phospho-mek ser217 Search Results


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  • 88
    Cell Signaling Technology Inc phospho mek ser217 221
    Phospho Mek Ser217 221, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 88/100, based on 27 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc anti phospho mek s217 221
    RXDX-105 inhibits tumor xenograft growth and inhibits <t>RET</t> phosphorylation and intracellular signaling in orthotopic neuroblastoma tumors. ( A ) SK-N-AS and SK-N-SH cells were injected into the left adrenal glands of nude mice as shown. Mice were then randomized and treated once daily orally with vehicle control or RXDX-105. SK-N-AS tumors were harvested at 4 weeks and SK-N-SH tumors at 6 weeks, based on tumor growth rates. ( B ) Final tumor weight was measured in harvested tumors and weights of tumors from treated mice were compared to weights of tumors from control mice. ( C ) Images and measurements from harvested tumors are shown, with untreated tumors in the top rows and treated tumors in the bottom rows. ( D ) Tumor cell lysates were analyzed by Western blot for expression and phosphorylation of RET, <t>MEK</t> and ERK in tumors from treated and control mice.
    Anti Phospho Mek S217 221, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 200 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc anti phospho mek
    RXDX-105 inhibits tumor xenograft growth and inhibits <t>RET</t> phosphorylation and intracellular signaling in orthotopic neuroblastoma tumors. ( A ) SK-N-AS and SK-N-SH cells were injected into the left adrenal glands of nude mice as shown. Mice were then randomized and treated once daily orally with vehicle control or RXDX-105. SK-N-AS tumors were harvested at 4 weeks and SK-N-SH tumors at 6 weeks, based on tumor growth rates. ( B ) Final tumor weight was measured in harvested tumors and weights of tumors from treated mice were compared to weights of tumors from control mice. ( C ) Images and measurements from harvested tumors are shown, with untreated tumors in the top rows and treated tumors in the bottom rows. ( D ) Tumor cell lysates were analyzed by Western blot for expression and phosphorylation of RET, <t>MEK</t> and ERK in tumors from treated and control mice.
    Anti Phospho Mek, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 138 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc phospho mitogen activated protein kinase erk kinase mek 1 2 ser217 221
    RXDX-105 inhibits tumor xenograft growth and inhibits <t>RET</t> phosphorylation and intracellular signaling in orthotopic neuroblastoma tumors. ( A ) SK-N-AS and SK-N-SH cells were injected into the left adrenal glands of nude mice as shown. Mice were then randomized and treated once daily orally with vehicle control or RXDX-105. SK-N-AS tumors were harvested at 4 weeks and SK-N-SH tumors at 6 weeks, based on tumor growth rates. ( B ) Final tumor weight was measured in harvested tumors and weights of tumors from treated mice were compared to weights of tumors from control mice. ( C ) Images and measurements from harvested tumors are shown, with untreated tumors in the top rows and treated tumors in the bottom rows. ( D ) Tumor cell lysates were analyzed by Western blot for expression and phosphorylation of RET, <t>MEK</t> and ERK in tumors from treated and control mice.
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    Santa Cruz Biotechnology phospho mek ser217 221 antibodies
    RXDX-105 inhibits tumor xenograft growth and inhibits <t>RET</t> phosphorylation and intracellular signaling in orthotopic neuroblastoma tumors. ( A ) SK-N-AS and SK-N-SH cells were injected into the left adrenal glands of nude mice as shown. Mice were then randomized and treated once daily orally with vehicle control or RXDX-105. SK-N-AS tumors were harvested at 4 weeks and SK-N-SH tumors at 6 weeks, based on tumor growth rates. ( B ) Final tumor weight was measured in harvested tumors and weights of tumors from treated mice were compared to weights of tumors from control mice. ( C ) Images and measurements from harvested tumors are shown, with untreated tumors in the top rows and treated tumors in the bottom rows. ( D ) Tumor cell lysates were analyzed by Western blot for expression and phosphorylation of RET, <t>MEK</t> and ERK in tumors from treated and control mice.
    Phospho Mek Ser217 221 Antibodies, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc phospho mek ser217 ser221
    HSV-1 decreased phosphorylated <t>MEK1/2,</t> and MG132 increased cytoplasmic phosphorylated MEK1/2 in virus infected cells. Subcellular localization of the phospho-MEK1/2 in HSV-infected and MG132-treated cells. Vero cells were infected with HSV-1 at an MOI of 1 and treated with (or without) 0.75 μM MG132 for 10 hours. Vero cells were stained with <t>anti-Ser217/Ser221-phospho-MEK1/2</t> (green), anti-ICP5 (red) and DAPI (blue) and observed by laser scanning confocal microscopy with a 40x water-immersion objective. Scale bars represent 20 μm. The upper and middle images show gray-scale images (single channel) of phospho-MEK1/2 and ICP5, respectively, and the lower images show triple staining of phospho-MEK1/2, ICP5 and DAPI.
    Phospho Mek Ser217 Ser221, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 90/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    RXDX-105 inhibits tumor xenograft growth and inhibits RET phosphorylation and intracellular signaling in orthotopic neuroblastoma tumors. ( A ) SK-N-AS and SK-N-SH cells were injected into the left adrenal glands of nude mice as shown. Mice were then randomized and treated once daily orally with vehicle control or RXDX-105. SK-N-AS tumors were harvested at 4 weeks and SK-N-SH tumors at 6 weeks, based on tumor growth rates. ( B ) Final tumor weight was measured in harvested tumors and weights of tumors from treated mice were compared to weights of tumors from control mice. ( C ) Images and measurements from harvested tumors are shown, with untreated tumors in the top rows and treated tumors in the bottom rows. ( D ) Tumor cell lysates were analyzed by Western blot for expression and phosphorylation of RET, MEK and ERK in tumors from treated and control mice.

    Journal: Oncotarget

    Article Title: The multikinase inhibitor RXDX-105 is effective against neuroblastoma in vitro and in vivo

    doi: 10.18632/oncotarget.27259

    Figure Lengend Snippet: RXDX-105 inhibits tumor xenograft growth and inhibits RET phosphorylation and intracellular signaling in orthotopic neuroblastoma tumors. ( A ) SK-N-AS and SK-N-SH cells were injected into the left adrenal glands of nude mice as shown. Mice were then randomized and treated once daily orally with vehicle control or RXDX-105. SK-N-AS tumors were harvested at 4 weeks and SK-N-SH tumors at 6 weeks, based on tumor growth rates. ( B ) Final tumor weight was measured in harvested tumors and weights of tumors from treated mice were compared to weights of tumors from control mice. ( C ) Images and measurements from harvested tumors are shown, with untreated tumors in the top rows and treated tumors in the bottom rows. ( D ) Tumor cell lysates were analyzed by Western blot for expression and phosphorylation of RET, MEK and ERK in tumors from treated and control mice.

    Article Snippet: Membranes were blocked with 3% BSA made in 1× TBS + 0.1% Tween 20 and then incubated with primary antibodies to total RET (#3220S), phospho-RET (#32212), total MEK1/2 (#9126S), phospho-MEK (#9154S), total ERK (#4695S), phospho-ERK (#4370S), PARP (#9542S), and GAPDH (#5174S) (all antibodies obtained from Cell Signaling Technology, Danvers, MA, USA).

    Techniques: Injection, Mouse Assay, Western Blot, Expressing

    HSV-1 decreased phosphorylated MEK1/2, and MG132 increased cytoplasmic phosphorylated MEK1/2 in virus infected cells. Subcellular localization of the phospho-MEK1/2 in HSV-infected and MG132-treated cells. Vero cells were infected with HSV-1 at an MOI of 1 and treated with (or without) 0.75 μM MG132 for 10 hours. Vero cells were stained with anti-Ser217/Ser221-phospho-MEK1/2 (green), anti-ICP5 (red) and DAPI (blue) and observed by laser scanning confocal microscopy with a 40x water-immersion objective. Scale bars represent 20 μm. The upper and middle images show gray-scale images (single channel) of phospho-MEK1/2 and ICP5, respectively, and the lower images show triple staining of phospho-MEK1/2, ICP5 and DAPI.

    Journal: Scientific Reports

    Article Title: MG132 exerts anti-viral activity against HSV-1 by overcoming virus-mediated suppression of the ERK signaling pathway

    doi: 10.1038/s41598-020-63438-1

    Figure Lengend Snippet: HSV-1 decreased phosphorylated MEK1/2, and MG132 increased cytoplasmic phosphorylated MEK1/2 in virus infected cells. Subcellular localization of the phospho-MEK1/2 in HSV-infected and MG132-treated cells. Vero cells were infected with HSV-1 at an MOI of 1 and treated with (or without) 0.75 μM MG132 for 10 hours. Vero cells were stained with anti-Ser217/Ser221-phospho-MEK1/2 (green), anti-ICP5 (red) and DAPI (blue) and observed by laser scanning confocal microscopy with a 40x water-immersion objective. Scale bars represent 20 μm. The upper and middle images show gray-scale images (single channel) of phospho-MEK1/2 and ICP5, respectively, and the lower images show triple staining of phospho-MEK1/2, ICP5 and DAPI.

    Article Snippet: Primary antibodies used in these experiments were Ser380-phospho-PTEN, lamin B1, cleaved caspase-3, cleaved PARP, Ser473-phospho-AKT, AKT, Tyr701-phospho-STAT1, Ser338-phospho-c-Raf, Ser217/Ser221-phospho-MEK1/2, Thr202/Tyr204-phospho-ERK1/2, Ser380-phospho-p90RSK, FGFR, and EGFR (1:1500 dilution, Cell Signaling Technology, MA, USA), Ras-GRF2 (1:1500 dilution, Abcam, OR, USA), IκBα, p65, β-catenin, ERK1, and ERK2 (1:1500 dilution, BD Biosciences, NJ, USA), β-Actin, p90RSK, ICP5, ICP8, ICP27, UL42, Ras-GRF1, and h-Ras (1:750 dilution, Santa Cruz Biotechnology, CA, USA).

    Techniques: Infection, Staining, Confocal Microscopy

    MG132 enhanced HSV-induced Raf-MEK-ERK-RSK cascade. ( a , b ) Effects of HSV-1 infection and MG132 treatment on ERK signaling. Vero cells infected with HSV-1 at an MOI of 1 or mock infected were cultured in media in the presence or absence MG132 for 0.4, 12, 24, or 36 hours. Whole-cell lysates were subjected to immunoblotting analysis with an anti-Thr202/Tyr204-phospho-ERK1/2, -ERK1, -ERK2, -Ser338-phospho-c-Raf, -Ser217/Ser221-phospho-MEK1/2, and –Ser380-phospho-p90RSK antibodies. The anti- Thr202/Tyr204 phospho-ERK1/2 antibody recognizes either Thr202- or Tyr204-phosphorylated ERK1 and also either Thr185- or Tyr187-phosphorylated ERK2. The values of p-c-Raf/β-actin, p-MEK/β-Actin and p-p90RSK/p90RSK are presented at the bottom of the image, and the values of 0.4 h nontreated and noninfected cells are presented as 1.0. ( b ) Densitometric analysis of the p-ERK1/2 in blotting data of ( a ). The quantitative analysis was performed using three separate membranes. The value of 0.4 h-nontreated and noninfected control was defined as 1.0. ( c ) Effects of HSV-1 infection and MG132 treatment on ERK signaling in human HepG2 cells. HepG2 cells infected with HSV-1 at an MOI of 1 and cultured with 0.75 μM MG132 for 18 and 21 hours. Cell lysates were subjected to immunoblotting using anti-Thr202/Tyr204 phospho-ERK1/2 antibody. The values of p-ERK1/2/β-Actin are presented at the bottom of the image, and the values of 18 h nontreated and noninfected cells are presented as 1. ( a , c ) Original images of blotting data are shown in Supplementary Fig. S5 .

    Journal: Scientific Reports

    Article Title: MG132 exerts anti-viral activity against HSV-1 by overcoming virus-mediated suppression of the ERK signaling pathway

    doi: 10.1038/s41598-020-63438-1

    Figure Lengend Snippet: MG132 enhanced HSV-induced Raf-MEK-ERK-RSK cascade. ( a , b ) Effects of HSV-1 infection and MG132 treatment on ERK signaling. Vero cells infected with HSV-1 at an MOI of 1 or mock infected were cultured in media in the presence or absence MG132 for 0.4, 12, 24, or 36 hours. Whole-cell lysates were subjected to immunoblotting analysis with an anti-Thr202/Tyr204-phospho-ERK1/2, -ERK1, -ERK2, -Ser338-phospho-c-Raf, -Ser217/Ser221-phospho-MEK1/2, and –Ser380-phospho-p90RSK antibodies. The anti- Thr202/Tyr204 phospho-ERK1/2 antibody recognizes either Thr202- or Tyr204-phosphorylated ERK1 and also either Thr185- or Tyr187-phosphorylated ERK2. The values of p-c-Raf/β-actin, p-MEK/β-Actin and p-p90RSK/p90RSK are presented at the bottom of the image, and the values of 0.4 h nontreated and noninfected cells are presented as 1.0. ( b ) Densitometric analysis of the p-ERK1/2 in blotting data of ( a ). The quantitative analysis was performed using three separate membranes. The value of 0.4 h-nontreated and noninfected control was defined as 1.0. ( c ) Effects of HSV-1 infection and MG132 treatment on ERK signaling in human HepG2 cells. HepG2 cells infected with HSV-1 at an MOI of 1 and cultured with 0.75 μM MG132 for 18 and 21 hours. Cell lysates were subjected to immunoblotting using anti-Thr202/Tyr204 phospho-ERK1/2 antibody. The values of p-ERK1/2/β-Actin are presented at the bottom of the image, and the values of 18 h nontreated and noninfected cells are presented as 1. ( a , c ) Original images of blotting data are shown in Supplementary Fig. S5 .

    Article Snippet: Primary antibodies used in these experiments were Ser380-phospho-PTEN, lamin B1, cleaved caspase-3, cleaved PARP, Ser473-phospho-AKT, AKT, Tyr701-phospho-STAT1, Ser338-phospho-c-Raf, Ser217/Ser221-phospho-MEK1/2, Thr202/Tyr204-phospho-ERK1/2, Ser380-phospho-p90RSK, FGFR, and EGFR (1:1500 dilution, Cell Signaling Technology, MA, USA), Ras-GRF2 (1:1500 dilution, Abcam, OR, USA), IκBα, p65, β-catenin, ERK1, and ERK2 (1:1500 dilution, BD Biosciences, NJ, USA), β-Actin, p90RSK, ICP5, ICP8, ICP27, UL42, Ras-GRF1, and h-Ras (1:750 dilution, Santa Cruz Biotechnology, CA, USA).

    Techniques: Infection, Cell Culture