Structured Review

Biomol GmbH monensin
In AML cells, FLT3-ITD can activate AKT, ERK, and STAT5 before it reaches the PM. (A.B) MOLM-14 cells were treated with <t>monensin</t> (inhibitor of Golgi export) for 8 hours. (A) Cells treated with 100 nM monensin were stained with anti-FLT3 (red) and lectin-HPA (Golgi marker, blue). Dashed line, cell border. Bars. 10 μm. (B) Lysates were immunoblotted with the indicated antibody. To examine phospho-FLT3 Tyr59l (pFLT3 Y591 ). FLT3 was immunoprecipitated, then immunoblotted. (C.D) MV4- 11 (C) or Kasumi-6 cells (D) were treated with monensin for 8 hours, then immunoblotted. Note that FLT3-ITD in the early secretory pathway can activate downstream in AML cells.
Monensin, supplied by Biomol GmbH, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Images

1) Product Images from "FLT3-ITD transduces autonomous growth signals during its biosynthetic trafficking in acute myelogenous leukemia cells"

Article Title: FLT3-ITD transduces autonomous growth signals during its biosynthetic trafficking in acute myelogenous leukemia cells

Journal: bioRxiv

doi: 10.1101/2021.01.01.424454

In AML cells, FLT3-ITD can activate AKT, ERK, and STAT5 before it reaches the PM. (A.B) MOLM-14 cells were treated with monensin (inhibitor of Golgi export) for 8 hours. (A) Cells treated with 100 nM monensin were stained with anti-FLT3 (red) and lectin-HPA (Golgi marker, blue). Dashed line, cell border. Bars. 10 μm. (B) Lysates were immunoblotted with the indicated antibody. To examine phospho-FLT3 Tyr59l (pFLT3 Y591 ). FLT3 was immunoprecipitated, then immunoblotted. (C.D) MV4- 11 (C) or Kasumi-6 cells (D) were treated with monensin for 8 hours, then immunoblotted. Note that FLT3-ITD in the early secretory pathway can activate downstream in AML cells.
Figure Legend Snippet: In AML cells, FLT3-ITD can activate AKT, ERK, and STAT5 before it reaches the PM. (A.B) MOLM-14 cells were treated with monensin (inhibitor of Golgi export) for 8 hours. (A) Cells treated with 100 nM monensin were stained with anti-FLT3 (red) and lectin-HPA (Golgi marker, blue). Dashed line, cell border. Bars. 10 μm. (B) Lysates were immunoblotted with the indicated antibody. To examine phospho-FLT3 Tyr59l (pFLT3 Y591 ). FLT3 was immunoprecipitated, then immunoblotted. (C.D) MV4- 11 (C) or Kasumi-6 cells (D) were treated with monensin for 8 hours, then immunoblotted. Note that FLT3-ITD in the early secretory pathway can activate downstream in AML cells.

Techniques Used: Staining, Marker, Immunoprecipitation

2) Product Images from "Oncogenic signaling by Kit tyrosine kinase occurs selectively on the Golgi apparatus in gastrointestinal stromal tumors"

Article Title: Oncogenic signaling by Kit tyrosine kinase occurs selectively on the Golgi apparatus in gastrointestinal stromal tumors

Journal: Oncogene

doi: 10.1038/onc.2016.519

Kit(mut) on the Golgi signals and activates the PI3K-Akt pathway, STAT5, and Erk. ( a – c ) GIST-T1 cells were treated with ( a ) 1 μ M BFA (brefeldin A; blocks ER export to the Golgi) for 16 h, ( b ) 250 n M monensin (blocks Golgi export) for 24 h, or ( c ) 100 n M bafilomycin A1 (BafA1; blocks endo/lysosomal trafficking) for 24 h. Cells were stained with anti-Kit (green) in conjunction with anti-calnexin (ER marker, red), anti-GM130 (Golgi marker, blue), or anti-LAMP1 (endo/lysosome marker, red). Arrows indicate the PM region. An inset shows a magnified image of the boxed area. Bars, 20 μm. Immunoblots are shown. Phosphorylated proteins are presented as pKit, pAkt, pSTAT5, and pErk. ( d ) GIST882 cells were treated with 1 μ M BFA for 16 h or 250 n M monensin for 24 h. Lysates were immunoblotted. ( e ) GIST-T1 and GIST882 were treated with 1 μ M BFA for 16 h or 250 n M monensin for 24 h. Anti-Kit immunoprecipitates were immunoblotted.
Figure Legend Snippet: Kit(mut) on the Golgi signals and activates the PI3K-Akt pathway, STAT5, and Erk. ( a – c ) GIST-T1 cells were treated with ( a ) 1 μ M BFA (brefeldin A; blocks ER export to the Golgi) for 16 h, ( b ) 250 n M monensin (blocks Golgi export) for 24 h, or ( c ) 100 n M bafilomycin A1 (BafA1; blocks endo/lysosomal trafficking) for 24 h. Cells were stained with anti-Kit (green) in conjunction with anti-calnexin (ER marker, red), anti-GM130 (Golgi marker, blue), or anti-LAMP1 (endo/lysosome marker, red). Arrows indicate the PM region. An inset shows a magnified image of the boxed area. Bars, 20 μm. Immunoblots are shown. Phosphorylated proteins are presented as pKit, pAkt, pSTAT5, and pErk. ( d ) GIST882 cells were treated with 1 μ M BFA for 16 h or 250 n M monensin for 24 h. Lysates were immunoblotted. ( e ) GIST-T1 and GIST882 were treated with 1 μ M BFA for 16 h or 250 n M monensin for 24 h. Anti-Kit immunoprecipitates were immunoblotted.

Techniques Used: Staining, Marker, Western Blot

3) Product Images from "M-COPA suppresses endolysosomal Kit-Akt oncogenic signalling through inhibiting the secretory pathway in neoplastic mast cells"

Article Title: M-COPA suppresses endolysosomal Kit-Akt oncogenic signalling through inhibiting the secretory pathway in neoplastic mast cells

Journal: PLoS ONE

doi: 10.1371/journal.pone.0175514

In neoplastic mast cells, Kit phosphorylation at Tyr568/570, Tyr703, Tyr721, and Tyr936 occurs on the ER. ( A ) Tyrosine phosphorylation sites in human Kit. ( B - F ) Cells were treated with vehicle or ( B - D ) 5 μM M-COPA for 16 hours or ( E and F ) 250 nM monensin for 24 hours. Anti-Kit immunoprecipitates ( B and E ) and cell lysates ( C , D , and F ) were immunoblotted with anti-Kit, anti-phospho-Kit Tyr568/570 (anti-pKit Tyr568/570 ), anti-pKit Tyr703 , anti-pKit Tyr721 , and anti-pKit Tyr936 . Note that ER-localized Kit was phosphorylated at Tyr568/570, Tyr703, Tyr721 and Tyr936 in neoplastic mast cells.
Figure Legend Snippet: In neoplastic mast cells, Kit phosphorylation at Tyr568/570, Tyr703, Tyr721, and Tyr936 occurs on the ER. ( A ) Tyrosine phosphorylation sites in human Kit. ( B - F ) Cells were treated with vehicle or ( B - D ) 5 μM M-COPA for 16 hours or ( E and F ) 250 nM monensin for 24 hours. Anti-Kit immunoprecipitates ( B and E ) and cell lysates ( C , D , and F ) were immunoblotted with anti-Kit, anti-phospho-Kit Tyr568/570 (anti-pKit Tyr568/570 ), anti-pKit Tyr703 , anti-pKit Tyr721 , and anti-pKit Tyr936 . Note that ER-localized Kit was phosphorylated at Tyr568/570, Tyr703, Tyr721 and Tyr936 in neoplastic mast cells.

Techniques Used:

4) Product Images from "Oncogenic Kit signals on endolysosomes and endoplasmic reticulum are essential for neoplastic mast cell proliferation"

Article Title: Oncogenic Kit signals on endolysosomes and endoplasmic reticulum are essential for neoplastic mast cell proliferation

Journal: Nature Communications

doi: 10.1038/ncomms6715

Kit(D814Y) at the ER activates STAT5 in mouse cells. ( a , b ) Inhibition of export of Kit(D814Y) from the Golgi. RCM cells were cultured with 250 nM monensin (inhibits Golgi transport) for 24 h. ( a ) RCM cells were stained with anti-Kit (green) and anti-GM130 (Golgi marker, blue). Magnified images of the boxed area are shown. Bars, 10 μm. The graph shows correlation coefficient (Pearson’s R) between Kit and GM130. Results are means±s.d. from 15 cells. *** P
Figure Legend Snippet: Kit(D814Y) at the ER activates STAT5 in mouse cells. ( a , b ) Inhibition of export of Kit(D814Y) from the Golgi. RCM cells were cultured with 250 nM monensin (inhibits Golgi transport) for 24 h. ( a ) RCM cells were stained with anti-Kit (green) and anti-GM130 (Golgi marker, blue). Magnified images of the boxed area are shown. Bars, 10 μm. The graph shows correlation coefficient (Pearson’s R) between Kit and GM130. Results are means±s.d. from 15 cells. *** P

Techniques Used: Inhibition, Cell Culture, Staining, Marker

Related Articles

other:

Article Title: Oncogenic signaling by Kit tyrosine kinase occurs selectively on the Golgi apparatus in gastrointestinal stromal tumors
Article Snippet: Bafilomycin A1, brefeldin A (Sigma) and monensin (Biomol, Exeter, UK) were dissolved in ethanol.

Staining:

Article Title: Long‐term peripheral immune cell profiling reveals further targets of oral cladribine in MS
Article Snippet: .. For intracellular staining, freshly thawed PBMCs were suspended in human AB serum overnight and subsequently stimulated with 10ng/mL phorbol myristate acetate (PMA, Sigma‐Aldrich, St. Louis, MO, USA) and 1µg/mL ionomycin (Sigma‐Aldrich) and supplemented with 0.2µM monensin (Biomol, Hamburg, Germany) for 6 h at 37°C. .. After harvesting, cells were incubated with viability dye staining (Zombie Green–Alexa488) for 20 min and after corresponding washing surface staining was performed (BD‐Biosciences: CD3‐APC‐H7, CD4‐BV510, CD196‐BV605, CD197‐A700, CXCR3‐PE‐Cy5; Biolegend: CD20‐BV711).

Article Title: Accumulation and therapeutic modulation of 6-sulfo LacNAc+ dendritic cells in multiple sclerosis
Article Snippet: .. After 6 hours, PBMCs were stimulated with 100 ng/mL lipopolysaccharide (LPS; Sigma–Aldrich) or 10 µM R848 (InvivoGen, Toulouse, France) in the presence of 0.2 µM Monensin (Biomol, Hamburg, Germany) for tumor necrosis factor (TNF)-α staining and harvested 12 hours later. .. For analysing CD150 expression, cells were incubated with LPS or R848 for 24 hours.

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    Biomol GmbH monensin
    Kit(mut) on the Golgi signals and activates the PI3K-Akt pathway, STAT5, and Erk. ( a – c ) GIST-T1 cells were treated with ( a ) 1 μ M BFA (brefeldin A; blocks ER export to the Golgi) for 16 h, ( b ) 250 n M <t>monensin</t> (blocks Golgi export) for 24 h, or ( c ) 100 n M bafilomycin A1 (BafA1; blocks endo/lysosomal trafficking) for 24 h. Cells were stained with anti-Kit (green) in conjunction with anti-calnexin (ER marker, red), anti-GM130 (Golgi marker, blue), or anti-LAMP1 (endo/lysosome marker, red). Arrows indicate the PM region. An inset shows a magnified image of the boxed area. Bars, 20 μm. Immunoblots are shown. Phosphorylated proteins are presented as pKit, pAkt, pSTAT5, and pErk. ( d ) GIST882 cells were treated with 1 μ M BFA for 16 h or 250 n M monensin for 24 h. Lysates were immunoblotted. ( e ) GIST-T1 and GIST882 were treated with 1 μ M BFA for 16 h or 250 n M monensin for 24 h. Anti-Kit immunoprecipitates were immunoblotted.
    Monensin, supplied by Biomol GmbH, 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/monensin/product/Biomol GmbH
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    monensin - by Bioz Stars, 2021-03
    86/100 stars
      Buy from Supplier

    86
    Biomol GmbH monensin sodium salt
    Fig. 2. hSpry2 enhances cell surface retention of EGFRs. ( A ) To quantify the surface EGFR population, COS-1 cells were co-transfected with 0.1 µg of an EGFR expression vector, together with 0.5 µg plasmid encoding c-Cbl alone (pink triangles) or with either 0.4 µg FLAG–hSpry2 (red squares), FLAG–hSpry2ΔN11 (blue squares) or FLAG–mSpry4 (yellow squares) cDNA, or with 1.0 µg plasmid encoding the RING finger-defective form of c-Cbl (C381A) alone (green triangles). Forty-eight hours post-transfection, serum-starved culture cells were subjected to stimulation without or with 100 ng/ml EGF at 37°C for the time periods indicated. Bound EGF was removed, and the level of surface receptors relative to the initial number of ligand-binding sites was determined by incubating sister cultures with [ 125 I]EGF (10 ng/ml) at 4°C for 2–4 h, in the absence or presence of a 100-fold excess of unlabelled EGF (1 µg/ml). Control cells were not exposed to EGF (circles). The results are expressed as the average fraction of original binding sites that remained on the cell surface after exposure to the unlabelled ligand at 37°C. The graphical plot shown is derived from a single experiment that is representative of four independent experiments. ( B ) Similar transfections (closed symbols) and treatment as in (A), except that cells were pre-incubated without or with 100 ng/ml EGF in the presence of 30 µM <t>monensin</t> at 4°C for 2 h before a temperature shift to 37°C for the various time periods. The residual level of surface-bound receptors that did not undergo down-regulation was then assayed by performing a direct binding assay with radiolabelled EGF. The average of duplicate determinations was expressed as the percentage of total radioactivity at time = 0 min. The experiment was repeated twice.
    Monensin Sodium Salt, supplied by Biomol GmbH, 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/monensin sodium salt/product/Biomol GmbH
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    monensin sodium salt - by Bioz Stars, 2021-03
    86/100 stars
      Buy from Supplier

    Image Search Results


    Kit(mut) on the Golgi signals and activates the PI3K-Akt pathway, STAT5, and Erk. ( a – c ) GIST-T1 cells were treated with ( a ) 1 μ M BFA (brefeldin A; blocks ER export to the Golgi) for 16 h, ( b ) 250 n M monensin (blocks Golgi export) for 24 h, or ( c ) 100 n M bafilomycin A1 (BafA1; blocks endo/lysosomal trafficking) for 24 h. Cells were stained with anti-Kit (green) in conjunction with anti-calnexin (ER marker, red), anti-GM130 (Golgi marker, blue), or anti-LAMP1 (endo/lysosome marker, red). Arrows indicate the PM region. An inset shows a magnified image of the boxed area. Bars, 20 μm. Immunoblots are shown. Phosphorylated proteins are presented as pKit, pAkt, pSTAT5, and pErk. ( d ) GIST882 cells were treated with 1 μ M BFA for 16 h or 250 n M monensin for 24 h. Lysates were immunoblotted. ( e ) GIST-T1 and GIST882 were treated with 1 μ M BFA for 16 h or 250 n M monensin for 24 h. Anti-Kit immunoprecipitates were immunoblotted.

    Journal: Oncogene

    Article Title: Oncogenic signaling by Kit tyrosine kinase occurs selectively on the Golgi apparatus in gastrointestinal stromal tumors

    doi: 10.1038/onc.2016.519

    Figure Lengend Snippet: Kit(mut) on the Golgi signals and activates the PI3K-Akt pathway, STAT5, and Erk. ( a – c ) GIST-T1 cells were treated with ( a ) 1 μ M BFA (brefeldin A; blocks ER export to the Golgi) for 16 h, ( b ) 250 n M monensin (blocks Golgi export) for 24 h, or ( c ) 100 n M bafilomycin A1 (BafA1; blocks endo/lysosomal trafficking) for 24 h. Cells were stained with anti-Kit (green) in conjunction with anti-calnexin (ER marker, red), anti-GM130 (Golgi marker, blue), or anti-LAMP1 (endo/lysosome marker, red). Arrows indicate the PM region. An inset shows a magnified image of the boxed area. Bars, 20 μm. Immunoblots are shown. Phosphorylated proteins are presented as pKit, pAkt, pSTAT5, and pErk. ( d ) GIST882 cells were treated with 1 μ M BFA for 16 h or 250 n M monensin for 24 h. Lysates were immunoblotted. ( e ) GIST-T1 and GIST882 were treated with 1 μ M BFA for 16 h or 250 n M monensin for 24 h. Anti-Kit immunoprecipitates were immunoblotted.

    Article Snippet: Bafilomycin A1, brefeldin A (Sigma) and monensin (Biomol, Exeter, UK) were dissolved in ethanol.

    Techniques: Staining, Marker, Western Blot

    In neoplastic mast cells, Kit phosphorylation at Tyr568/570, Tyr703, Tyr721, and Tyr936 occurs on the ER. ( A ) Tyrosine phosphorylation sites in human Kit. ( B - F ) Cells were treated with vehicle or ( B - D ) 5 μM M-COPA for 16 hours or ( E and F ) 250 nM monensin for 24 hours. Anti-Kit immunoprecipitates ( B and E ) and cell lysates ( C , D , and F ) were immunoblotted with anti-Kit, anti-phospho-Kit Tyr568/570 (anti-pKit Tyr568/570 ), anti-pKit Tyr703 , anti-pKit Tyr721 , and anti-pKit Tyr936 . Note that ER-localized Kit was phosphorylated at Tyr568/570, Tyr703, Tyr721 and Tyr936 in neoplastic mast cells.

    Journal: PLoS ONE

    Article Title: M-COPA suppresses endolysosomal Kit-Akt oncogenic signalling through inhibiting the secretory pathway in neoplastic mast cells

    doi: 10.1371/journal.pone.0175514

    Figure Lengend Snippet: In neoplastic mast cells, Kit phosphorylation at Tyr568/570, Tyr703, Tyr721, and Tyr936 occurs on the ER. ( A ) Tyrosine phosphorylation sites in human Kit. ( B - F ) Cells were treated with vehicle or ( B - D ) 5 μM M-COPA for 16 hours or ( E and F ) 250 nM monensin for 24 hours. Anti-Kit immunoprecipitates ( B and E ) and cell lysates ( C , D , and F ) were immunoblotted with anti-Kit, anti-phospho-Kit Tyr568/570 (anti-pKit Tyr568/570 ), anti-pKit Tyr703 , anti-pKit Tyr721 , and anti-pKit Tyr936 . Note that ER-localized Kit was phosphorylated at Tyr568/570, Tyr703, Tyr721 and Tyr936 in neoplastic mast cells.

    Article Snippet: Monensin (Biomol, Exeter, UK), brefeldin A (Wako, Osaka, Japan), and bafilomycin A1 (Sigma) were dissolved in ethanol.

    Techniques:

    Kit(D814Y) at the ER activates STAT5 in mouse cells. ( a , b ) Inhibition of export of Kit(D814Y) from the Golgi. RCM cells were cultured with 250 nM monensin (inhibits Golgi transport) for 24 h. ( a ) RCM cells were stained with anti-Kit (green) and anti-GM130 (Golgi marker, blue). Magnified images of the boxed area are shown. Bars, 10 μm. The graph shows correlation coefficient (Pearson’s R) between Kit and GM130. Results are means±s.d. from 15 cells. *** P

    Journal: Nature Communications

    Article Title: Oncogenic Kit signals on endolysosomes and endoplasmic reticulum are essential for neoplastic mast cell proliferation

    doi: 10.1038/ncomms6715

    Figure Lengend Snippet: Kit(D814Y) at the ER activates STAT5 in mouse cells. ( a , b ) Inhibition of export of Kit(D814Y) from the Golgi. RCM cells were cultured with 250 nM monensin (inhibits Golgi transport) for 24 h. ( a ) RCM cells were stained with anti-Kit (green) and anti-GM130 (Golgi marker, blue). Magnified images of the boxed area are shown. Bars, 10 μm. The graph shows correlation coefficient (Pearson’s R) between Kit and GM130. Results are means±s.d. from 15 cells. *** P

    Article Snippet: Bafilomycin A1 (Sigma-Aldrich), brefeldin A (Sigma-Aldrich) and monensin (Biomol) were dissolved in ethanol.

    Techniques: Inhibition, Cell Culture, Staining, Marker

    Fig. 2. hSpry2 enhances cell surface retention of EGFRs. ( A ) To quantify the surface EGFR population, COS-1 cells were co-transfected with 0.1 µg of an EGFR expression vector, together with 0.5 µg plasmid encoding c-Cbl alone (pink triangles) or with either 0.4 µg FLAG–hSpry2 (red squares), FLAG–hSpry2ΔN11 (blue squares) or FLAG–mSpry4 (yellow squares) cDNA, or with 1.0 µg plasmid encoding the RING finger-defective form of c-Cbl (C381A) alone (green triangles). Forty-eight hours post-transfection, serum-starved culture cells were subjected to stimulation without or with 100 ng/ml EGF at 37°C for the time periods indicated. Bound EGF was removed, and the level of surface receptors relative to the initial number of ligand-binding sites was determined by incubating sister cultures with [ 125 I]EGF (10 ng/ml) at 4°C for 2–4 h, in the absence or presence of a 100-fold excess of unlabelled EGF (1 µg/ml). Control cells were not exposed to EGF (circles). The results are expressed as the average fraction of original binding sites that remained on the cell surface after exposure to the unlabelled ligand at 37°C. The graphical plot shown is derived from a single experiment that is representative of four independent experiments. ( B ) Similar transfections (closed symbols) and treatment as in (A), except that cells were pre-incubated without or with 100 ng/ml EGF in the presence of 30 µM monensin at 4°C for 2 h before a temperature shift to 37°C for the various time periods. The residual level of surface-bound receptors that did not undergo down-regulation was then assayed by performing a direct binding assay with radiolabelled EGF. The average of duplicate determinations was expressed as the percentage of total radioactivity at time = 0 min. The experiment was repeated twice.

    Journal: The EMBO Journal

    Article Title: Sprouty2 attenuates epidermal growth factor receptor ubiquitylation and endocytosis, and consequently enhances Ras/ERK signalling

    doi: 10.1093/emboj/cdf493

    Figure Lengend Snippet: Fig. 2. hSpry2 enhances cell surface retention of EGFRs. ( A ) To quantify the surface EGFR population, COS-1 cells were co-transfected with 0.1 µg of an EGFR expression vector, together with 0.5 µg plasmid encoding c-Cbl alone (pink triangles) or with either 0.4 µg FLAG–hSpry2 (red squares), FLAG–hSpry2ΔN11 (blue squares) or FLAG–mSpry4 (yellow squares) cDNA, or with 1.0 µg plasmid encoding the RING finger-defective form of c-Cbl (C381A) alone (green triangles). Forty-eight hours post-transfection, serum-starved culture cells were subjected to stimulation without or with 100 ng/ml EGF at 37°C for the time periods indicated. Bound EGF was removed, and the level of surface receptors relative to the initial number of ligand-binding sites was determined by incubating sister cultures with [ 125 I]EGF (10 ng/ml) at 4°C for 2–4 h, in the absence or presence of a 100-fold excess of unlabelled EGF (1 µg/ml). Control cells were not exposed to EGF (circles). The results are expressed as the average fraction of original binding sites that remained on the cell surface after exposure to the unlabelled ligand at 37°C. The graphical plot shown is derived from a single experiment that is representative of four independent experiments. ( B ) Similar transfections (closed symbols) and treatment as in (A), except that cells were pre-incubated without or with 100 ng/ml EGF in the presence of 30 µM monensin at 4°C for 2 h before a temperature shift to 37°C for the various time periods. The residual level of surface-bound receptors that did not undergo down-regulation was then assayed by performing a direct binding assay with radiolabelled EGF. The average of duplicate determinations was expressed as the percentage of total radioactivity at time = 0 min. The experiment was repeated twice.

    Article Snippet: Monensin sodium salt was obtained from Biomol Research Laboratories, Inc (Plymouth, PA).

    Techniques: Transfection, Expressing, Plasmid Preparation, Ligand Binding Assay, Binding Assay, Derivative Assay, Incubation, Radioactivity