellet was lysed with Lysis Buffer (Cell Signaling Technology) containing Protease Inhibitor Cocktail (Roche, Basel, Switzerland). ..

Lysis:

Article Title: Nucleotide-mediated SPDEF modulates TFF3-mediated wound healing and intestinal barrier function during the weaning process
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Protease Inhibitor:

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Blocking Assay:

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Binding Assay:

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Negative Control:

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Article Snippet: .. Free binding sites on beads were saturated with 110 μl of 1 M glycine at RT for 30 min. Exosomes-coated beads were resuspended into 400 μL PBS containing 2% BSA and a 25 μL aliquot was incubated with the following antibodies: CD63 (sc-5275, Santa Cruz), CD9 (#655433, BD Bioscience), TSG101 (ab83, Abcam), ANXA1 (AF3770, R & D Biosystems), H2AFZ (sc-67218, Santa Cruz), HSPA8 (NB100-41377, Novus), PKM2 (D78A4, Cell Signaling), and anti-human IgG (#409309, BioLegend), or an isotype-matched negative control antibody for 30 min at 4 °C followed, when needed, by incubation with FITC-conjugated secondary antibody (BD Bioscience). ..

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    Cell Signaling Technology Inc pbs controls
    <t>Cortistatin</t> regulates the inflammatory cytokine milieu in the heart during EAM progression. Mice with MyHC 614–629 ‐induced EAM were treated i.p. with <t>PBS</t> (EAM) or cortistatin (EAM + CST) three times per week for 2 weeks, and the heart was isolated at day 21. Naïve mice were used as reference. RNA expression of cytokines was assayed by quantitative real‐time PCR and normalized with GAPDH gene expression. n = 5 mice per group. * P
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    Cell Signaling Technology Inc pbs control
    AnxA1 2–26 does not induce tube formation. HUVECs (2 × 10 4 cells/well) were incubated with <t>PBS</t> (control), AnxA1 2–26 (30 μM), and/or <t>VEGF</t> (50 ng/mL) for 6 h on Matrigel ® and the number of tube structures were quantified using an optical microscope (A,B) . PECAM-1 expression was evaluated by flow cytometry (C) . Scale bar = 10 μm. Results are expressed as the mean ± SEM of two independent experiments in triplicate (ANOVA followed by the Tukey’s multiple comparisons test). ∗ p
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    Cell Signaling Technology Inc control pbs
    <t>WPF-induced</t> activation of EGFR-ERK pathway. Human gastric epithelial cell line (GES-1) cells were treated with control <t>(PBS)</t> or WPF (1.3 mg/mL) for 12 h before protein was extracted by cell lysis buffer and analyzed using Western blot. GAPDH was used as a loading control. ( A ) Representative blots of p-ERK, ERK, p-EGFR and EGFR; ( B ) Changes of p-ERK/ERK; ( C ) Changes of p-EGFR/EGFR. Data are presented as mean ± SD. * p
    Control Pbs, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/control pbs/product/Cell Signaling Technology Inc
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    Cortistatin regulates the inflammatory cytokine milieu in the heart during EAM progression. Mice with MyHC 614–629 ‐induced EAM were treated i.p. with PBS (EAM) or cortistatin (EAM + CST) three times per week for 2 weeks, and the heart was isolated at day 21. Naïve mice were used as reference. RNA expression of cytokines was assayed by quantitative real‐time PCR and normalized with GAPDH gene expression. n = 5 mice per group. * P

    Journal: British Journal of Pharmacology

    Article Title: The neuropeptide cortistatin attenuates experimental autoimmune myocarditis via inhibition of cardiomyogenic T cell‐driven inflammatory responses) The neuropeptide cortistatin attenuates experimental autoimmune myocarditis via inhibition of cardiomyogenic T cell‐driven inflammatory responses

    doi: 10.1111/bph.13682

    Figure Lengend Snippet: Cortistatin regulates the inflammatory cytokine milieu in the heart during EAM progression. Mice with MyHC 614–629 ‐induced EAM were treated i.p. with PBS (EAM) or cortistatin (EAM + CST) three times per week for 2 weeks, and the heart was isolated at day 21. Naïve mice were used as reference. RNA expression of cytokines was assayed by quantitative real‐time PCR and normalized with GAPDH gene expression. n = 5 mice per group. * P

    Article Snippet: Mice were injected s.c. with MyHC614–629 on days 0 and 7 (red arrows) and were then randomly distributed in different experimental groups that were treated i.p. with PBS (controls) or with cortistatin (CST, blue arrows) following three different profiles: treatment 1 consisted in six injections of 1 nmol of cortistatin starting at day 7 (early at the effector phase); treatment 2 consisted in six injections of 1, 0.5 or 0.1 nmol of cortisatin starting at day 11 (during the effector phase); and treatment 3 consisted in six injections of 1 nmol of cortistatin starting at day 15 (late during the effector phase).

    Techniques: Mouse Assay, Isolation, RNA Expression, Real-time Polymerase Chain Reaction, Expressing

    Cortistatin alleviates clinical signs of EAM. Mice with MyHC 614–629 ‐induced EAM were treated i.p. with PBS (EAM) or cortistatin (EAM + CST, 1 nmol per mouse) three times per week for 2 weeks starting at day 7. At day 21, hearts and sera were obtained from each experimental group for analysis. Naïve mice were used as a reference. (A) Macroscopic evaluation of hearts. Scale bars: 2 mm. (B) Ratio between heart weight and body weight. (C) Levels of BNP in serum ( n = 16 mice per group). (D) Haematoxylin–eosin staining of heart sections showing areas of myocardial inflammatory infiltration and pericardial myocyte necrosis and histopathological scores measuring extension of myocardial inflammation. Scale bars: 100 μm. The identity of inflammatory infiltrates was confirmed by immunostaining of CD45 + A). (E) Sirius Red staining of heart sections showing areas of incipient collagen deposits in pericardium and the measurement of areas positive for Sirius Red staining. Scale bars: 50 μm. In (B, D and E), each symbol represents one mouse, horizontal lines are the mean and vertical lines represent SEM for each experimental group. Results correspond to three independent experiments. * P

    Journal: British Journal of Pharmacology

    Article Title: The neuropeptide cortistatin attenuates experimental autoimmune myocarditis via inhibition of cardiomyogenic T cell‐driven inflammatory responses) The neuropeptide cortistatin attenuates experimental autoimmune myocarditis via inhibition of cardiomyogenic T cell‐driven inflammatory responses

    doi: 10.1111/bph.13682

    Figure Lengend Snippet: Cortistatin alleviates clinical signs of EAM. Mice with MyHC 614–629 ‐induced EAM were treated i.p. with PBS (EAM) or cortistatin (EAM + CST, 1 nmol per mouse) three times per week for 2 weeks starting at day 7. At day 21, hearts and sera were obtained from each experimental group for analysis. Naïve mice were used as a reference. (A) Macroscopic evaluation of hearts. Scale bars: 2 mm. (B) Ratio between heart weight and body weight. (C) Levels of BNP in serum ( n = 16 mice per group). (D) Haematoxylin–eosin staining of heart sections showing areas of myocardial inflammatory infiltration and pericardial myocyte necrosis and histopathological scores measuring extension of myocardial inflammation. Scale bars: 100 μm. The identity of inflammatory infiltrates was confirmed by immunostaining of CD45 + A). (E) Sirius Red staining of heart sections showing areas of incipient collagen deposits in pericardium and the measurement of areas positive for Sirius Red staining. Scale bars: 50 μm. In (B, D and E), each symbol represents one mouse, horizontal lines are the mean and vertical lines represent SEM for each experimental group. Results correspond to three independent experiments. * P

    Article Snippet: Mice were injected s.c. with MyHC614–629 on days 0 and 7 (red arrows) and were then randomly distributed in different experimental groups that were treated i.p. with PBS (controls) or with cortistatin (CST, blue arrows) following three different profiles: treatment 1 consisted in six injections of 1 nmol of cortistatin starting at day 7 (early at the effector phase); treatment 2 consisted in six injections of 1, 0.5 or 0.1 nmol of cortisatin starting at day 11 (during the effector phase); and treatment 3 consisted in six injections of 1 nmol of cortistatin starting at day 15 (late during the effector phase).

    Techniques: Mouse Assay, Staining, Immunostaining

    Treatment with cortistatin reduces the number of inflammatory cells infiltrating the heart of mice with EAM. Mice with MyHC 614–629 ‐induced EAM were treated i.p. with PBS (EAM) or cortistatin (EAM + CST) three times per week for 2 weeks starting at day 7. At day 21, inflammatory cells infiltrating the heart were isolated and analysed by flow cytometry. Frequency and/or absolute number of CD45 + , CD4 + , CD11b + , IFNγ + and IL‐17 + cells within live cells were determined. Naïve mice were used as reference. Representative plots are shown in Figure S2B–C. n = 6 mice per group. * P

    Journal: British Journal of Pharmacology

    Article Title: The neuropeptide cortistatin attenuates experimental autoimmune myocarditis via inhibition of cardiomyogenic T cell‐driven inflammatory responses) The neuropeptide cortistatin attenuates experimental autoimmune myocarditis via inhibition of cardiomyogenic T cell‐driven inflammatory responses

    doi: 10.1111/bph.13682

    Figure Lengend Snippet: Treatment with cortistatin reduces the number of inflammatory cells infiltrating the heart of mice with EAM. Mice with MyHC 614–629 ‐induced EAM were treated i.p. with PBS (EAM) or cortistatin (EAM + CST) three times per week for 2 weeks starting at day 7. At day 21, inflammatory cells infiltrating the heart were isolated and analysed by flow cytometry. Frequency and/or absolute number of CD45 + , CD4 + , CD11b + , IFNγ + and IL‐17 + cells within live cells were determined. Naïve mice were used as reference. Representative plots are shown in Figure S2B–C. n = 6 mice per group. * P

    Article Snippet: Mice were injected s.c. with MyHC614–629 on days 0 and 7 (red arrows) and were then randomly distributed in different experimental groups that were treated i.p. with PBS (controls) or with cortistatin (CST, blue arrows) following three different profiles: treatment 1 consisted in six injections of 1 nmol of cortistatin starting at day 7 (early at the effector phase); treatment 2 consisted in six injections of 1, 0.5 or 0.1 nmol of cortisatin starting at day 11 (during the effector phase); and treatment 3 consisted in six injections of 1 nmol of cortistatin starting at day 15 (late during the effector phase).

    Techniques: Mouse Assay, Isolation, Flow Cytometry, Cytometry

    Treatment with cortistatin impairs cardiomyogenic T‐cell responses in vivo . Mice with MyHC 614–629 ‐induced EAM were treated i.p. with PBS (EAM) or cortistatin (EAM + CST) three times per week for 2 weeks. (A) At day 21, DLN cells were isolated. Proliferation and cytokine production by DLN cells cultured in medium or restimulated with MyHC 614–629 was determined. We obtained similar results when splenocytes were analysed. n = 10 mice per group, performed in two independent experiments. * P

    Journal: British Journal of Pharmacology

    Article Title: The neuropeptide cortistatin attenuates experimental autoimmune myocarditis via inhibition of cardiomyogenic T cell‐driven inflammatory responses) The neuropeptide cortistatin attenuates experimental autoimmune myocarditis via inhibition of cardiomyogenic T cell‐driven inflammatory responses

    doi: 10.1111/bph.13682

    Figure Lengend Snippet: Treatment with cortistatin impairs cardiomyogenic T‐cell responses in vivo . Mice with MyHC 614–629 ‐induced EAM were treated i.p. with PBS (EAM) or cortistatin (EAM + CST) three times per week for 2 weeks. (A) At day 21, DLN cells were isolated. Proliferation and cytokine production by DLN cells cultured in medium or restimulated with MyHC 614–629 was determined. We obtained similar results when splenocytes were analysed. n = 10 mice per group, performed in two independent experiments. * P

    Article Snippet: Mice were injected s.c. with MyHC614–629 on days 0 and 7 (red arrows) and were then randomly distributed in different experimental groups that were treated i.p. with PBS (controls) or with cortistatin (CST, blue arrows) following three different profiles: treatment 1 consisted in six injections of 1 nmol of cortistatin starting at day 7 (early at the effector phase); treatment 2 consisted in six injections of 1, 0.5 or 0.1 nmol of cortisatin starting at day 11 (during the effector phase); and treatment 3 consisted in six injections of 1 nmol of cortistatin starting at day 15 (late during the effector phase).

    Techniques: In Vivo, Mouse Assay, Isolation, Cell Culture

    AnxA1 2–26 does not induce tube formation. HUVECs (2 × 10 4 cells/well) were incubated with PBS (control), AnxA1 2–26 (30 μM), and/or VEGF (50 ng/mL) for 6 h on Matrigel ® and the number of tube structures were quantified using an optical microscope (A,B) . PECAM-1 expression was evaluated by flow cytometry (C) . Scale bar = 10 μm. Results are expressed as the mean ± SEM of two independent experiments in triplicate (ANOVA followed by the Tukey’s multiple comparisons test). ∗ p

    Journal: Frontiers in Pharmacology

    Article Title: Annexin A12–26 Treatment Improves Skin Heterologous Transplantation by Modulating Inflammation and Angiogenesis Processes

    doi: 10.3389/fphar.2018.01015

    Figure Lengend Snippet: AnxA1 2–26 does not induce tube formation. HUVECs (2 × 10 4 cells/well) were incubated with PBS (control), AnxA1 2–26 (30 μM), and/or VEGF (50 ng/mL) for 6 h on Matrigel ® and the number of tube structures were quantified using an optical microscope (A,B) . PECAM-1 expression was evaluated by flow cytometry (C) . Scale bar = 10 μm. Results are expressed as the mean ± SEM of two independent experiments in triplicate (ANOVA followed by the Tukey’s multiple comparisons test). ∗ p

    Article Snippet: HUVECs were seeded (1 × 104 cells/well) and, after cell adhesion, were incubated with PBS (control), AnxA12–26 peptide (30 μM) and/or VEGF-A (10 ng/mL) (Cell Signaling Technology, Danvers, MA, Unites States) for 24, 48, or 72 h to measure proliferation.

    Techniques: Incubation, Microscopy, Expressing, Flow Cytometry, Cytometry

    AnxA1 2–26 increases endothelial cell migration and actin polymerization. HUVECs (1 × 10 4 cells/well) were incubated with PBS (control), AnxA1 2–26 (30 μM), and/or VEGF-A (10 or 50 ng/mL) and cell proliferation was evaluated at 24, 48, and 72 h. Results are expressed as the mean ± SEM of cells of two independent experiments in triplicate (A) . HUVECs were incubated with different treatments for 48 h, later labeled with PI (50 μg/mL) and the cell cycle phases were evaluated (ANOVA followed by the Tukey’s multiple comparisons test) (B) . HUVEC migration was evaluated after 12 h of incubation with PBS (control), AnxA1 2–26 (1, 10, or 30 μM) and/or VEGF-A (50 ng/mL). Cell migration was monitored with images obtained before (0 h) and after (12 h) treatments (C,D) . HUVECs (1 × 10 4 cells/well) were incubated with different treatments for 2 h and later incubated with rhodamine-phalloidin to evaluate actin polymerization. The intensity of fluorescence was monitored using a fluorescent plate reader (E) and by confocal microscopy (F) . Scale bar = 10 μm. Results are expressed as the mean ± SEM of cells of two independent experiments in triplicate (ANOVA followed by the Bonferroni’s test). ∗ p

    Journal: Frontiers in Pharmacology

    Article Title: Annexin A12–26 Treatment Improves Skin Heterologous Transplantation by Modulating Inflammation and Angiogenesis Processes

    doi: 10.3389/fphar.2018.01015

    Figure Lengend Snippet: AnxA1 2–26 increases endothelial cell migration and actin polymerization. HUVECs (1 × 10 4 cells/well) were incubated with PBS (control), AnxA1 2–26 (30 μM), and/or VEGF-A (10 or 50 ng/mL) and cell proliferation was evaluated at 24, 48, and 72 h. Results are expressed as the mean ± SEM of cells of two independent experiments in triplicate (A) . HUVECs were incubated with different treatments for 48 h, later labeled with PI (50 μg/mL) and the cell cycle phases were evaluated (ANOVA followed by the Tukey’s multiple comparisons test) (B) . HUVEC migration was evaluated after 12 h of incubation with PBS (control), AnxA1 2–26 (1, 10, or 30 μM) and/or VEGF-A (50 ng/mL). Cell migration was monitored with images obtained before (0 h) and after (12 h) treatments (C,D) . HUVECs (1 × 10 4 cells/well) were incubated with different treatments for 2 h and later incubated with rhodamine-phalloidin to evaluate actin polymerization. The intensity of fluorescence was monitored using a fluorescent plate reader (E) and by confocal microscopy (F) . Scale bar = 10 μm. Results are expressed as the mean ± SEM of cells of two independent experiments in triplicate (ANOVA followed by the Bonferroni’s test). ∗ p

    Article Snippet: HUVECs were seeded (1 × 104 cells/well) and, after cell adhesion, were incubated with PBS (control), AnxA12–26 peptide (30 μM) and/or VEGF-A (10 ng/mL) (Cell Signaling Technology, Danvers, MA, Unites States) for 24, 48, or 72 h to measure proliferation.

    Techniques: Migration, Incubation, Labeling, Fluorescence, Confocal Microscopy

    AnxA1 2–26 treatment improves the heterologous transplantation and induces angiogenesis. Histopathological analyses of skin transplanted fragments without (PBS) and with AnxA1 2–26 peptide treatment after 3 (A) , 10 (B) , 15 (C) , and 60 (D) days post-surgery. Cell infiltration (E) , TGF-β (F) , α-SMA (G) , FGF-b (H) , and VEGF-A (I) gene expression and VEGF-A protein (J) in the transplanted tissue. Host tissue (TH), transplanted scaffold (Sc), vessels ( ∗ ), fibroblasts (arrows). The inserts show high magnifications of the fibroblasts. The values express the mean ± SEM of five animals per group (ANOVA followed by the Bonferroni’s test). ∗ p

    Journal: Frontiers in Pharmacology

    Article Title: Annexin A12–26 Treatment Improves Skin Heterologous Transplantation by Modulating Inflammation and Angiogenesis Processes

    doi: 10.3389/fphar.2018.01015

    Figure Lengend Snippet: AnxA1 2–26 treatment improves the heterologous transplantation and induces angiogenesis. Histopathological analyses of skin transplanted fragments without (PBS) and with AnxA1 2–26 peptide treatment after 3 (A) , 10 (B) , 15 (C) , and 60 (D) days post-surgery. Cell infiltration (E) , TGF-β (F) , α-SMA (G) , FGF-b (H) , and VEGF-A (I) gene expression and VEGF-A protein (J) in the transplanted tissue. Host tissue (TH), transplanted scaffold (Sc), vessels ( ∗ ), fibroblasts (arrows). The inserts show high magnifications of the fibroblasts. The values express the mean ± SEM of five animals per group (ANOVA followed by the Bonferroni’s test). ∗ p

    Article Snippet: HUVECs were seeded (1 × 104 cells/well) and, after cell adhesion, were incubated with PBS (control), AnxA12–26 peptide (30 μM) and/or VEGF-A (10 ng/mL) (Cell Signaling Technology, Danvers, MA, Unites States) for 24, 48, or 72 h to measure proliferation.

    Techniques: Transplantation Assay, Expressing

    WPF-induced activation of EGFR-ERK pathway. Human gastric epithelial cell line (GES-1) cells were treated with control (PBS) or WPF (1.3 mg/mL) for 12 h before protein was extracted by cell lysis buffer and analyzed using Western blot. GAPDH was used as a loading control. ( A ) Representative blots of p-ERK, ERK, p-EGFR and EGFR; ( B ) Changes of p-ERK/ERK; ( C ) Changes of p-EGFR/EGFR. Data are presented as mean ± SD. * p

    Journal: Nutrients

    Article Title: A Novel Combination of Wheat Peptides and Fucoidan Attenuates Ethanol-Induced Gastric Mucosal Damage through Anti-Oxidant, Anti-Inflammatory, and Pro-Survival Mechanisms

    doi: 10.3390/nu9090978

    Figure Lengend Snippet: WPF-induced activation of EGFR-ERK pathway. Human gastric epithelial cell line (GES-1) cells were treated with control (PBS) or WPF (1.3 mg/mL) for 12 h before protein was extracted by cell lysis buffer and analyzed using Western blot. GAPDH was used as a loading control. ( A ) Representative blots of p-ERK, ERK, p-EGFR and EGFR; ( B ) Changes of p-ERK/ERK; ( C ) Changes of p-EGFR/EGFR. Data are presented as mean ± SD. * p

    Article Snippet: Western Blot GES-1 cells were treated with control (PBS) or WPF (1.3 mg/mL) for 12 h before protein extraction with cell lysis buffer (Cell Signaling, Danvers, MA, USA).

    Techniques: Activation Assay, Lysis, Western Blot