elisa kit  (Millipore)

 
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    Name:
    Human GH ELISA Kit
    Description:
    The Human GH ELISA Enzyme Linked Immunosorbent Assay kit is an in vitro enzyme linked immunosorbent assay for the quantitative measurement of human GH in serum plasma cell culture supernatants and urine
    Catalog Number:
    rab0206
    Price:
    None
    Applications:
    For research use only. Not for use in diagnostic procedures.Please refer to the attached General ELISA KIT Procedure (sandwich, competitive & Indirect ELISA)
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    Structured Review

    Millipore elisa kit
    Human GH ELISA Kit
    The Human GH ELISA Enzyme Linked Immunosorbent Assay kit is an in vitro enzyme linked immunosorbent assay for the quantitative measurement of human GH in serum plasma cell culture supernatants and urine
    https://www.bioz.com/result/elisa kit/product/Millipore
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    elisa kit - by Bioz Stars, 2021-03
    86/100 stars

    Images

    1) Product Images from "The incretin hormone GIP is upregulated in patients with atherosclerosis and stabilizes plaques in ApoE−/− mice by blocking monocyte/macrophage activation"

    Article Title: The incretin hormone GIP is upregulated in patients with atherosclerosis and stabilizes plaques in ApoE−/− mice by blocking monocyte/macrophage activation

    Journal: Molecular Metabolism

    doi: 10.1016/j.molmet.2018.05.014

    In vitro effects of GIP (1–42) on monocyte/macrophage inflammatory activation. Chemokine-induced migration of murine (RAW 264.7 cells) and human THP-1 monocytes. Monocytes were pretreated with GIP (1–42) for 30 min at the concentrations indicated before migration experiments using MCP-1 (10 nM) were performed in a modified Boyden chamber (A) (n = 3–4; r = 4), MMP-9 protein expression and activity analyzed by western blotting (IB) or zymography (Z) in the supernatant of RAW 264.7 cells 72 h after LPS stimulation (100 ng/mL) and 30 min pretreatment with GIP (1–42) at the indicated concentrations (B, C), IL-6 secretion of RAW 264.7 cells analyzed by ELISA 24 h after LPS stimulation (100 ng/mL) and 30 min pretreatment with 1 nM GIP (1–42) (D) (n = 4; r = 3), NF-κB p65 activation of RAW 264.7 cells at the indicated timepoints after LPS stimulation (100 ng/mL) and 30 min pretreatment with GIP (1–42) (n = 2; r = 3) (E) and western blot analysis of JNK, ERK, and p38 phosphorylation 30 min after LPS stimulation (100 ng/mL) and 30 min pretreatment with GIP (1–42) at the indicated concentrations (n = 3; r = 2). N: number of independent experiments; r: number of replicates. Results are expressed as the mean ± SEM. *p
    Figure Legend Snippet: In vitro effects of GIP (1–42) on monocyte/macrophage inflammatory activation. Chemokine-induced migration of murine (RAW 264.7 cells) and human THP-1 monocytes. Monocytes were pretreated with GIP (1–42) for 30 min at the concentrations indicated before migration experiments using MCP-1 (10 nM) were performed in a modified Boyden chamber (A) (n = 3–4; r = 4), MMP-9 protein expression and activity analyzed by western blotting (IB) or zymography (Z) in the supernatant of RAW 264.7 cells 72 h after LPS stimulation (100 ng/mL) and 30 min pretreatment with GIP (1–42) at the indicated concentrations (B, C), IL-6 secretion of RAW 264.7 cells analyzed by ELISA 24 h after LPS stimulation (100 ng/mL) and 30 min pretreatment with 1 nM GIP (1–42) (D) (n = 4; r = 3), NF-κB p65 activation of RAW 264.7 cells at the indicated timepoints after LPS stimulation (100 ng/mL) and 30 min pretreatment with GIP (1–42) (n = 2; r = 3) (E) and western blot analysis of JNK, ERK, and p38 phosphorylation 30 min after LPS stimulation (100 ng/mL) and 30 min pretreatment with GIP (1–42) at the indicated concentrations (n = 3; r = 2). N: number of independent experiments; r: number of replicates. Results are expressed as the mean ± SEM. *p

    Techniques Used: In Vitro, Activation Assay, Migration, Modification, Expressing, Activity Assay, Western Blot, Zymography, Enzyme-linked Immunosorbent Assay

    2) Product Images from "Geniposide Protects against Obesity-Related Cardiac Injury through AMPKα- and Sirt1-Dependent Mechanisms"

    Article Title: Geniposide Protects against Obesity-Related Cardiac Injury through AMPKα- and Sirt1-Dependent Mechanisms

    Journal: Oxidative Medicine and Cellular Longevity

    doi: 10.1155/2018/6053727

    Geniposide (50 mg/kg) treatment for 3 weeks attenuated myocardial inflammation in obese mice. (a, b) Representative Western blots and quantitative results of NF- κ B in the nucleus and cytoplasm ( n = 6). (c) Cardiac TNF- α levels as detected by ELISA ( n = 6). (d) The mRNA levels of inflammatory factors ( n = 6). The data are expressed as the mean ± SD. ∗ P
    Figure Legend Snippet: Geniposide (50 mg/kg) treatment for 3 weeks attenuated myocardial inflammation in obese mice. (a, b) Representative Western blots and quantitative results of NF- κ B in the nucleus and cytoplasm ( n = 6). (c) Cardiac TNF- α levels as detected by ELISA ( n = 6). (d) The mRNA levels of inflammatory factors ( n = 6). The data are expressed as the mean ± SD. ∗ P

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

    3) Product Images from "Morphine hyperalgesia gated through microglia-mediated disruption of neuronal Cl− homeostasis"

    Article Title: Morphine hyperalgesia gated through microglia-mediated disruption of neuronal Cl− homeostasis

    Journal: Nature neuroscience

    doi: 10.1038/nn.3295

    Altered Cl − homeostasis in spinal neurons and morphine-induced hyperalgesia are depend on P2X4R-BDNF-TrkB signaling a . ELISA-based measurement of BDNF release from cultured microglia treated with 100 nM morphine ( n = 14 trials, H: 30.17, *** P
    Figure Legend Snippet: Altered Cl − homeostasis in spinal neurons and morphine-induced hyperalgesia are depend on P2X4R-BDNF-TrkB signaling a . ELISA-based measurement of BDNF release from cultured microglia treated with 100 nM morphine ( n = 14 trials, H: 30.17, *** P

    Techniques Used: Enzyme-linked Immunosorbent Assay, Cell Culture

    4) Product Images from "An excessive increase in glutamate contributes to glucose-toxicity in β-cells via activation of pancreatic NMDA receptors in rodent diabetes"

    Article Title: An excessive increase in glutamate contributes to glucose-toxicity in β-cells via activation of pancreatic NMDA receptors in rodent diabetes

    Journal: Scientific Reports

    doi: 10.1038/srep44120

    MK801 inhibited the expression of inflammatory cytokine and oxidative stress in high-glucose-treated β-cells. MK801 decreased the mRNA expression of TNF-α ( a ) and IL-1β ( b ) in MIN6 cells treated with glucose (33.3 mM) for 72 h, detected by real-time PCR. MK801 decreased the content of TNF-α ( c ) and IL-1β ( d ) protein content in the supernatant of MIN6 cells treated with glucose (33.3 mM) for 72 h, detected by ELISA. (n = 6, * p
    Figure Legend Snippet: MK801 inhibited the expression of inflammatory cytokine and oxidative stress in high-glucose-treated β-cells. MK801 decreased the mRNA expression of TNF-α ( a ) and IL-1β ( b ) in MIN6 cells treated with glucose (33.3 mM) for 72 h, detected by real-time PCR. MK801 decreased the content of TNF-α ( c ) and IL-1β ( d ) protein content in the supernatant of MIN6 cells treated with glucose (33.3 mM) for 72 h, detected by ELISA. (n = 6, * p

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

    5) Product Images from "SARS-CoV-2 membrane glycoprotein M antagonizes the MAVS-mediated innate antiviral response"

    Article Title: SARS-CoV-2 membrane glycoprotein M antagonizes the MAVS-mediated innate antiviral response

    Journal: Cellular and Molecular Immunology

    doi: 10.1038/s41423-020-00571-x

    Identification of SARS-CoV-2 M as an inhibitor of the viral RNA-triggered innate immune response. a Screening for SARS-CoV-2 proteins that inhibit the SeV-triggered activation of the IFN-β promoter. HEK293T cells were transfected with an IFN-β promoter luciferase plasmid and the indicated SARS-CoV-2 protein expression plasmids for 20 h and then infected with SeV (MOI = 1) or left untreated for 12 h before luciferase assays were performed. b The M protein inhibits the SeV-triggered activation of the IFNβ promoter, ISRE and NF-κB in a dose-dependent manner. HEK293T cells were transfected with the indicated reporter plasmids and increasing amounts of the Flag-M plasmid for 20 h and then infected with SeV (MOI = 1) or left untreated for 12 h before luciferase assays were performed. c The M protein inhibits the SeV-triggered transcription of antiviral genes in HEK293 cells. HEK293 cells stably expressing the M protein were left uninfected or infected with SeV (MOI = 1) for the indicated times before qPCR analysis was performed. d The M protein inhibits the poly (I:C)-triggered transcription of antiviral genes in HEK293 cells. HEK293 cells stably expressing the M protein were mock-transfected or transfected with poly (I:C) for 6 h before qPCR analysis was performed. e The M protein inhibits the SARS-CoV-2-triggered transcription of antiviral genes in HEK293 cells. HEK293-ACE2 cells were transfected with the Flag-M plasmid for 20 h and then infected with SARS-CoV-2 (MOI = 1) or left uninfected for the indicated times before qPCR analysis was performed. f Effects of M on viral genome replication during SARS-CoV-2 infection in HEK293-ACE2 cells. HEK293-ACE2 cells were transfected with the Flag-M plasmid for 20 h and then infected with SARS-CoV-2 (MOI = 1) or left uninfected for the indicated times before qPCR analysis was performed. g The M protein inhibits the SeV- and poly (I:C)-induced secretion of IFN-β and TNF-α in HEK293 cells. HEK293 cells stably expressing the M protein were infected with SeV (MOI = 1) or transfected with poly (I:C) for 8 h before measurement of IFN-β and TNF-α by ELISA. h The M protein impairs the SeV- and poly (I:C)-induced phosphorylation of downstream components. HEK293 cells stably expressing the M protein were infected with SeV (MOI = 1) or transfected with poly (I:C) for the indicated times before immunoblot analysis was performed. i M impairs the SeV-induced nuclear translocation of IRF3. HeLa cells were transfected with the Flag-M plasmid for 20 h and then infected with SeV (MOI = 1) or left uninfected for 10 h before confocal microscopy was performed. j Effects of the M protein on the IFN-β-induced transcription of the ISG56 and CXCL10 genes. HEK293 cells stably expressing the M protein were untreated or treated with IFN-β for 4 h before qPCR analysis was performed. k Effects of the M protein on cell viability. HEK293 cells stably expressing the M protein and vector were measured by MTT assays. Graphs show the mean ± SD; n = 3; ns not significant; * p
    Figure Legend Snippet: Identification of SARS-CoV-2 M as an inhibitor of the viral RNA-triggered innate immune response. a Screening for SARS-CoV-2 proteins that inhibit the SeV-triggered activation of the IFN-β promoter. HEK293T cells were transfected with an IFN-β promoter luciferase plasmid and the indicated SARS-CoV-2 protein expression plasmids for 20 h and then infected with SeV (MOI = 1) or left untreated for 12 h before luciferase assays were performed. b The M protein inhibits the SeV-triggered activation of the IFNβ promoter, ISRE and NF-κB in a dose-dependent manner. HEK293T cells were transfected with the indicated reporter plasmids and increasing amounts of the Flag-M plasmid for 20 h and then infected with SeV (MOI = 1) or left untreated for 12 h before luciferase assays were performed. c The M protein inhibits the SeV-triggered transcription of antiviral genes in HEK293 cells. HEK293 cells stably expressing the M protein were left uninfected or infected with SeV (MOI = 1) for the indicated times before qPCR analysis was performed. d The M protein inhibits the poly (I:C)-triggered transcription of antiviral genes in HEK293 cells. HEK293 cells stably expressing the M protein were mock-transfected or transfected with poly (I:C) for 6 h before qPCR analysis was performed. e The M protein inhibits the SARS-CoV-2-triggered transcription of antiviral genes in HEK293 cells. HEK293-ACE2 cells were transfected with the Flag-M plasmid for 20 h and then infected with SARS-CoV-2 (MOI = 1) or left uninfected for the indicated times before qPCR analysis was performed. f Effects of M on viral genome replication during SARS-CoV-2 infection in HEK293-ACE2 cells. HEK293-ACE2 cells were transfected with the Flag-M plasmid for 20 h and then infected with SARS-CoV-2 (MOI = 1) or left uninfected for the indicated times before qPCR analysis was performed. g The M protein inhibits the SeV- and poly (I:C)-induced secretion of IFN-β and TNF-α in HEK293 cells. HEK293 cells stably expressing the M protein were infected with SeV (MOI = 1) or transfected with poly (I:C) for 8 h before measurement of IFN-β and TNF-α by ELISA. h The M protein impairs the SeV- and poly (I:C)-induced phosphorylation of downstream components. HEK293 cells stably expressing the M protein were infected with SeV (MOI = 1) or transfected with poly (I:C) for the indicated times before immunoblot analysis was performed. i M impairs the SeV-induced nuclear translocation of IRF3. HeLa cells were transfected with the Flag-M plasmid for 20 h and then infected with SeV (MOI = 1) or left uninfected for 10 h before confocal microscopy was performed. j Effects of the M protein on the IFN-β-induced transcription of the ISG56 and CXCL10 genes. HEK293 cells stably expressing the M protein were untreated or treated with IFN-β for 4 h before qPCR analysis was performed. k Effects of the M protein on cell viability. HEK293 cells stably expressing the M protein and vector were measured by MTT assays. Graphs show the mean ± SD; n = 3; ns not significant; * p

    Techniques Used: Activation Assay, Transfection, Luciferase, Plasmid Preparation, Expressing, Infection, Stable Transfection, Real-time Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay, Translocation Assay, Confocal Microscopy, MTT Assay

    Related Articles

    Enzyme-linked Immunosorbent Assay:

    Article Title: Chronic Over-Expression of Heat Shock Protein 27 Attenuates Atherogenesis and Enhances Plaque Remodeling: A Combined Histological and Mechanical Assessment of Aortic Lesions
    Article Snippet: Serum Cholesterol and HSP27 Measurements An enzymatic assay kit (Wako Pure Chemical Industries, Ltd, Osaka, Japan) was employed to determine serum levels of total cholesterol. .. Serum HSP27 levels were measured using an ELISA kit specific to human HSP27 (QIA119, Calbiochem, San Diego, CA). ..

    Article Title: S100β in Newborns after C-Section with General versus Epidural Anesthesia: a prospective observational study
    Article Snippet: S100β serum concentrations were measured using ELISA assay. .. Commercially available ELISA kits were used: EZHS100B-33K, Human S100β ELISA, EMD Millipore, Billerica, MA, USA was used at SFMIH, and Sangtec ® 100 ELISA, DiaSorin Inc., Stillwater, MN, USA was used at HUP. ..

    Article Title: Diazonium-Modified Screen-Printed Electrodes for Immunosensing Growth Hormone in Blood Samples
    Article Snippet: A picture was captured for each droplet on modified surfaces, and the contact angle was calculated using Young’s equation. .. ELISA-Based Detection GH detection kit was purchased from EMD Millipore (Etobicoke, ON, Canada). .. In the sandwich-based assay, the GH samples were captured by the pre-tittered anti-GH polyclonal antibodies on the 96-well plate, and then, the binding of a second biotinylated anti-GH polyclonal antibody would form a “sandwich” by capturing the target protein on the surface.

    Article Title: Inhibition of Nuclear Translocation of Apoptosis-Inducing Factor Is an Essential Mechanism of the Neuroprotective Activity of Pigment Epithelium-Derived Factor in a Rat Model of Retinal Degeneration
    Article Snippet: The immunoreactivity was visualized using the ECL Plus detection reagents (Amersham Biosciences, Buckinghamshire, UK). .. The protein contents in rat eyes were determined using an ELISA kit for human PEDF (not available for rat PEDF; Chemicon International). ..

    Article Title: Transforming growth factor‐β blocks glucose‐induced inflammation and apoptosis in corneal epithelial cells
    Article Snippet: The 2−ΔΔCq method was used to analyze the relative changes in gene expression. .. The concentrations of TGF‐β in the supernatant were determined using a human ELISA kit (Sigma) in accordance with the manufacturer's protocol. .. Human corneal epithelial cells were cultured for attachment and growth in a six‐well plate and then treated with glucose at varying concentrations for 24 h. Intracellular ROS levels were detected using 2′,7′‐dichlorofluorescein diacetate (DCFH‐DA; Life Technologies, Grand Island, NE, USA) during a 30‐min incubation in the dark.

    Article Title: Production of recombinant human proinsulin in the milk of transgenic mice
    Article Snippet: The resulting supernatant (plasma) was saved and used for ELISA analysis. .. Two different ELISA kits were used: 1) a Human Insulin ELISA Kit (RAB0327, Sigma), which is specifically used to measure human insulin and proinsulin; and 2) a mouse Ultrasensitive Insulin ELISA kit (80-INSMSU-E10, Alpco, Salem, NH), which has 147% and 0.27% cross-reactivity against human insulin and proinsulin, respectively. .. RT-PCR and qRT-PCR Total RNA was isolated from various tissues (mammary gland, kidney, spleen, lung, thymus, salivary gland, ovary, liver, blood, muscle, and heart) of the transgenic and non-transgenic mice using Trizol reagent (Invitrogen) and digested by RNase-free DNase I (Invitrogen).

    Article Title: Role of proNGF/p75 signaling in bladder dysfunction after spinal cord injury
    Article Snippet: Both proNGF ELISA kits are specific to proNGF and do not detect mature NGF. .. The ELISA kit for human mature NGF was purchased from Sigma-Aldrich. ..

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    • stat3 inhibitor  (Millipore)
    95
    Millipore stat3 inhibitor
    Impact of <t>STAT3</t> pathway down-modulation on SF763 cells. (A and D) Cells were treated with JSI-124 (7 hours) or with anti-gp130-blocking antibody (24 hours). Total proteins were electrophoresed by SDS–PAGE, followed by immunoblotting with anti-STAT3, anti-pSTAT3-Tyr705, and anti-β-actin antibody. (B) Clonogenic survival of SF763 cell line exposed 24 hours to a concentration range of JSI-124. One representative experiment performed in triplicate is shown. (C) Clonogenic survival of SF763 cell line exposed to 0.01 µM of JSI-124 during 24 hours. After 7 hours of treatment, cells were irradiated to 4 Gy and the surviving fraction was compared with that of control (DMSO). One representative of 3 independent experiments (performed in triplicate) is shown. (E) Clonogenic survival of SF763 cell line exposed to blocking anti-gp130 or to control (IgG2a) antibody when cells were attached in flasks (8 hours after seeding), before or after irradiation. Cells were irradiated to 4 Gy and the surviving fraction was compared with that of control (IgG2a). Representative experiment performed in triplicate is shown.
    Stat3 Inhibitor, supplied by Millipore, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/stat3 inhibitor/product/Millipore
    Average 95 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    stat3 inhibitor - by Bioz Stars, 2021-03
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    mouse il 11 elisa kit  (Millipore)
    90
    Millipore mouse il 11 elisa kit
    Increased expression of Il11 in polyps and Lkb1-deficient fibroblasts. ( A ) Western blot and ( B ) mRNA expression of Lkb1 in primary Lkb1 fl/fl MEFs 2 passages after AdCre transduction. Control cells were transduced with AdGFP. ( C ) Relative mRNA expression of indicated genes after Lkb1 deletion. Data are shown relative to β-actin mRNA levels for triplicate samples and normalized relative to control (AdGFP) cells. MEFs derived from 3 independent embryos of the same genotype were used and data shown are the average of 3 experiments. ( D ) Relative mRNA expression of indicated genes after Lkb1 deletion. Average of triplicate samples is shown relative to control (AdGFP) cells. Primary gastric fibroblasts derived from 3 independent mice of the same genotype were used and data shown are the average of 3 experiments. ( E ) Relative expression of Il11 mRNA in PJS mouse model polyps compared with adjacent normal mucosa (genotypes indicated). n = 3–5 mice per data point. ( F ) <t>ELISA</t> measurement of secreted <t>IL-11</t> from primary Lkb1 fl/fl MEFs after Lkb1 deletion. MEFs derived from 3 independent embryos of the same genotype were used and data shown are the average of 3 experiments. ( G ) Western blot analysis of p-STAT3-Y705 in wild-type intestinal epithelial crypts incubated for 45 minutes with IL-6 or IL-11 (20 ng/ml). Representative blot of 2 independent experiments is shown. ( H ) qPCR analysis of Reg3b , Reg3b , and Lrg1 mRNA expression in intestinal organoids cultured with IL-6 and IL-11 (20 ng/ml). Average of 3 experiments is shown. Error bars denote SEM. * P
    Mouse Il 11 Elisa Kit, supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 90 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    mouse il 11 elisa kit - by Bioz Stars, 2021-03
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    leptin  (Millipore)
    93
    Millipore leptin
    Insulin (a), <t>leptin</t> (b), and <t>ghrelin</t> level (c) of obese mice treated with UP601 at oral doses of 1.3 g/kg for 7 weeks. † P ≤ 0.0001; ∗ P ≤ 0.05.
    Leptin, supplied by Millipore, 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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    cdh1  (Millipore)
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    Millipore cdh1
    UL97 phosphorylates <t>Cdh1</t> at multiple sites in vitro . (A) In vitro kinase assays using purified Cdh1 and GST-UL97 were performed with [γ- 32 P]ATP in the presence or absence of maribavir (MBV). 32 P incorporation was imaged on a phosphor screen, and
    Cdh1, supplied by Millipore, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    Impact of STAT3 pathway down-modulation on SF763 cells. (A and D) Cells were treated with JSI-124 (7 hours) or with anti-gp130-blocking antibody (24 hours). Total proteins were electrophoresed by SDS–PAGE, followed by immunoblotting with anti-STAT3, anti-pSTAT3-Tyr705, and anti-β-actin antibody. (B) Clonogenic survival of SF763 cell line exposed 24 hours to a concentration range of JSI-124. One representative experiment performed in triplicate is shown. (C) Clonogenic survival of SF763 cell line exposed to 0.01 µM of JSI-124 during 24 hours. After 7 hours of treatment, cells were irradiated to 4 Gy and the surviving fraction was compared with that of control (DMSO). One representative of 3 independent experiments (performed in triplicate) is shown. (E) Clonogenic survival of SF763 cell line exposed to blocking anti-gp130 or to control (IgG2a) antibody when cells were attached in flasks (8 hours after seeding), before or after irradiation. Cells were irradiated to 4 Gy and the surviving fraction was compared with that of control (IgG2a). Representative experiment performed in triplicate is shown.

    Journal: Neuro-Oncology

    Article Title: Akt signaling pathway: a target for radiosensitizing human malignant glioma

    doi: 10.1093/neuonc/nop059

    Figure Lengend Snippet: Impact of STAT3 pathway down-modulation on SF763 cells. (A and D) Cells were treated with JSI-124 (7 hours) or with anti-gp130-blocking antibody (24 hours). Total proteins were electrophoresed by SDS–PAGE, followed by immunoblotting with anti-STAT3, anti-pSTAT3-Tyr705, and anti-β-actin antibody. (B) Clonogenic survival of SF763 cell line exposed 24 hours to a concentration range of JSI-124. One representative experiment performed in triplicate is shown. (C) Clonogenic survival of SF763 cell line exposed to 0.01 µM of JSI-124 during 24 hours. After 7 hours of treatment, cells were irradiated to 4 Gy and the surviving fraction was compared with that of control (DMSO). One representative of 3 independent experiments (performed in triplicate) is shown. (E) Clonogenic survival of SF763 cell line exposed to blocking anti-gp130 or to control (IgG2a) antibody when cells were attached in flasks (8 hours after seeding), before or after irradiation. Cells were irradiated to 4 Gy and the surviving fraction was compared with that of control (IgG2a). Representative experiment performed in triplicate is shown.

    Article Snippet: Akt inhibitor IV (B2311) was from Sigma and STAT3 inhibitor (JSI-124) was from Calbiochem (VWR).

    Techniques: Blocking Assay, SDS Page, Concentration Assay, Irradiation

    Akt and STAT3 basal signaling pathways activation. (A) Cells were harvested during the exponential growth phase and 30 µg of total proteins were loaded per lane and electrophoresed by SDS–PAGE. Transfer membranes were immunoblotted with anti-STAT3, anti-Akt, anti-pSTAT3-Tyr705, and anti-pAkt-Ser473. To ensure equal protein loading, the blots were stripped and reprobed with anti-β-actin antibody. The blot is representative of 3 independent experiments with consistent results. (B and C) Densitometric analyses of the blots are presented as relative ratios of phosphoprotein/total protein. Data were plotted as mean values ± SE of triplicate determinations (arbitrary units).

    Journal: Neuro-Oncology

    Article Title: Akt signaling pathway: a target for radiosensitizing human malignant glioma

    doi: 10.1093/neuonc/nop059

    Figure Lengend Snippet: Akt and STAT3 basal signaling pathways activation. (A) Cells were harvested during the exponential growth phase and 30 µg of total proteins were loaded per lane and electrophoresed by SDS–PAGE. Transfer membranes were immunoblotted with anti-STAT3, anti-Akt, anti-pSTAT3-Tyr705, and anti-pAkt-Ser473. To ensure equal protein loading, the blots were stripped and reprobed with anti-β-actin antibody. The blot is representative of 3 independent experiments with consistent results. (B and C) Densitometric analyses of the blots are presented as relative ratios of phosphoprotein/total protein. Data were plotted as mean values ± SE of triplicate determinations (arbitrary units).

    Article Snippet: Akt inhibitor IV (B2311) was from Sigma and STAT3 inhibitor (JSI-124) was from Calbiochem (VWR).

    Techniques: Activation Assay, SDS Page

    Impact of STAT3 pathway down-modulation on SNB19 cells. (A) Cells were treated with anti-gp130-blocking antibody (24 hours). Total proteins were electrophoresed by SDS–PAGE, followed by immunoblotting with anti-STAT3, anti-pSTAT3-Tyr705, and anti-β-actin antibody. (B) Clonogenic survival of SNB19 cell line exposed to blocking anti-gp130 or to control (IgG2a) antibody when cells were attached in flasks (8 hours after seeding). Cells were irradiated to 2 Gy and the surviving fraction was compared with that of control (IgG2a). Representative experiment performed in triplicate is shown.

    Journal: Neuro-Oncology

    Article Title: Akt signaling pathway: a target for radiosensitizing human malignant glioma

    doi: 10.1093/neuonc/nop059

    Figure Lengend Snippet: Impact of STAT3 pathway down-modulation on SNB19 cells. (A) Cells were treated with anti-gp130-blocking antibody (24 hours). Total proteins were electrophoresed by SDS–PAGE, followed by immunoblotting with anti-STAT3, anti-pSTAT3-Tyr705, and anti-β-actin antibody. (B) Clonogenic survival of SNB19 cell line exposed to blocking anti-gp130 or to control (IgG2a) antibody when cells were attached in flasks (8 hours after seeding). Cells were irradiated to 2 Gy and the surviving fraction was compared with that of control (IgG2a). Representative experiment performed in triplicate is shown.

    Article Snippet: Akt inhibitor IV (B2311) was from Sigma and STAT3 inhibitor (JSI-124) was from Calbiochem (VWR).

    Techniques: Blocking Assay, SDS Page, Irradiation

    Increased expression of Il11 in polyps and Lkb1-deficient fibroblasts. ( A ) Western blot and ( B ) mRNA expression of Lkb1 in primary Lkb1 fl/fl MEFs 2 passages after AdCre transduction. Control cells were transduced with AdGFP. ( C ) Relative mRNA expression of indicated genes after Lkb1 deletion. Data are shown relative to β-actin mRNA levels for triplicate samples and normalized relative to control (AdGFP) cells. MEFs derived from 3 independent embryos of the same genotype were used and data shown are the average of 3 experiments. ( D ) Relative mRNA expression of indicated genes after Lkb1 deletion. Average of triplicate samples is shown relative to control (AdGFP) cells. Primary gastric fibroblasts derived from 3 independent mice of the same genotype were used and data shown are the average of 3 experiments. ( E ) Relative expression of Il11 mRNA in PJS mouse model polyps compared with adjacent normal mucosa (genotypes indicated). n = 3–5 mice per data point. ( F ) ELISA measurement of secreted IL-11 from primary Lkb1 fl/fl MEFs after Lkb1 deletion. MEFs derived from 3 independent embryos of the same genotype were used and data shown are the average of 3 experiments. ( G ) Western blot analysis of p-STAT3-Y705 in wild-type intestinal epithelial crypts incubated for 45 minutes with IL-6 or IL-11 (20 ng/ml). Representative blot of 2 independent experiments is shown. ( H ) qPCR analysis of Reg3b , Reg3b , and Lrg1 mRNA expression in intestinal organoids cultured with IL-6 and IL-11 (20 ng/ml). Average of 3 experiments is shown. Error bars denote SEM. * P

    Journal: The Journal of Clinical Investigation

    Article Title: Stromal Lkb1 deficiency leads to gastrointestinal tumorigenesis involving the IL-11–JAK/STAT3 pathway

    doi: 10.1172/JCI93597

    Figure Lengend Snippet: Increased expression of Il11 in polyps and Lkb1-deficient fibroblasts. ( A ) Western blot and ( B ) mRNA expression of Lkb1 in primary Lkb1 fl/fl MEFs 2 passages after AdCre transduction. Control cells were transduced with AdGFP. ( C ) Relative mRNA expression of indicated genes after Lkb1 deletion. Data are shown relative to β-actin mRNA levels for triplicate samples and normalized relative to control (AdGFP) cells. MEFs derived from 3 independent embryos of the same genotype were used and data shown are the average of 3 experiments. ( D ) Relative mRNA expression of indicated genes after Lkb1 deletion. Average of triplicate samples is shown relative to control (AdGFP) cells. Primary gastric fibroblasts derived from 3 independent mice of the same genotype were used and data shown are the average of 3 experiments. ( E ) Relative expression of Il11 mRNA in PJS mouse model polyps compared with adjacent normal mucosa (genotypes indicated). n = 3–5 mice per data point. ( F ) ELISA measurement of secreted IL-11 from primary Lkb1 fl/fl MEFs after Lkb1 deletion. MEFs derived from 3 independent embryos of the same genotype were used and data shown are the average of 3 experiments. ( G ) Western blot analysis of p-STAT3-Y705 in wild-type intestinal epithelial crypts incubated for 45 minutes with IL-6 or IL-11 (20 ng/ml). Representative blot of 2 independent experiments is shown. ( H ) qPCR analysis of Reg3b , Reg3b , and Lrg1 mRNA expression in intestinal organoids cultured with IL-6 and IL-11 (20 ng/ml). Average of 3 experiments is shown. Error bars denote SEM. * P

    Article Snippet: A Mouse IL-11 ELISA Kit (MilliporeSigma) was used to quantify the IL-11 in the culture media.

    Techniques: Expressing, Western Blot, Transduction, Derivative Assay, Mouse Assay, Enzyme-linked Immunosorbent Assay, Incubation, Real-time Polymerase Chain Reaction, Cell Culture

    Insulin (a), leptin (b), and ghrelin level (c) of obese mice treated with UP601 at oral doses of 1.3 g/kg for 7 weeks. † P ≤ 0.0001; ∗ P ≤ 0.05.

    Journal: Journal of Obesity

    Article Title: Appetite Suppression and Antiobesity Effect of a Botanical Composition Composed of Morus alba, Yerba mate, and Magnolia officinalis

    doi: 10.1155/2016/4670818

    Figure Lengend Snippet: Insulin (a), leptin (b), and ghrelin level (c) of obese mice treated with UP601 at oral doses of 1.3 g/kg for 7 weeks. † P ≤ 0.0001; ∗ P ≤ 0.05.

    Article Snippet: Enzyme-linked immunosorbent assay (ELISA) kits were used to determine the levels of leptin (#EZML-82K, Millipore Co., USA), active ghrelin (#EZRGRA-90K, Millipore Co., USA), and insulin (#EZRMI-13K, Millipore Co., USA).

    Techniques: Mouse Assay

    UL97 phosphorylates Cdh1 at multiple sites in vitro . (A) In vitro kinase assays using purified Cdh1 and GST-UL97 were performed with [γ- 32 P]ATP in the presence or absence of maribavir (MBV). 32 P incorporation was imaged on a phosphor screen, and

    Journal: Journal of Virology

    Article Title: Inactivation and Disassembly of the Anaphase-Promoting Complex during Human Cytomegalovirus Infection Is Associated with Degradation of the APC5 and APC4 Subunits and Does Not Require UL97-Mediated Phosphorylation of Cdh1 ▿

    doi: 10.1128/JVI.01260-10

    Figure Lengend Snippet: UL97 phosphorylates Cdh1 at multiple sites in vitro . (A) In vitro kinase assays using purified Cdh1 and GST-UL97 were performed with [γ- 32 P]ATP in the presence or absence of maribavir (MBV). 32 P incorporation was imaged on a phosphor screen, and

    Article Snippet: Samples from reaction mixtures in which Cdh1 was phosphorylated by GST-UL97 in the presence of unlabeled ATP were analyzed by mass spectrometry for the sites of phosphorylation to determine whether UL97 also utilizes the same sites on Cdh1 as Cdks.

    Techniques: In Vitro, Purification

    Inactivation of the APC during HCMV infection. (A) Schematic diagram of the APC Cdh1 . The essential mammalian APC core subunits are shown and numbered accordingly. (B) Model illustrating the mechanisms by which the APC is disabled during HCMV infection.

    Journal: Journal of Virology

    Article Title: Inactivation and Disassembly of the Anaphase-Promoting Complex during Human Cytomegalovirus Infection Is Associated with Degradation of the APC5 and APC4 Subunits and Does Not Require UL97-Mediated Phosphorylation of Cdh1 ▿

    doi: 10.1128/JVI.01260-10

    Figure Lengend Snippet: Inactivation of the APC during HCMV infection. (A) Schematic diagram of the APC Cdh1 . The essential mammalian APC core subunits are shown and numbered accordingly. (B) Model illustrating the mechanisms by which the APC is disabled during HCMV infection.

    Article Snippet: Samples from reaction mixtures in which Cdh1 was phosphorylated by GST-UL97 in the presence of unlabeled ATP were analyzed by mass spectrometry for the sites of phosphorylation to determine whether UL97 also utilizes the same sites on Cdh1 as Cdks.

    Techniques: Infection