jak2 ip buffer  (Millipore)


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    Millipore jak2 ip buffer
    Erythropoietin Receptor-Mediated Activation of the <t>JAK2/STAT5,</t> RAS/MAPK, and PI3K/AKT Signaling Pathways is Attenuated by BCR-ABL Kinase Activity in K562 Cells A. Normalized hEPO-mediated (10′ stimulation) JAK2 activation in K562 cells treated for 1hr with either 100nM dasatinib or 1μM imatinib. Data represents the average ± SD (n=3). JAK2 activation was monitored by immunoprecipitation and activation loop (Y1007) phosphorylation. JAK2 activation was normalized to the level of phospho-Y1007 observed in the “DMSO” condition for each experimental replicate. B. Upper: Line diagram representation of duration of serum starve, kinase inhibitor treatment, and growth-factor stimulation. Lower: Western immunoblot analysis of whole cell lysates from K562 cells after short-term and prolonged BCR-ABL inhibition (100nM dasatinib: 2hrs, 4hrs, 8hrs, 24hrs; 0.2% DMSO, 24hrs) followed by hEPO stimulation (10′). C. Normalized hEPO-mediated JAK2 activation in K562 cells after short-term (1hr) and prolonged (24hrs) 100nM dasatinib treatment followed hEPO stimulation (10′). Data is representative of triplicate experimental analysis. JAK2 activation and normalization was performed as in (A). D. Normalized RAS-GTP loading in K562 cells after short-term (1hr) and prolonged (24hrs) 100nM dasatinib treatment followed by hEPO stimulation (10′). Data is representative of triplicate experimental analysis. RAS activation was monitored using a RAS-GTP pulldown assay and RAS-GTP levels were normalized to the “DMSO” condition. E. Normalized hEPO-mediated (10′ stimulation) JAK2 activation in K562 cells pretreated for 24hrs with 0.2% DMSO, 100nM dasatinib, 1μM imatinib, 500nM TG101348, dasatinib/TG101348, or imatinib/TG101348. JAK2 activation was monitored and normalized as in (A). F. Upper: Line diagram representation of duration of serum starve, kinase inhibitor treatment, and growth-factor stimulation. Lower: Western immunoblot analysis of whole cell lysates in K562 cells pretreated for 24hrs with 0.2% DMSO, 100nM dasatinib, 1μM imatinib, 500nM TG101348, dasatinib/TG101348, or imatinib/TG101348 followed by hEPO stimulation (10′).
    Jak2 Ip Buffer, supplied by Millipore, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/jak2 ip buffer/product/Millipore
    Average 85 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    jak2 ip buffer - by Bioz Stars, 2020-07
    85/100 stars

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    ras ip buffer
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    Images

    1) Product Images from "MEK-Dependent Negative Feedback Underlies BCR-ABL-Mediated Oncogene Addiction"

    Article Title: MEK-Dependent Negative Feedback Underlies BCR-ABL-Mediated Oncogene Addiction

    Journal: Cancer discovery

    doi: 10.1158/2159-8290.CD-13-0235

    Erythropoietin Receptor-Mediated Activation of the JAK2/STAT5, RAS/MAPK, and PI3K/AKT Signaling Pathways is Attenuated by BCR-ABL Kinase Activity in K562 Cells A. Normalized hEPO-mediated (10′ stimulation) JAK2 activation in K562 cells treated for 1hr with either 100nM dasatinib or 1μM imatinib. Data represents the average ± SD (n=3). JAK2 activation was monitored by immunoprecipitation and activation loop (Y1007) phosphorylation. JAK2 activation was normalized to the level of phospho-Y1007 observed in the “DMSO” condition for each experimental replicate. B. Upper: Line diagram representation of duration of serum starve, kinase inhibitor treatment, and growth-factor stimulation. Lower: Western immunoblot analysis of whole cell lysates from K562 cells after short-term and prolonged BCR-ABL inhibition (100nM dasatinib: 2hrs, 4hrs, 8hrs, 24hrs; 0.2% DMSO, 24hrs) followed by hEPO stimulation (10′). C. Normalized hEPO-mediated JAK2 activation in K562 cells after short-term (1hr) and prolonged (24hrs) 100nM dasatinib treatment followed hEPO stimulation (10′). Data is representative of triplicate experimental analysis. JAK2 activation and normalization was performed as in (A). D. Normalized RAS-GTP loading in K562 cells after short-term (1hr) and prolonged (24hrs) 100nM dasatinib treatment followed by hEPO stimulation (10′). Data is representative of triplicate experimental analysis. RAS activation was monitored using a RAS-GTP pulldown assay and RAS-GTP levels were normalized to the “DMSO” condition. E. Normalized hEPO-mediated (10′ stimulation) JAK2 activation in K562 cells pretreated for 24hrs with 0.2% DMSO, 100nM dasatinib, 1μM imatinib, 500nM TG101348, dasatinib/TG101348, or imatinib/TG101348. JAK2 activation was monitored and normalized as in (A). F. Upper: Line diagram representation of duration of serum starve, kinase inhibitor treatment, and growth-factor stimulation. Lower: Western immunoblot analysis of whole cell lysates in K562 cells pretreated for 24hrs with 0.2% DMSO, 100nM dasatinib, 1μM imatinib, 500nM TG101348, dasatinib/TG101348, or imatinib/TG101348 followed by hEPO stimulation (10′).
    Figure Legend Snippet: Erythropoietin Receptor-Mediated Activation of the JAK2/STAT5, RAS/MAPK, and PI3K/AKT Signaling Pathways is Attenuated by BCR-ABL Kinase Activity in K562 Cells A. Normalized hEPO-mediated (10′ stimulation) JAK2 activation in K562 cells treated for 1hr with either 100nM dasatinib or 1μM imatinib. Data represents the average ± SD (n=3). JAK2 activation was monitored by immunoprecipitation and activation loop (Y1007) phosphorylation. JAK2 activation was normalized to the level of phospho-Y1007 observed in the “DMSO” condition for each experimental replicate. B. Upper: Line diagram representation of duration of serum starve, kinase inhibitor treatment, and growth-factor stimulation. Lower: Western immunoblot analysis of whole cell lysates from K562 cells after short-term and prolonged BCR-ABL inhibition (100nM dasatinib: 2hrs, 4hrs, 8hrs, 24hrs; 0.2% DMSO, 24hrs) followed by hEPO stimulation (10′). C. Normalized hEPO-mediated JAK2 activation in K562 cells after short-term (1hr) and prolonged (24hrs) 100nM dasatinib treatment followed hEPO stimulation (10′). Data is representative of triplicate experimental analysis. JAK2 activation and normalization was performed as in (A). D. Normalized RAS-GTP loading in K562 cells after short-term (1hr) and prolonged (24hrs) 100nM dasatinib treatment followed by hEPO stimulation (10′). Data is representative of triplicate experimental analysis. RAS activation was monitored using a RAS-GTP pulldown assay and RAS-GTP levels were normalized to the “DMSO” condition. E. Normalized hEPO-mediated (10′ stimulation) JAK2 activation in K562 cells pretreated for 24hrs with 0.2% DMSO, 100nM dasatinib, 1μM imatinib, 500nM TG101348, dasatinib/TG101348, or imatinib/TG101348. JAK2 activation was monitored and normalized as in (A). F. Upper: Line diagram representation of duration of serum starve, kinase inhibitor treatment, and growth-factor stimulation. Lower: Western immunoblot analysis of whole cell lysates in K562 cells pretreated for 24hrs with 0.2% DMSO, 100nM dasatinib, 1μM imatinib, 500nM TG101348, dasatinib/TG101348, or imatinib/TG101348 followed by hEPO stimulation (10′).

    Techniques Used: Activation Assay, Activity Assay, Immunoprecipitation, Western Blot, Inhibition

    Global Gene Expression Analysis of Dasatinib Treated K562 Cells Identifies Candidate Mediators Responsible for the Attenuation of Myeloid GF-R Signaling in CML Cells A. ). The heat map at the bottom highlights a few of the genes with increased expression following dasatinib treatment in K562 cells. B. Quantitative PCR (qPCR) analysis of potential negative feedback genes in K562 cells treated with dasatinib (100nM), imatinib (1μM), or PD0325901 (500nM). The average fold expression change (2 (−ΔΔCt) ) and standard deviation (SD fold-change ) for each gene is represented (n=3). C. Upper: Line diagram representation of duration of serum starve, kinase inhibitor treatment, and growth-factor stimulation. Lower: Western immunoblot analysis of RAS and ERK activity before and after hEPO-stimulation (10′) in K562 cells pretreated for 24hrs with 0.2% DMSO, 100nM dasatinib, 500nM PD0325901, or dasatinib/PD0325901. RAS activity was monitored using a RAS-GTP pulldown assay. D. Upper: Line diagram representation of duration of serum starve, kinase inhibitor treatment, and growth-factor stimulation. Lower: Western immunoblot analysis of JAK2 and STAT5 activity before and after hEPO-stimulation in K562 cells treated under the same experimental conditions as (A). JAK2 activation was determined by immunoprecipitation and activation loop (Y1007) phosphorylation.
    Figure Legend Snippet: Global Gene Expression Analysis of Dasatinib Treated K562 Cells Identifies Candidate Mediators Responsible for the Attenuation of Myeloid GF-R Signaling in CML Cells A. ). The heat map at the bottom highlights a few of the genes with increased expression following dasatinib treatment in K562 cells. B. Quantitative PCR (qPCR) analysis of potential negative feedback genes in K562 cells treated with dasatinib (100nM), imatinib (1μM), or PD0325901 (500nM). The average fold expression change (2 (−ΔΔCt) ) and standard deviation (SD fold-change ) for each gene is represented (n=3). C. Upper: Line diagram representation of duration of serum starve, kinase inhibitor treatment, and growth-factor stimulation. Lower: Western immunoblot analysis of RAS and ERK activity before and after hEPO-stimulation (10′) in K562 cells pretreated for 24hrs with 0.2% DMSO, 100nM dasatinib, 500nM PD0325901, or dasatinib/PD0325901. RAS activity was monitored using a RAS-GTP pulldown assay. D. Upper: Line diagram representation of duration of serum starve, kinase inhibitor treatment, and growth-factor stimulation. Lower: Western immunoblot analysis of JAK2 and STAT5 activity before and after hEPO-stimulation in K562 cells treated under the same experimental conditions as (A). JAK2 activation was determined by immunoprecipitation and activation loop (Y1007) phosphorylation.

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction, Standard Deviation, Western Blot, Activity Assay, Activation Assay, Immunoprecipitation

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    Millipore jak2 ip buffer
    Erythropoietin Receptor-Mediated Activation of the <t>JAK2/STAT5,</t> RAS/MAPK, and PI3K/AKT Signaling Pathways is Attenuated by BCR-ABL Kinase Activity in K562 Cells A. Normalized hEPO-mediated (10′ stimulation) JAK2 activation in K562 cells treated for 1hr with either 100nM dasatinib or 1μM imatinib. Data represents the average ± SD (n=3). JAK2 activation was monitored by immunoprecipitation and activation loop (Y1007) phosphorylation. JAK2 activation was normalized to the level of phospho-Y1007 observed in the “DMSO” condition for each experimental replicate. B. Upper: Line diagram representation of duration of serum starve, kinase inhibitor treatment, and growth-factor stimulation. Lower: Western immunoblot analysis of whole cell lysates from K562 cells after short-term and prolonged BCR-ABL inhibition (100nM dasatinib: 2hrs, 4hrs, 8hrs, 24hrs; 0.2% DMSO, 24hrs) followed by hEPO stimulation (10′). C. Normalized hEPO-mediated JAK2 activation in K562 cells after short-term (1hr) and prolonged (24hrs) 100nM dasatinib treatment followed hEPO stimulation (10′). Data is representative of triplicate experimental analysis. JAK2 activation and normalization was performed as in (A). D. Normalized RAS-GTP loading in K562 cells after short-term (1hr) and prolonged (24hrs) 100nM dasatinib treatment followed by hEPO stimulation (10′). Data is representative of triplicate experimental analysis. RAS activation was monitored using a RAS-GTP pulldown assay and RAS-GTP levels were normalized to the “DMSO” condition. E. Normalized hEPO-mediated (10′ stimulation) JAK2 activation in K562 cells pretreated for 24hrs with 0.2% DMSO, 100nM dasatinib, 1μM imatinib, 500nM TG101348, dasatinib/TG101348, or imatinib/TG101348. JAK2 activation was monitored and normalized as in (A). F. Upper: Line diagram representation of duration of serum starve, kinase inhibitor treatment, and growth-factor stimulation. Lower: Western immunoblot analysis of whole cell lysates in K562 cells pretreated for 24hrs with 0.2% DMSO, 100nM dasatinib, 1μM imatinib, 500nM TG101348, dasatinib/TG101348, or imatinib/TG101348 followed by hEPO stimulation (10′).
    Jak2 Ip Buffer, supplied by Millipore, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/jak2 ip buffer/product/Millipore
    Average 85 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    jak2 ip buffer - by Bioz Stars, 2020-07
    85/100 stars
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    Erythropoietin Receptor-Mediated Activation of the JAK2/STAT5, RAS/MAPK, and PI3K/AKT Signaling Pathways is Attenuated by BCR-ABL Kinase Activity in K562 Cells A. Normalized hEPO-mediated (10′ stimulation) JAK2 activation in K562 cells treated for 1hr with either 100nM dasatinib or 1μM imatinib. Data represents the average ± SD (n=3). JAK2 activation was monitored by immunoprecipitation and activation loop (Y1007) phosphorylation. JAK2 activation was normalized to the level of phospho-Y1007 observed in the “DMSO” condition for each experimental replicate. B. Upper: Line diagram representation of duration of serum starve, kinase inhibitor treatment, and growth-factor stimulation. Lower: Western immunoblot analysis of whole cell lysates from K562 cells after short-term and prolonged BCR-ABL inhibition (100nM dasatinib: 2hrs, 4hrs, 8hrs, 24hrs; 0.2% DMSO, 24hrs) followed by hEPO stimulation (10′). C. Normalized hEPO-mediated JAK2 activation in K562 cells after short-term (1hr) and prolonged (24hrs) 100nM dasatinib treatment followed hEPO stimulation (10′). Data is representative of triplicate experimental analysis. JAK2 activation and normalization was performed as in (A). D. Normalized RAS-GTP loading in K562 cells after short-term (1hr) and prolonged (24hrs) 100nM dasatinib treatment followed by hEPO stimulation (10′). Data is representative of triplicate experimental analysis. RAS activation was monitored using a RAS-GTP pulldown assay and RAS-GTP levels were normalized to the “DMSO” condition. E. Normalized hEPO-mediated (10′ stimulation) JAK2 activation in K562 cells pretreated for 24hrs with 0.2% DMSO, 100nM dasatinib, 1μM imatinib, 500nM TG101348, dasatinib/TG101348, or imatinib/TG101348. JAK2 activation was monitored and normalized as in (A). F. Upper: Line diagram representation of duration of serum starve, kinase inhibitor treatment, and growth-factor stimulation. Lower: Western immunoblot analysis of whole cell lysates in K562 cells pretreated for 24hrs with 0.2% DMSO, 100nM dasatinib, 1μM imatinib, 500nM TG101348, dasatinib/TG101348, or imatinib/TG101348 followed by hEPO stimulation (10′).

    Journal: Cancer discovery

    Article Title: MEK-Dependent Negative Feedback Underlies BCR-ABL-Mediated Oncogene Addiction

    doi: 10.1158/2159-8290.CD-13-0235

    Figure Lengend Snippet: Erythropoietin Receptor-Mediated Activation of the JAK2/STAT5, RAS/MAPK, and PI3K/AKT Signaling Pathways is Attenuated by BCR-ABL Kinase Activity in K562 Cells A. Normalized hEPO-mediated (10′ stimulation) JAK2 activation in K562 cells treated for 1hr with either 100nM dasatinib or 1μM imatinib. Data represents the average ± SD (n=3). JAK2 activation was monitored by immunoprecipitation and activation loop (Y1007) phosphorylation. JAK2 activation was normalized to the level of phospho-Y1007 observed in the “DMSO” condition for each experimental replicate. B. Upper: Line diagram representation of duration of serum starve, kinase inhibitor treatment, and growth-factor stimulation. Lower: Western immunoblot analysis of whole cell lysates from K562 cells after short-term and prolonged BCR-ABL inhibition (100nM dasatinib: 2hrs, 4hrs, 8hrs, 24hrs; 0.2% DMSO, 24hrs) followed by hEPO stimulation (10′). C. Normalized hEPO-mediated JAK2 activation in K562 cells after short-term (1hr) and prolonged (24hrs) 100nM dasatinib treatment followed hEPO stimulation (10′). Data is representative of triplicate experimental analysis. JAK2 activation and normalization was performed as in (A). D. Normalized RAS-GTP loading in K562 cells after short-term (1hr) and prolonged (24hrs) 100nM dasatinib treatment followed by hEPO stimulation (10′). Data is representative of triplicate experimental analysis. RAS activation was monitored using a RAS-GTP pulldown assay and RAS-GTP levels were normalized to the “DMSO” condition. E. Normalized hEPO-mediated (10′ stimulation) JAK2 activation in K562 cells pretreated for 24hrs with 0.2% DMSO, 100nM dasatinib, 1μM imatinib, 500nM TG101348, dasatinib/TG101348, or imatinib/TG101348. JAK2 activation was monitored and normalized as in (A). F. Upper: Line diagram representation of duration of serum starve, kinase inhibitor treatment, and growth-factor stimulation. Lower: Western immunoblot analysis of whole cell lysates in K562 cells pretreated for 24hrs with 0.2% DMSO, 100nM dasatinib, 1μM imatinib, 500nM TG101348, dasatinib/TG101348, or imatinib/TG101348 followed by hEPO stimulation (10′).

    Article Snippet: Cells were lysed in JAK2 IP buffer (50mM Tris pH 7.6, 100mM NaCl, 1mM EDTA, 1mM EGTA, 0.5% NP40, 0.1% Triton) or RAS IP buffer (50mM Tris pH 7.5, 125mM NaCl, 6.5mM MgCl2 , 5% glycerol, 0.2% NP40) supplemented with 1% protease and 1% phosphatase inhibitors (Calbiochem).

    Techniques: Activation Assay, Activity Assay, Immunoprecipitation, Western Blot, Inhibition

    Global Gene Expression Analysis of Dasatinib Treated K562 Cells Identifies Candidate Mediators Responsible for the Attenuation of Myeloid GF-R Signaling in CML Cells A. ). The heat map at the bottom highlights a few of the genes with increased expression following dasatinib treatment in K562 cells. B. Quantitative PCR (qPCR) analysis of potential negative feedback genes in K562 cells treated with dasatinib (100nM), imatinib (1μM), or PD0325901 (500nM). The average fold expression change (2 (−ΔΔCt) ) and standard deviation (SD fold-change ) for each gene is represented (n=3). C. Upper: Line diagram representation of duration of serum starve, kinase inhibitor treatment, and growth-factor stimulation. Lower: Western immunoblot analysis of RAS and ERK activity before and after hEPO-stimulation (10′) in K562 cells pretreated for 24hrs with 0.2% DMSO, 100nM dasatinib, 500nM PD0325901, or dasatinib/PD0325901. RAS activity was monitored using a RAS-GTP pulldown assay. D. Upper: Line diagram representation of duration of serum starve, kinase inhibitor treatment, and growth-factor stimulation. Lower: Western immunoblot analysis of JAK2 and STAT5 activity before and after hEPO-stimulation in K562 cells treated under the same experimental conditions as (A). JAK2 activation was determined by immunoprecipitation and activation loop (Y1007) phosphorylation.

    Journal: Cancer discovery

    Article Title: MEK-Dependent Negative Feedback Underlies BCR-ABL-Mediated Oncogene Addiction

    doi: 10.1158/2159-8290.CD-13-0235

    Figure Lengend Snippet: Global Gene Expression Analysis of Dasatinib Treated K562 Cells Identifies Candidate Mediators Responsible for the Attenuation of Myeloid GF-R Signaling in CML Cells A. ). The heat map at the bottom highlights a few of the genes with increased expression following dasatinib treatment in K562 cells. B. Quantitative PCR (qPCR) analysis of potential negative feedback genes in K562 cells treated with dasatinib (100nM), imatinib (1μM), or PD0325901 (500nM). The average fold expression change (2 (−ΔΔCt) ) and standard deviation (SD fold-change ) for each gene is represented (n=3). C. Upper: Line diagram representation of duration of serum starve, kinase inhibitor treatment, and growth-factor stimulation. Lower: Western immunoblot analysis of RAS and ERK activity before and after hEPO-stimulation (10′) in K562 cells pretreated for 24hrs with 0.2% DMSO, 100nM dasatinib, 500nM PD0325901, or dasatinib/PD0325901. RAS activity was monitored using a RAS-GTP pulldown assay. D. Upper: Line diagram representation of duration of serum starve, kinase inhibitor treatment, and growth-factor stimulation. Lower: Western immunoblot analysis of JAK2 and STAT5 activity before and after hEPO-stimulation in K562 cells treated under the same experimental conditions as (A). JAK2 activation was determined by immunoprecipitation and activation loop (Y1007) phosphorylation.

    Article Snippet: Cells were lysed in JAK2 IP buffer (50mM Tris pH 7.6, 100mM NaCl, 1mM EDTA, 1mM EGTA, 0.5% NP40, 0.1% Triton) or RAS IP buffer (50mM Tris pH 7.5, 125mM NaCl, 6.5mM MgCl2 , 5% glycerol, 0.2% NP40) supplemented with 1% protease and 1% phosphatase inhibitors (Calbiochem).

    Techniques: Expressing, Real-time Polymerase Chain Reaction, Standard Deviation, Western Blot, Activity Assay, Activation Assay, Immunoprecipitation