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  • 93
    Bio-Techne corporation pf 3644022
    A Immunoblot analysis of ERBB2, AKT, MEK1/2, and ERK1/2 signaling inhibition after treatment with increasing doses of lapatinib for 24 h. Status of ERBB2 (phospho-tyrosine 1221/1222 and total), AKT (phospho-serine 473 and total pan AKT), ERK1/2 (Phospho-threonine 202/phospho-tyrosine 204 and total), MEK1/2 (Ser217/221), and ZFP36/TTP are shown. A blot from at least two experiments is shown. B Immunoblot analysis for the inhibition of <t>MK2</t> activation after treatment with lapatinib. SKBR3 cells were treated with increasing doses of lapatinib, as indicated for 24 h. Phospho-threonine MK2 (T222) and total MK2 protein abundance are shown. A representative blot from two experiments is shown. C Immunoblot analysis for ZFP36/TTP phosphorylation in MAPKAPK-2 silenced SKBR3 cells. SKBR3 cells transfected with 100 nM of si Ctrl or si MAPKAPK-2 for 24 h were tested for ZFP36/TTP protein abundance. Total MK2, phosphorylated ZFP36/TTP, and β-actin protein abundances are shown. A representative blot from three experiments is shown. Effect of the MK2 inhibitor <t>PF-3644022</t> (1 µM, 4 h) on the abundance of phosphorylated ZFP36/TTP in ERBB2-expressing SKBR3 ( D ) or SKBR3 transfected with ZFP36 expression plasmid ( E ). Western blots are from two independent experiments. F Immunoblot analysis of total and phosphorylated ZFP36/TTP, and MK2 in MK2 -knockout MEF cells in the absence or presence of overnight transfected ERBB2.
    Pf 3644022, supplied by Bio-Techne corporation, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/pf 3644022/product/Bio-Techne corporation
    Average 93 stars, based on 1 article reviews
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    pf 3644022 - by Bioz Stars, 2024-06
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    90
    ATCC a hydrophila atcc 7966t
    A Immunoblot analysis of ERBB2, AKT, MEK1/2, and ERK1/2 signaling inhibition after treatment with increasing doses of lapatinib for 24 h. Status of ERBB2 (phospho-tyrosine 1221/1222 and total), AKT (phospho-serine 473 and total pan AKT), ERK1/2 (Phospho-threonine 202/phospho-tyrosine 204 and total), MEK1/2 (Ser217/221), and ZFP36/TTP are shown. A blot from at least two experiments is shown. B Immunoblot analysis for the inhibition of <t>MK2</t> activation after treatment with lapatinib. SKBR3 cells were treated with increasing doses of lapatinib, as indicated for 24 h. Phospho-threonine MK2 (T222) and total MK2 protein abundance are shown. A representative blot from two experiments is shown. C Immunoblot analysis for ZFP36/TTP phosphorylation in MAPKAPK-2 silenced SKBR3 cells. SKBR3 cells transfected with 100 nM of si Ctrl or si MAPKAPK-2 for 24 h were tested for ZFP36/TTP protein abundance. Total MK2, phosphorylated ZFP36/TTP, and β-actin protein abundances are shown. A representative blot from three experiments is shown. Effect of the MK2 inhibitor <t>PF-3644022</t> (1 µM, 4 h) on the abundance of phosphorylated ZFP36/TTP in ERBB2-expressing SKBR3 ( D ) or SKBR3 transfected with ZFP36 expression plasmid ( E ). Western blots are from two independent experiments. F Immunoblot analysis of total and phosphorylated ZFP36/TTP, and MK2 in MK2 -knockout MEF cells in the absence or presence of overnight transfected ERBB2.
    A Hydrophila Atcc 7966t, supplied by ATCC, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/a hydrophila atcc 7966t/product/ATCC
    Average 90 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    a hydrophila atcc 7966t - by Bioz Stars, 2024-06
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    94
    Cell Signaling Technology Inc mouse pan keratin
    A Immunoblot analysis of ERBB2, AKT, MEK1/2, and ERK1/2 signaling inhibition after treatment with increasing doses of lapatinib for 24 h. Status of ERBB2 (phospho-tyrosine 1221/1222 and total), AKT (phospho-serine 473 and total pan AKT), ERK1/2 (Phospho-threonine 202/phospho-tyrosine 204 and total), MEK1/2 (Ser217/221), and ZFP36/TTP are shown. A blot from at least two experiments is shown. B Immunoblot analysis for the inhibition of <t>MK2</t> activation after treatment with lapatinib. SKBR3 cells were treated with increasing doses of lapatinib, as indicated for 24 h. Phospho-threonine MK2 (T222) and total MK2 protein abundance are shown. A representative blot from two experiments is shown. C Immunoblot analysis for ZFP36/TTP phosphorylation in MAPKAPK-2 silenced SKBR3 cells. SKBR3 cells transfected with 100 nM of si Ctrl or si MAPKAPK-2 for 24 h were tested for ZFP36/TTP protein abundance. Total MK2, phosphorylated ZFP36/TTP, and β-actin protein abundances are shown. A representative blot from three experiments is shown. Effect of the MK2 inhibitor <t>PF-3644022</t> (1 µM, 4 h) on the abundance of phosphorylated ZFP36/TTP in ERBB2-expressing SKBR3 ( D ) or SKBR3 transfected with ZFP36 expression plasmid ( E ). Western blots are from two independent experiments. F Immunoblot analysis of total and phosphorylated ZFP36/TTP, and MK2 in MK2 -knockout MEF cells in the absence or presence of overnight transfected ERBB2.
    Mouse Pan Keratin, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mouse pan keratin/product/Cell Signaling Technology Inc
    Average 94 stars, based on 1 article reviews
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    mouse pan keratin - by Bioz Stars, 2024-06
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    94
    Tocris protein kinase 2 mk2 inhibitor pf
    TGFβ induces post-translational modification of MRTF in a p38- and <t>MK2-dependent</t> manner. A and B, C3H/10T1/2 cells were pretreated with vehicle (DMSO) or DORA (A) or AKTi (B) and, where indicated, exposed to TGFβ for 6 h. Whole-cell extracts were run in 6% SDS gels, and the relative shift is the molecular mass of MRTF (see dotted lines) was determined and normalized to the change detected in the vehicle-treated controls as described under “Experimental procedures.” C and D, cells were transfected with 300 nm non-related (siNR) or α (100 nm)-, β (100 nm)-, and γ (100 nm)-p38 siRNA (sip38) for 48 h and then, where indicated, exposed to TGFβ for 6 h. Cortactin was used as loading control. TAZ expression (C) and the relative molecular shift of MRTF (D) were assessed by Western blotting (n = 3) as in Figs. 1A and ​and88B, respectively. α-Actinin (α-act) was used as loading control. E, cells were cotransfected with 3DA firefly reporter and Renilla luciferase and, where indicated (panel iii) with Smad3 siRNA or NR siRNA for 24 h. Subsequently cells were preincubated with vehicle (DMSO) or DORA (panel i) or AKTi (panel ii) for 30 min. Cells were then exposed to TGFβ for 6 h, as indicated. Normalized luciferase activities were determined (n = 3 for each condition). F and G, C3H/10T1/2 cells were pretreated with vehicle or the MK2 inhibitor <t>PF-3644022</t> (PF, 10 μm) followed by 6 h of treatment with TGFβ as indicated and then processed for Western blotting to assess TAZ expression (F) or the shift of MRTF (G) (n = 3). H and I, conditions were as in F and G, except the cells were pretreated where indicated with the antifibrotic drug, pirfenidone (Pirf, 1 mg/ml). n.s., non-significant.
    Protein Kinase 2 Mk2 Inhibitor Pf, supplied by Tocris, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/protein kinase 2 mk2 inhibitor pf/product/Tocris
    Average 94 stars, based on 1 article reviews
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    86
    Gilead Sciences gs us 418 4279
    TGFβ induces post-translational modification of MRTF in a p38- and <t>MK2-dependent</t> manner. A and B, C3H/10T1/2 cells were pretreated with vehicle (DMSO) or DORA (A) or AKTi (B) and, where indicated, exposed to TGFβ for 6 h. Whole-cell extracts were run in 6% SDS gels, and the relative shift is the molecular mass of MRTF (see dotted lines) was determined and normalized to the change detected in the vehicle-treated controls as described under “Experimental procedures.” C and D, cells were transfected with 300 nm non-related (siNR) or α (100 nm)-, β (100 nm)-, and γ (100 nm)-p38 siRNA (sip38) for 48 h and then, where indicated, exposed to TGFβ for 6 h. Cortactin was used as loading control. TAZ expression (C) and the relative molecular shift of MRTF (D) were assessed by Western blotting (n = 3) as in Figs. 1A and ​and88B, respectively. α-Actinin (α-act) was used as loading control. E, cells were cotransfected with 3DA firefly reporter and Renilla luciferase and, where indicated (panel iii) with Smad3 siRNA or NR siRNA for 24 h. Subsequently cells were preincubated with vehicle (DMSO) or DORA (panel i) or AKTi (panel ii) for 30 min. Cells were then exposed to TGFβ for 6 h, as indicated. Normalized luciferase activities were determined (n = 3 for each condition). F and G, C3H/10T1/2 cells were pretreated with vehicle or the MK2 inhibitor <t>PF-3644022</t> (PF, 10 μm) followed by 6 h of treatment with TGFβ as indicated and then processed for Western blotting to assess TAZ expression (F) or the shift of MRTF (G) (n = 3). H and I, conditions were as in F and G, except the cells were pretreated where indicated with the antifibrotic drug, pirfenidone (Pirf, 1 mg/ml). n.s., non-significant.
    Gs Us 418 4279, supplied by Gilead Sciences, 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/gs us 418 4279/product/Gilead Sciences
    Average 86 stars, based on 1 article reviews
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    gs us 418 4279 - by Bioz Stars, 2024-06
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    Image Search Results


    A Immunoblot analysis of ERBB2, AKT, MEK1/2, and ERK1/2 signaling inhibition after treatment with increasing doses of lapatinib for 24 h. Status of ERBB2 (phospho-tyrosine 1221/1222 and total), AKT (phospho-serine 473 and total pan AKT), ERK1/2 (Phospho-threonine 202/phospho-tyrosine 204 and total), MEK1/2 (Ser217/221), and ZFP36/TTP are shown. A blot from at least two experiments is shown. B Immunoblot analysis for the inhibition of MK2 activation after treatment with lapatinib. SKBR3 cells were treated with increasing doses of lapatinib, as indicated for 24 h. Phospho-threonine MK2 (T222) and total MK2 protein abundance are shown. A representative blot from two experiments is shown. C Immunoblot analysis for ZFP36/TTP phosphorylation in MAPKAPK-2 silenced SKBR3 cells. SKBR3 cells transfected with 100 nM of si Ctrl or si MAPKAPK-2 for 24 h were tested for ZFP36/TTP protein abundance. Total MK2, phosphorylated ZFP36/TTP, and β-actin protein abundances are shown. A representative blot from three experiments is shown. Effect of the MK2 inhibitor PF-3644022 (1 µM, 4 h) on the abundance of phosphorylated ZFP36/TTP in ERBB2-expressing SKBR3 ( D ) or SKBR3 transfected with ZFP36 expression plasmid ( E ). Western blots are from two independent experiments. F Immunoblot analysis of total and phosphorylated ZFP36/TTP, and MK2 in MK2 -knockout MEF cells in the absence or presence of overnight transfected ERBB2.

    Journal: Oncogenesis

    Article Title: Post-transcriptional screen of cancer amplified genes identifies ERBB2 / Her2 signaling as AU-rich mRNA stability-promoting pathway

    doi: 10.1038/s41389-021-00351-w

    Figure Lengend Snippet: A Immunoblot analysis of ERBB2, AKT, MEK1/2, and ERK1/2 signaling inhibition after treatment with increasing doses of lapatinib for 24 h. Status of ERBB2 (phospho-tyrosine 1221/1222 and total), AKT (phospho-serine 473 and total pan AKT), ERK1/2 (Phospho-threonine 202/phospho-tyrosine 204 and total), MEK1/2 (Ser217/221), and ZFP36/TTP are shown. A blot from at least two experiments is shown. B Immunoblot analysis for the inhibition of MK2 activation after treatment with lapatinib. SKBR3 cells were treated with increasing doses of lapatinib, as indicated for 24 h. Phospho-threonine MK2 (T222) and total MK2 protein abundance are shown. A representative blot from two experiments is shown. C Immunoblot analysis for ZFP36/TTP phosphorylation in MAPKAPK-2 silenced SKBR3 cells. SKBR3 cells transfected with 100 nM of si Ctrl or si MAPKAPK-2 for 24 h were tested for ZFP36/TTP protein abundance. Total MK2, phosphorylated ZFP36/TTP, and β-actin protein abundances are shown. A representative blot from three experiments is shown. Effect of the MK2 inhibitor PF-3644022 (1 µM, 4 h) on the abundance of phosphorylated ZFP36/TTP in ERBB2-expressing SKBR3 ( D ) or SKBR3 transfected with ZFP36 expression plasmid ( E ). Western blots are from two independent experiments. F Immunoblot analysis of total and phosphorylated ZFP36/TTP, and MK2 in MK2 -knockout MEF cells in the absence or presence of overnight transfected ERBB2.

    Article Snippet: PF-3644022 (MK2 inhibitor) was purchased from Tocris (Tocris Bioscience, Minneapolis, MN).

    Techniques: Western Blot, Inhibition, Activation Assay, Transfection, Expressing, Plasmid Preparation, Knock-Out

    TGFβ induces post-translational modification of MRTF in a p38- and MK2-dependent manner. A and B, C3H/10T1/2 cells were pretreated with vehicle (DMSO) or DORA (A) or AKTi (B) and, where indicated, exposed to TGFβ for 6 h. Whole-cell extracts were run in 6% SDS gels, and the relative shift is the molecular mass of MRTF (see dotted lines) was determined and normalized to the change detected in the vehicle-treated controls as described under “Experimental procedures.” C and D, cells were transfected with 300 nm non-related (siNR) or α (100 nm)-, β (100 nm)-, and γ (100 nm)-p38 siRNA (sip38) for 48 h and then, where indicated, exposed to TGFβ for 6 h. Cortactin was used as loading control. TAZ expression (C) and the relative molecular shift of MRTF (D) were assessed by Western blotting (n = 3) as in Figs. 1A and ​and88B, respectively. α-Actinin (α-act) was used as loading control. E, cells were cotransfected with 3DA firefly reporter and Renilla luciferase and, where indicated (panel iii) with Smad3 siRNA or NR siRNA for 24 h. Subsequently cells were preincubated with vehicle (DMSO) or DORA (panel i) or AKTi (panel ii) for 30 min. Cells were then exposed to TGFβ for 6 h, as indicated. Normalized luciferase activities were determined (n = 3 for each condition). F and G, C3H/10T1/2 cells were pretreated with vehicle or the MK2 inhibitor PF-3644022 (PF, 10 μm) followed by 6 h of treatment with TGFβ as indicated and then processed for Western blotting to assess TAZ expression (F) or the shift of MRTF (G) (n = 3). H and I, conditions were as in F and G, except the cells were pretreated where indicated with the antifibrotic drug, pirfenidone (Pirf, 1 mg/ml). n.s., non-significant.

    Journal: The Journal of Biological Chemistry

    Article Title: TGF-β1 regulates the expression and transcriptional activity of TAZ protein via a Smad3-independent, myocardin-related transcription factor-mediated mechanism

    doi: 10.1074/jbc.M117.780502

    Figure Lengend Snippet: TGFβ induces post-translational modification of MRTF in a p38- and MK2-dependent manner. A and B, C3H/10T1/2 cells were pretreated with vehicle (DMSO) or DORA (A) or AKTi (B) and, where indicated, exposed to TGFβ for 6 h. Whole-cell extracts were run in 6% SDS gels, and the relative shift is the molecular mass of MRTF (see dotted lines) was determined and normalized to the change detected in the vehicle-treated controls as described under “Experimental procedures.” C and D, cells were transfected with 300 nm non-related (siNR) or α (100 nm)-, β (100 nm)-, and γ (100 nm)-p38 siRNA (sip38) for 48 h and then, where indicated, exposed to TGFβ for 6 h. Cortactin was used as loading control. TAZ expression (C) and the relative molecular shift of MRTF (D) were assessed by Western blotting (n = 3) as in Figs. 1A and ​and88B, respectively. α-Actinin (α-act) was used as loading control. E, cells were cotransfected with 3DA firefly reporter and Renilla luciferase and, where indicated (panel iii) with Smad3 siRNA or NR siRNA for 24 h. Subsequently cells were preincubated with vehicle (DMSO) or DORA (panel i) or AKTi (panel ii) for 30 min. Cells were then exposed to TGFβ for 6 h, as indicated. Normalized luciferase activities were determined (n = 3 for each condition). F and G, C3H/10T1/2 cells were pretreated with vehicle or the MK2 inhibitor PF-3644022 (PF, 10 μm) followed by 6 h of treatment with TGFβ as indicated and then processed for Western blotting to assess TAZ expression (F) or the shift of MRTF (G) (n = 3). H and I, conditions were as in F and G, except the cells were pretreated where indicated with the antifibrotic drug, pirfenidone (Pirf, 1 mg/ml). n.s., non-significant.

    Article Snippet: The p38 MAPK inhibitor doramapimod (BIRB-76) was from Cayman Chemical Co. (Ann Arbor, MI); MEK1/2 inhibitor U0126 was from Alexis Biochemicals (San Diego, CA); Smad3 inhibitor SIS3 and NADPH oxidase inhibitor VAS2870 were from Calbiochem/EDM Millipore (Billerica, MA); mTORC1 inhibitor rapamycin was from Abcam (Cambridge, UK); Food and Drug Administration-approved anti-fibrotic drug pirfenidone and MAPK-activated protein kinase-2 (MK2) inhibitor PF-3644022 were from Tocris (Minneapolis, MN).

    Techniques: Modification, Transfection, Expressing, Western Blot, Luciferase