Structured Review

Enzo Biochem monensin
ASMase is responsible for the effects of SPL on the DDR. ( a ) Control and SPL hi cells were left untreated or pretreated with <t>Monensin</t> (50 nM) for 3 h then cells were exposed to IR and caspase-3 activity was measured 24 h after radiation exposure. ( b ) SPL hi cells were either mock transfected or transfected with siRNA against human ASMase gene ( SMPD1 ). After 48 h, cells were irradiated and harvested after 24 h. ASMase activity in knockdown and mock transfected cells was assayed. Caspase-3 activity was measured using DEVD-pNA as a substrate. Data represent mean±S.D. of three independent experiments. ( * P
Monensin, supplied by Enzo Biochem, 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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1) Product Images from "S1P lyase regulates DNA damage responses through a novel sphingolipid feedback mechanism"

Article Title: S1P lyase regulates DNA damage responses through a novel sphingolipid feedback mechanism

Journal: Cell Death & Disease

doi: 10.1038/cddis.2011.3

ASMase is responsible for the effects of SPL on the DDR. ( a ) Control and SPL hi cells were left untreated or pretreated with Monensin (50 nM) for 3 h then cells were exposed to IR and caspase-3 activity was measured 24 h after radiation exposure. ( b ) SPL hi cells were either mock transfected or transfected with siRNA against human ASMase gene ( SMPD1 ). After 48 h, cells were irradiated and harvested after 24 h. ASMase activity in knockdown and mock transfected cells was assayed. Caspase-3 activity was measured using DEVD-pNA as a substrate. Data represent mean±S.D. of three independent experiments. ( * P
Figure Legend Snippet: ASMase is responsible for the effects of SPL on the DDR. ( a ) Control and SPL hi cells were left untreated or pretreated with Monensin (50 nM) for 3 h then cells were exposed to IR and caspase-3 activity was measured 24 h after radiation exposure. ( b ) SPL hi cells were either mock transfected or transfected with siRNA against human ASMase gene ( SMPD1 ). After 48 h, cells were irradiated and harvested after 24 h. ASMase activity in knockdown and mock transfected cells was assayed. Caspase-3 activity was measured using DEVD-pNA as a substrate. Data represent mean±S.D. of three independent experiments. ( * P

Techniques Used: Activity Assay, Transfection, Irradiation

2) Product Images from "Image-based drug screen identifies HDAC inhibitors as novel Golgi disruptors synergizing with JQ1"

Article Title: Image-based drug screen identifies HDAC inhibitors as novel Golgi disruptors synergizing with JQ1

Journal: Molecular Biology of the Cell

doi: 10.1091/mbc.E17-03-0176

Connectivity map analysis of classical Golgi-fragmenting drugs predicts HDAC inhibitors and DNA-damaging agents as compounds with a similar mode of action. The gene expression signatures of A549 cells treated for 20 h with 71 nM BFA, 5 µM GCA, or 10 µM monensin were determined and used to query the LINCS L1000 database to identify compounds with similar gene expression profiles. (A) Heat map representation of all the gene expression signatures in the L1000 database and their connectivity scores in comparison with our own BFA, GCA, and monensin input expression profiles. The data were sorted based on the similarity score for BFA. (B) Detailed view of the top 50 correlations identified in this analysis and sorted by their similarity to the BFA profile. Blue boxes indicate DNA-damaging agents; red boxes indicate HDAC inhibitors. (C) Pie chart summarizing the compounds in the top 50 hit list.
Figure Legend Snippet: Connectivity map analysis of classical Golgi-fragmenting drugs predicts HDAC inhibitors and DNA-damaging agents as compounds with a similar mode of action. The gene expression signatures of A549 cells treated for 20 h with 71 nM BFA, 5 µM GCA, or 10 µM monensin were determined and used to query the LINCS L1000 database to identify compounds with similar gene expression profiles. (A) Heat map representation of all the gene expression signatures in the L1000 database and their connectivity scores in comparison with our own BFA, GCA, and monensin input expression profiles. The data were sorted based on the similarity score for BFA. (B) Detailed view of the top 50 correlations identified in this analysis and sorted by their similarity to the BFA profile. Blue boxes indicate DNA-damaging agents; red boxes indicate HDAC inhibitors. (C) Pie chart summarizing the compounds in the top 50 hit list.

Techniques Used: Expressing

3) Product Images from "Aberrant T Helper 17 Cells and Related Cytokines in Bone Marrow Microenvironment of Patients with Acute Myeloid Leukemia"

Article Title: Aberrant T Helper 17 Cells and Related Cytokines in Bone Marrow Microenvironment of Patients with Acute Myeloid Leukemia

Journal: Clinical and Developmental Immunology

doi: 10.1155/2013/915873

Th subsets and their related cytokines in ND, relapsed-refractory, and CR AML patients and controls. (a) The percentage of BM Th17 cells was significantly decreased in ND AML patients compared with CR patients or controls after stimulation with phorbol myristate acetate, ionomycin, and monensin for 4 h. (b) The level of BM plasma IL-17A showed the decreased trend in the ND, relapsed-refractory, or CR AML patients compared with controls, though no statistical significance exists. (c) The percentage of BM Th1 cells was significantly decreased in ND AML patients compared with relapsed-refractory or CR patients or controls. (d) The level of BM plasma IFN- γ was decreased in the ND AML patients compared with CR patients.
Figure Legend Snippet: Th subsets and their related cytokines in ND, relapsed-refractory, and CR AML patients and controls. (a) The percentage of BM Th17 cells was significantly decreased in ND AML patients compared with CR patients or controls after stimulation with phorbol myristate acetate, ionomycin, and monensin for 4 h. (b) The level of BM plasma IL-17A showed the decreased trend in the ND, relapsed-refractory, or CR AML patients compared with controls, though no statistical significance exists. (c) The percentage of BM Th1 cells was significantly decreased in ND AML patients compared with relapsed-refractory or CR patients or controls. (d) The level of BM plasma IFN- γ was decreased in the ND AML patients compared with CR patients.

Techniques Used:

Related Articles

other:

Article Title: Preferential Recruitment of Th17 Cells to Cervical Cancer via CCR6-CCL20 Pathway
Article Snippet: Cells were stimulated to secrete cytokines for 4h with 100 ng/mL phorbol myristate acetate (PMA), 1 μg/mL ionomycin (Sigma—Aldrich) and 2 μM monensin (Enzo, Plymouth, PA).

Article Title: Thymic Stromal Lymphopoietin Attenuates the Development of Atherosclerosis in ApoE−/− Mice
Article Snippet: Cultures were stimulated with phorbol myristate acetate (20 ng/mL) plus ionomycin (1 μg/mL) from Alexis Biochemicals for 4 hours in the presence of 2 μmol/mL monensin (Alexis Biochemicals).

Article Title: The Treg/Th17 Imbalance in Patients with Obstructive Sleep Apnoea Syndrome
Article Snippet: Cultures were stimulated with phorbol myristate acetate (PMA, 50 ng/mL) plus ionomycin (1 μ M) for 4 h in the presence of monensin (500 ng/mL; all from Alexis Biochemicals, San Diego, CA).

Article Title: Peripheral Th17/Treg imbalance in patients with atherosclerotic cerebral infarction
Article Snippet: Cultures were stimulated with phorbol myristate acetate (PMA, 25 ng/ml) plus ionomycin (1 μg/ml) for 4 h, in the presence of monensin (1.7 μg/ml, all from Alexis Biochemicals, San Diego, CA, USA).

Article Title: Intranasal immunization with heat shock protein 60 induces CD4+CD25+GARP+ and type 1 regulatory T cells and inhibits early atherosclerosis
Article Snippet: For the analysis of CD4+ IFN‐γ+ (Th1), CD4+ IL‐4+ (Th2) and CD4+ IL‐17+ (Th17) T cells, the cells were stimulated with phorbol myristate acetate (PMA, 20 ng/ml) plus ionomycin (1 μg/ml; Alexis Biochemicals, San Diego, CA, USA) for 4 h in the presence of 2 μmol/ml monensin (Alexis Biochemicals).

Incubation:

Article Title: Accumulation of T-helper 22 cells, interleukin-22 and myeloid-derived suppressor cells promotes gastric cancer progression in elderly patients
Article Snippet: Flow cytometric analysis of Th1, Th17 and Th22 cells Peripheral blood was collected from all subjects and cultured under stimulation conditions. .. Heparinized peripheral whole blood (400 µl) in an equal volume of RPMI-1640 medium (Tiangen Biotech Co., Ltd., Beijing, China) were incubated for 4 h at 37°C with 5% CO2 in the presence of 25 ng/ml phorbol myristate acetate, 1 µg/ml ionomycin and 1.7 µg/ml monensin (all from Enzo Biochem, Inc., Farmingdale, NY, USA). .. Following incubation, the cells were fixed and permeabilized using FIX and PERM Reagent (MultiSciences Co., Ltd., Hangzhou, China), followed by staining with peridinin-chlorophyll-protein (PerCP)-cyanine (Cy) 5.5-conjugated anti-CD4 monoclonal antibody (cat. no., 45-0048-42; dilution,1:20; eBioscience; Thermo Fisher Scientific, Inc., Waltham, MA, USA) at room temperature in the dark for 30 min.

Article Title: Aberrant Circulating Th17 Cells in Patients with B-Cell Non-Hodgkin’s Lymphoma
Article Snippet: Flow Cytometric Analysis Flow cytometry was used to study membrane makers and intracellular cytokines to identify the cytokine-producing cells. .. Briefly, heparinized peripheral blood (400 μl) with an equal volume of RPMI 1640 medium (Hyclone, USA) was incubated for 4 h at 37°C, 5% CO2 in the presence of 25 ng/ml of phorbol myristate acetate (PMA), 1 μg/ml of ionomycin, and 1.7 μg/ml monensin (all from Alexis Biochemicals, USA). .. After incubation, the cells were stained with Alexa Fluor® 647 or PerCP/Cy 5.5 anti-CD4 (isotype mouse IgG1, κ; clone RPA-T4) monoclonal antibody at room temperature in the dark for 20 min. After surface staining, the cells were next stained with FITC anti-IFN-γ (isotype mouse IgG1, κ; clone 4S.B3), PerCP/Cy 5.5 or PE anti-IL-17 (isotype mouse IgG1, κ; clone BL168) monoclonal antibodies after fixation and permeabilization.

Article Title: The existence of Th22, pure Th17 and Th1 cells in CIN and Cervical Cancer along with their frequency variation in different stages of cervical cancer
Article Snippet: Flow Cytometric Analysis Intracellular cytokines were evaluated by flow cytometry to identify the cytokine-producing cells. .. Briefly, heparinized peripheral whole blood (200 μl) with an equal volume of Roswell Park Memorial Institute (RPMI) 1640 medium (Sigma Chemical, St Louis, MO, USA) was incubated for 4 h at 37 °C and 5 % CO2 in the presence of 25 ng/ml of phorbolmyristate acetate (PMA), 1 μg/ml of ionomycin and 1.7 μg/ml of Monensin (all from Alexis Biochemicals, San Diego, CA, USA). .. After incubation, the cells were stained with anti-CD4-PE-Cy5 monoclonal antibodies at room temperature (RT) in the dark for 15 minutes to delimitate CD4+ T cells.

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    Enzo Biochem monensin
    Golgi stress causes ARF4 upregulation (a) Several cancer cell lines were cultured with or without 20 ng/mL BFA for 29 hours before cell lysis, and protein extracts were analyzed with the indicated antibodies. The blot is representative of two independent experiments. Note the induction of ARF4 and GBF1 levels in the presence of BFA. (b) A549 cells were left untreated or exposed to 40 ng/mL BFA, 5 μM GCA, 75 μM Exo1 or 10 μM <t>Monensin</t> for 29 hours revealing increased ARF4 expression. The experiment was repeated three times. (c) Immunoblots showing ARF4 and ER stress marker expression of HeLa and A549 cells treated for 29 hours with following compounds and concentrations: lane 1: untreated, lanes 2 and 3 Brefeldin A (BFA; used at 10 ng/mL= 36 nM and 50 ng/mL= 180 nM); lanes 4–6: Tunicamycin (TM; used at 100 ng/mL (119 nM), 500 ng/mL (597 nM) and 2 mg/mL (2.39 μM); lanes 7–9: Thapsigargin (TG; used at 10 nM, 100 nM and 500 nM); lane 10: Golgicide A (GCA; used at 5 μM). Western blots are representative of two independent experiments. (d, e) Co-treatment of A549 or HeLa cells with BFA and increasing amounts of H-89 or Forskolin, two compounds that antagonize BFA-induced Golgi dispersal, mitigates upregulation of ARF4 and UPR parameters. The experiment was repeated twice with qualitatively similar results.
    Monensin, supplied by Enzo Biochem, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/monensin/product/Enzo Biochem
    Average 92 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    monensin - by Bioz Stars, 2021-03
    92/100 stars
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    Golgi stress causes ARF4 upregulation (a) Several cancer cell lines were cultured with or without 20 ng/mL BFA for 29 hours before cell lysis, and protein extracts were analyzed with the indicated antibodies. The blot is representative of two independent experiments. Note the induction of ARF4 and GBF1 levels in the presence of BFA. (b) A549 cells were left untreated or exposed to 40 ng/mL BFA, 5 μM GCA, 75 μM Exo1 or 10 μM Monensin for 29 hours revealing increased ARF4 expression. The experiment was repeated three times. (c) Immunoblots showing ARF4 and ER stress marker expression of HeLa and A549 cells treated for 29 hours with following compounds and concentrations: lane 1: untreated, lanes 2 and 3 Brefeldin A (BFA; used at 10 ng/mL= 36 nM and 50 ng/mL= 180 nM); lanes 4–6: Tunicamycin (TM; used at 100 ng/mL (119 nM), 500 ng/mL (597 nM) and 2 mg/mL (2.39 μM); lanes 7–9: Thapsigargin (TG; used at 10 nM, 100 nM and 500 nM); lane 10: Golgicide A (GCA; used at 5 μM). Western blots are representative of two independent experiments. (d, e) Co-treatment of A549 or HeLa cells with BFA and increasing amounts of H-89 or Forskolin, two compounds that antagonize BFA-induced Golgi dispersal, mitigates upregulation of ARF4 and UPR parameters. The experiment was repeated twice with qualitatively similar results.

    Journal: Nature cell biology

    Article Title: A Luman/CREB3-ADP-ribosylation factor 4 (ARF4) signaling pathway mediates the response to Golgi stress and susceptibility to pathogens

    doi: 10.1038/ncb2865

    Figure Lengend Snippet: Golgi stress causes ARF4 upregulation (a) Several cancer cell lines were cultured with or without 20 ng/mL BFA for 29 hours before cell lysis, and protein extracts were analyzed with the indicated antibodies. The blot is representative of two independent experiments. Note the induction of ARF4 and GBF1 levels in the presence of BFA. (b) A549 cells were left untreated or exposed to 40 ng/mL BFA, 5 μM GCA, 75 μM Exo1 or 10 μM Monensin for 29 hours revealing increased ARF4 expression. The experiment was repeated three times. (c) Immunoblots showing ARF4 and ER stress marker expression of HeLa and A549 cells treated for 29 hours with following compounds and concentrations: lane 1: untreated, lanes 2 and 3 Brefeldin A (BFA; used at 10 ng/mL= 36 nM and 50 ng/mL= 180 nM); lanes 4–6: Tunicamycin (TM; used at 100 ng/mL (119 nM), 500 ng/mL (597 nM) and 2 mg/mL (2.39 μM); lanes 7–9: Thapsigargin (TG; used at 10 nM, 100 nM and 500 nM); lane 10: Golgicide A (GCA; used at 5 μM). Western blots are representative of two independent experiments. (d, e) Co-treatment of A549 or HeLa cells with BFA and increasing amounts of H-89 or Forskolin, two compounds that antagonize BFA-induced Golgi dispersal, mitigates upregulation of ARF4 and UPR parameters. The experiment was repeated twice with qualitatively similar results.

    Article Snippet: Compounds were obtained from following companies: Brefeldin A (Sigma-Aldrich), Golgicide A (Santa Cruz Biotechnology), Exo1 (Santa Cruz Biotechnology), H-89 (Santa Cruz Biotechnology), Forskolin (Santa Cruz Biotechnology), Monensin (Enzo Life Sciences), AEBSF (VWR), PF 429242 (AdooQ BioScience).

    Techniques: Cell Culture, Lysis, Expressing, Western Blot, Marker

    The percentages of circulating Tc17 and Th17 cells in ITP patients and controls. Heparinized peripheral whole blood from all subjects was stimulated with phorbol myristate acetate, ionomycin, and monensin for 4 h, then stained with labeled antibodies as described in the Design and Methods section. (a) Lymphocytes were gated by flow cytometry in Gate 1. (b,d,f) CD3+ T subsets were gated by flow cytometry; the plots in intern box Gate 2 represent CD3+ T cells. (c, e, g) The percentages of circulating Tc17 and Th17 cells from ITP patients and controls; the percentage of positive cells is shown in each panel.

    Journal: PLoS ONE

    Article Title: Increased Number of Tc17 and Correlation with Th17 Cells in Patients with Immune Thrombocytopenia

    doi: 10.1371/journal.pone.0026522

    Figure Lengend Snippet: The percentages of circulating Tc17 and Th17 cells in ITP patients and controls. Heparinized peripheral whole blood from all subjects was stimulated with phorbol myristate acetate, ionomycin, and monensin for 4 h, then stained with labeled antibodies as described in the Design and Methods section. (a) Lymphocytes were gated by flow cytometry in Gate 1. (b,d,f) CD3+ T subsets were gated by flow cytometry; the plots in intern box Gate 2 represent CD3+ T cells. (c, e, g) The percentages of circulating Tc17 and Th17 cells from ITP patients and controls; the percentage of positive cells is shown in each panel.

    Article Snippet: Briefly, heparinized peripheral whole blood (400 µl) with an equal volume of Roswell Park Memorial Institute (RPMI)-1640 medium was incubated for 4 h at 37°C in 5% CO2 in the presence of 25 ng/mL of phorbol myristate acetate (PMA), 1 µg/mL of ionomycin, and 1.7 µg/mL of monensin (all from Alexis Biochemicals, San Diego, CA, USA).

    Techniques: Staining, Labeling, Flow Cytometry, Cytometry

    Th subsets and their related cytokines in ND, relapsed-refractory, and CR AML patients and controls. (a) The percentage of BM Th17 cells was significantly decreased in ND AML patients compared with CR patients or controls after stimulation with phorbol myristate acetate, ionomycin, and monensin for 4 h. (b) The level of BM plasma IL-17A showed the decreased trend in the ND, relapsed-refractory, or CR AML patients compared with controls, though no statistical significance exists. (c) The percentage of BM Th1 cells was significantly decreased in ND AML patients compared with relapsed-refractory or CR patients or controls. (d) The level of BM plasma IFN- γ was decreased in the ND AML patients compared with CR patients.

    Journal: Clinical and Developmental Immunology

    Article Title: Aberrant T Helper 17 Cells and Related Cytokines in Bone Marrow Microenvironment of Patients with Acute Myeloid Leukemia

    doi: 10.1155/2013/915873

    Figure Lengend Snippet: Th subsets and their related cytokines in ND, relapsed-refractory, and CR AML patients and controls. (a) The percentage of BM Th17 cells was significantly decreased in ND AML patients compared with CR patients or controls after stimulation with phorbol myristate acetate, ionomycin, and monensin for 4 h. (b) The level of BM plasma IL-17A showed the decreased trend in the ND, relapsed-refractory, or CR AML patients compared with controls, though no statistical significance exists. (c) The percentage of BM Th1 cells was significantly decreased in ND AML patients compared with relapsed-refractory or CR patients or controls. (d) The level of BM plasma IFN- γ was decreased in the ND AML patients compared with CR patients.

    Article Snippet: Briefly, heparinized whole BM (400 uL) with an equal volume of Roswell Park Memorial Institute (RPMI)-1640 medium was incubated for 4 h at 37°C in 5% CO2 in the presence of 2.5 ng/mL of phorbol myristate acetate (PMA), 1 mg/mL of ionomycin, and 1.7 mg/mL of monensin (all from Alexis Biochemicals, San Diego, CA, USA).

    Techniques:

    Connectivity map analysis of classical Golgi-fragmenting drugs predicts HDAC inhibitors and DNA-damaging agents as compounds with a similar mode of action. The gene expression signatures of A549 cells treated for 20 h with 71 nM BFA, 5 µM GCA, or 10 µM monensin were determined and used to query the LINCS L1000 database to identify compounds with similar gene expression profiles. (A) Heat map representation of all the gene expression signatures in the L1000 database and their connectivity scores in comparison with our own BFA, GCA, and monensin input expression profiles. The data were sorted based on the similarity score for BFA. (B) Detailed view of the top 50 correlations identified in this analysis and sorted by their similarity to the BFA profile. Blue boxes indicate DNA-damaging agents; red boxes indicate HDAC inhibitors. (C) Pie chart summarizing the compounds in the top 50 hit list.

    Journal: Molecular Biology of the Cell

    Article Title: Image-based drug screen identifies HDAC inhibitors as novel Golgi disruptors synergizing with JQ1

    doi: 10.1091/mbc.E17-03-0176

    Figure Lengend Snippet: Connectivity map analysis of classical Golgi-fragmenting drugs predicts HDAC inhibitors and DNA-damaging agents as compounds with a similar mode of action. The gene expression signatures of A549 cells treated for 20 h with 71 nM BFA, 5 µM GCA, or 10 µM monensin were determined and used to query the LINCS L1000 database to identify compounds with similar gene expression profiles. (A) Heat map representation of all the gene expression signatures in the L1000 database and their connectivity scores in comparison with our own BFA, GCA, and monensin input expression profiles. The data were sorted based on the similarity score for BFA. (B) Detailed view of the top 50 correlations identified in this analysis and sorted by their similarity to the BFA profile. Blue boxes indicate DNA-damaging agents; red boxes indicate HDAC inhibitors. (C) Pie chart summarizing the compounds in the top 50 hit list.

    Article Snippet: Compounds were obtained from the following companies: brefeldin A (Sigma-Aldrich), golgicide A (Santa Cruz Biotechnology), monensin (Enzo Life Sciences), AG-1478 (Sigma), tunicamycin (Santa Cruz Biotechnology), thapsigargin (Santa Cruz Biotechnology), nocodazole (Santa Cruz Biotechnology), (+)-JQ1 (Cayman Chemical), CBP30 (TargetMol), doxorubicin (Sigma), etoposide (Sigma), teniposide (Santa Cruz Biotechnology), mitomycin-C (Santa Cruz Biotechnology), cisplatin (Santa Cruz Biotechnology), hydroxyurea (Sigma), 5-fluorouracil (Sigma), gemcitabine (Santa Cruz Biotechnology), irinotecan (Santa Cruz Biotechnology), bleomycin (Santa Cruz Biotechnology), NU7441 (Selleckchem), KU55933 (Sigma), Flavopiridol (Santa Cruz Biotechnology), phorbol 12-myristate 13-acetate (PMA; Santa Cruz Biotechnology), Panobinostat (Selleckchem), Tubastatin (Selleckchem), Entinostat (Santa Cruz Biotechnology), Pracinostat (Selleckchem), Givinostat (Selleckchem), Triptolide (Santa Cruz Biotechnology), α-Amanitin (Santa Cruz Biotechnology), and Z-VAD-FMK (Santa Cruz Biotechnology).

    Techniques: Expressing