u0124 Search Results


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  • 99
    Millipore control u0124
    Control U0124, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Tocris u0124
    Infusion of U0126 but not <t>U0124</t> in PVA blocks the SNI-induced cardioprotection. a Schematic of experimental design showing the timeline for sham/SNI surgery (D0), intra-PVA infusion of U0126/or U0124 (1.5 mM in 0.3 μL 50% DMSO, D3) and myocardial IR surgery (D5). b Immunohistochemical staining of pERK, an indication of ERK activation, in PVA (outlined by dashed line ) from sham and SNI animals received U0126 or U0124 infusion. Scale bar = 100 μm. Immunofluorescent imaging of pERK ( green ) and NeuN ( red ) in PVA from SNI animal. Scale bar = 50 μm (lower magnification) and 10 μm (higher magnification), respectively. Quantification results of pERK-positive cells in PVA from these animals. c Mechanical responses of hind paws at D0 (basal) and D5, after intra-PVA infusion of U0124 or U0126 (D3). * p
    U0124, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 45 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    90
    Millipore u0124
    A small molecule MEK1/2 inhibitor U0126 inhibits migration and invasion of human MM cells in vitro. (A) A transwell insert model shows significantly increased migration of the sarcomatoid MO line in comparison to other MM lines. (B) The MEK1/2 inhibitor, U0126, inhibits migration of the MO line. (C) Increased invasion of the MO line using a transwell insert coated with Matrigel. (D) The MEK1/2 inhibitor, U0126 (20 μM) inhibits invasion of MO cells, whereas its inactive analog, <t>U0124</t> (20 μM) is ineffective. Results are expressed as Mean +/− SEM. *=p
    U0124, supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 156 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    90
    Santa Cruz Biotechnology u0124
    U0126 application during a specific time-window decreases ERK phosphorylation specifically . A : Diphospho-Erk staining in the trunk of wt 24 hpf embryos. B : U0126 eliminates ERK1/2 phosphorylation (green) in the trunk and tail of 24 hpf zebrafish embryos. Notice that U0126-treated embryos have been overexposed (can be judged by the autofluorescence of the yolk sac extension) and still fail to show specific staining. C : <t>U0124</t> does not eliminate the p-Erk staining. D : PD98059 also does not eliminate p-Erk staining when given just below the level of lethal toxicity (25 μM). E : Somewhat weaker but still significant p-Erk staining in embryos treated with U0126 starting at 10 hpf. F : Western-blot analysis demonstrated a slight but incomplete reduction in pErk1/2 levels in 10-somite embryos. G : Stage and dose-dependency of U0126 application. There is a dramatic drop in the percentage of affected embryos when treatment is applied after epiboly is completed. H : Washout experiments reveal the necessity of U0126 to be present until at least the 18 somite stage to produce the full phenotype.
    U0124, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 90/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    90
    Avantor u0124
    Effects of intra-amygdala infusion of U0126 on nociceptive behavior. a , Spontaneous nociceptive responses to formalin were not significantly different in U0126- versus vehicle-injected mice ( n = 8–10 animals per treatment). b , Baseline mechanical thresholds (in the absence of inflammation) are not affected by intra-amygdala infusion of vehicle (50% DMSO) or U0126 (1.5 nmol) ( n = 3 mice per treatment). c , d , Five days after cannulation, animals were injected with 5% formalin into the hindpaw. Two hours after the paw injection, the MEK inhibitor U0126, the structural analog control compound <t>U0124,</t> or vehicle was infused into the amygdala. One hour after the amygdala injection, the effects of these treatments on thermal latencies ( c ) or mechanical thresholds ( d ) were analyzed. c , U0126 infusion into the amygdala did not affect formalin-induced thermal hypersensitivity ( n = 4 animals per treatment). d , U0126 infusion significantly reduced formalin-induced mechanical hypersensitivity in both the injected and the noninjected hindpaw ( n = 6–7 animals per treatment; p
    U0124, supplied by Avantor, used in various techniques. Bioz Stars score: 90/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    90
    Merck KGaA u0124
    TRTS-induced changes in PC12 cell differentiation after exposure to various inhibitors. (A–K) PC12 cells in the differentiation medium were treated with TRTS at 39.5°C (18 h/day), 40 ng/ml BMP4, or left untreated for 7 days in the presence or absence of 2.5 μM U0126, 2.5 μM <t>U0124,</t> 0.5 μM SB203580, or 1.0 μM GW441756. (A) Representative phase-contrast images of PC12 cells on day 7 after treatment with no stimulation; (B) TRTS (18 h/day); (C) TRTS (18 h/day) plus 2.5 μM U0126; (D) TRTS (18 h/day) plus 2.5 μM U0124; (E) TRTS (18 h/day) plus 0.5 μM SB203580; (F) TRTS (18 h/day) plus 1.0 μM GW441756; (G) 40 ng/ml BMP4; (H) 40 ng/ml BMP4 plus 2.5 μM U0126; (I) 40 ng/ml BMP4 plus 2.5 μM U0124; (J) 40 ng/ml BMP4 plus 0.5 μM SB203580; (K) 40 ng/ml BMP4 plus 1.0 μM GW441756. Scale bar, 100 μm. (L, M) PC12 cells were treated with TRTS at 39.5°C (18 h/day), 40 ng/ml BMP4, or left untreated for 7 days in the presence of the indicated concentrations of U0126, U0124, SB203580, or GW441756. The percentage of neurite-bearing cells on day 7 was assayed. The data represent the mean ± SD of three replicates. †† P
    U0124, supplied by Merck KGaA, used in various techniques. Bioz Stars score: 90/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Millipore inactive analog u0124
    Effects of small molecule inhibitors on the growth of MCF10 cell variants in 3D rBM overlay cultures. Cells were incubated for 9 days in 3D rBM overlay cultures under control (DMSO vehicle) or drug treatment conditions. Inhibitors used were U0126 at 10 μM, <t>U0124</t> at 10 μM, wortmannin at 200 nM, CI-1040 at 100 nM, and doxorubicin at 1 μM. Phase-contrast images are shown. Scale bar, 100 μm.
    Inactive Analog U0124, supplied by Millipore, used in various techniques. Bioz Stars score: 92/100, based on 27 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    90
    Promega u0124
    MEK inhibition decreases NIS protein levels and NIS-mediated RA radioactive iodide uptake in tRA/H-treated MCF-7 human breast cancer cells (A) Western blot analysis showed that MEK inhibitor U0126 (left panel) or recombinant adenovirus carrying dominant negative MEK1 A217/A221 (right panel) decreased NIS protein levels in MCF-7-tRA/H cells. MCF-7 cells treated with tRA/H were cultured in the presence of DMSO, U0126, or inactive analog <t>U0124</t> for 24 hours, or were infected with recombinant adenovirus carrying LacZ (rAdLacZ) or dominant negative MEK1 (rAdDNMEK1) at a multiplicity of infection (MOI) of 5 for 24 hours prior to western blot analysis. β-actin served as a loading control. The results are representative of at least two independent experiments. (B) Bar graph indicates the densitometry values of NIS protein level normalized with β-actin of cells under various treatments (represented as percentage relative to MCF-7/tRA/H or MCF-7/tRA/H/Lac-Z control). (C) U0126 decreased radioactive iodide uptake in a dose-dependent manner in tRA/H-induced MCF-7 cells. The results are representative of three independent experiments performed in triplicate and the mean ± SD are shown. Asterisk indicates statistically significant difference (P
    U0124, supplied by Promega, used in various techniques. Bioz Stars score: 90/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Cell Signaling Technology Inc u0124
    U0126 reduces H 2 O 2 -induced ROS level in PC12 cells. (a) Representative images of the green channel (DCHFDA fluorescence) at 10 min and 2 h after H 2 O 2 addition. The fluorescence intensity is correlated with the amount of ROS in cells. All images are shown with the same intensity scale bar. (b) Quantitative measurements of the fluorescence intensity show that U0126 and <t>U0124</t> are able to reduce the amount of ROS in PC-12 cells within 10 min of incubation. The ROS level is maintained low at 2 h. Trametinib increases the amount of ROS in PC-12 cells. Images are collated from three sets of individual experiments and the error bars depict ± SD. Scale bar = 100 μm.
    U0124, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    88
    Millipore inactive analogue u0124
    U0126 reduces H 2 O 2 -induced ROS level in PC12 cells. (a) Representative images of the green channel (DCHFDA fluorescence) at 10 min and 2 h after H 2 O 2 addition. The fluorescence intensity is correlated with the amount of ROS in cells. All images are shown with the same intensity scale bar. (b) Quantitative measurements of the fluorescence intensity show that U0126 and <t>U0124</t> are able to reduce the amount of ROS in PC-12 cells within 10 min of incubation. The ROS level is maintained low at 2 h. Trametinib increases the amount of ROS in PC-12 cells. Images are collated from three sets of individual experiments and the error bars depict ± SD. Scale bar = 100 μm.
    Inactive Analogue U0124, supplied by Millipore, used in various techniques. Bioz Stars score: 88/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    85
    Millipore compound u0124
    U0126 reduces H 2 O 2 -induced ROS level in PC12 cells. (a) Representative images of the green channel (DCHFDA fluorescence) at 10 min and 2 h after H 2 O 2 addition. The fluorescence intensity is correlated with the amount of ROS in cells. All images are shown with the same intensity scale bar. (b) Quantitative measurements of the fluorescence intensity show that U0126 and <t>U0124</t> are able to reduce the amount of ROS in PC-12 cells within 10 min of incubation. The ROS level is maintained low at 2 h. Trametinib increases the amount of ROS in PC-12 cells. Images are collated from three sets of individual experiments and the error bars depict ± SD. Scale bar = 100 μm.
    Compound U0124, supplied by Millipore, used in various techniques. Bioz Stars score: 85/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    88
    Merck & Co inactive analogue u0124
    Inhibition of MEK1/2 could reverse NRG1-induced microgliosis and mechanical and cold pain-related hypersensitivity. NRG1 was administered intrathecally (4 ng given daily for 3 days) together with the MEK inhibitor U0126 (10 μg) or the inactive analogue <t>U0124</t> (10μg). a and b : Dorsal horn of animals treated with NRG1 + U0124 (in a) or NRG1 + U0126 (in b) immunostained with Iba1. Note that U0126 but not U0124 could prevent NRG1 associated increase in numbers of microglia with an effector morphology. In c quantification of this response is shown. In d – k we assessed proliferation (pulse labeling with BrdU) after injections (Iba1 is shown in red, DAPI in blue, BrdU in yellow and in the last panel merged images are shown). d–g: Dorsal horn microglia from a NRG1 + U0124 treated animal. h–k: Dorsal horn microglia from a NRG1 + U0126 treated animal. In ( l ) quantification of all BrdU-positive microglia in the dorsal horn is shown. Again, U0126 but not U0124 prevented NRG1 induced increase in microglial proliferation. Mechanical (shown in m ) and cold (shown in n ) pain related hypersensitivity developed after NRG1 injections which were reversed by U0126 but not by U0124. Scale bars: a and b: 100 μm, d–k: 50 μm. * P
    Inactive Analogue U0124, supplied by Merck & Co, used in various techniques. Bioz Stars score: 88/100, based on 16 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Merck KGaA inactive analog u0124
    Inhibition of MEK1/2 could reverse NRG1-induced microgliosis and mechanical and cold pain-related hypersensitivity. NRG1 was administered intrathecally (4 ng given daily for 3 days) together with the MEK inhibitor U0126 (10 μg) or the inactive analogue <t>U0124</t> (10μg). a and b : Dorsal horn of animals treated with NRG1 + U0124 (in a) or NRG1 + U0126 (in b) immunostained with Iba1. Note that U0126 but not U0124 could prevent NRG1 associated increase in numbers of microglia with an effector morphology. In c quantification of this response is shown. In d – k we assessed proliferation (pulse labeling with BrdU) after injections (Iba1 is shown in red, DAPI in blue, BrdU in yellow and in the last panel merged images are shown). d–g: Dorsal horn microglia from a NRG1 + U0124 treated animal. h–k: Dorsal horn microglia from a NRG1 + U0126 treated animal. In ( l ) quantification of all BrdU-positive microglia in the dorsal horn is shown. Again, U0126 but not U0124 prevented NRG1 induced increase in microglial proliferation. Mechanical (shown in m ) and cold (shown in n ) pain related hypersensitivity developed after NRG1 injections which were reversed by U0126 but not by U0124. Scale bars: a and b: 100 μm, d–k: 50 μm. * P
    Inactive Analog U0124, supplied by Merck KGaA, used in various techniques. Bioz Stars score: 88/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    85
    LC Laboratories u0124 1 4 diamino 2 3 dicyano 1 4 bis methylthio butadiene
    Inhibition of MEK1/2 could reverse NRG1-induced microgliosis and mechanical and cold pain-related hypersensitivity. NRG1 was administered intrathecally (4 ng given daily for 3 days) together with the MEK inhibitor U0126 (10 μg) or the inactive analogue <t>U0124</t> (10μg). a and b : Dorsal horn of animals treated with NRG1 + U0124 (in a) or NRG1 + U0126 (in b) immunostained with Iba1. Note that U0126 but not U0124 could prevent NRG1 associated increase in numbers of microglia with an effector morphology. In c quantification of this response is shown. In d – k we assessed proliferation (pulse labeling with BrdU) after injections (Iba1 is shown in red, DAPI in blue, BrdU in yellow and in the last panel merged images are shown). d–g: Dorsal horn microglia from a NRG1 + U0124 treated animal. h–k: Dorsal horn microglia from a NRG1 + U0126 treated animal. In ( l ) quantification of all BrdU-positive microglia in the dorsal horn is shown. Again, U0126 but not U0124 prevented NRG1 induced increase in microglial proliferation. Mechanical (shown in m ) and cold (shown in n ) pain related hypersensitivity developed after NRG1 injections which were reversed by U0126 but not by U0124. Scale bars: a and b: 100 μm, d–k: 50 μm. * P
    U0124 1 4 Diamino 2 3 Dicyano 1 4 Bis Methylthio Butadiene, supplied by LC Laboratories, used in various techniques. Bioz Stars score: 85/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    98
    Millipore 1 4 diamino 2 3 dicyano1 4 bis
    Inhibition of MEK1/2 could reverse NRG1-induced microgliosis and mechanical and cold pain-related hypersensitivity. NRG1 was administered intrathecally (4 ng given daily for 3 days) together with the MEK inhibitor U0126 (10 μg) or the inactive analogue <t>U0124</t> (10μg). a and b : Dorsal horn of animals treated with NRG1 + U0124 (in a) or NRG1 + U0126 (in b) immunostained with Iba1. Note that U0126 but not U0124 could prevent NRG1 associated increase in numbers of microglia with an effector morphology. In c quantification of this response is shown. In d – k we assessed proliferation (pulse labeling with BrdU) after injections (Iba1 is shown in red, DAPI in blue, BrdU in yellow and in the last panel merged images are shown). d–g: Dorsal horn microglia from a NRG1 + U0124 treated animal. h–k: Dorsal horn microglia from a NRG1 + U0126 treated animal. In ( l ) quantification of all BrdU-positive microglia in the dorsal horn is shown. Again, U0126 but not U0124 prevented NRG1 induced increase in microglial proliferation. Mechanical (shown in m ) and cold (shown in n ) pain related hypersensitivity developed after NRG1 injections which were reversed by U0126 but not by U0124. Scale bars: a and b: 100 μm, d–k: 50 μm. * P
    1 4 Diamino 2 3 Dicyano1 4 Bis, supplied by Millipore, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Tocris erk blockers
    FLNA overexpression is sensitive to MEK-ERK1/2 blockade but insensitive to mTOR blockade (A) Immunoblots for FLNA, S6K1, S6, ERK1/2, and their respective phosphorylated forms from P14 OB of R Tsc1 cHet and R Tsc1 cKO mice (N=3 each). (B) Normalized % changes for pS6/S6, FLNA/ERK1/2, and pERK1/2/ERK1/2 in R Tsc1 cHet (black) and R Tsc1 cKO mice (red) with or without rapamycin treatment in vivo . (C) Immunoblots for FLNA, S6, ERK1/2, and their phosphorylated forms in GFP (control) and Rheb CA -transfected Neuro2a cells treated with vehicle, mTOR (rapamycin and <t>Torin</t> 1) blockers, or MEK-ERK1/2 blockers, PD0325901 (PD, 2 μM) and U0126 (20 μM, n=3 sets of Neuro2a cells). U0124 (20 μM) is the inactive form of U0126. (D) Normalized % changes for pS6/S6, <t>FLNA/ERK,</t> and pERK/ERK in GFP and Rheb CA -transfected cells. (E) .
    Erk Blockers, supplied by Tocris, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Merck KGaA u0126
    TRTS-induced changes in PC12 cell differentiation after exposure to various inhibitors. (A–K) PC12 cells in the differentiation medium were treated with TRTS at 39.5°C (18 h/day), 40 ng/ml BMP4, or left untreated for 7 days in the presence or absence of 2.5 μM <t>U0126,</t> 2.5 μM U0124, 0.5 μM SB203580, or 1.0 μM GW441756. (A) Representative phase-contrast images of PC12 cells on day 7 after treatment with no stimulation; (B) TRTS (18 h/day); (C) TRTS (18 h/day) plus 2.5 μM U0126; (D) TRTS (18 h/day) plus 2.5 μM U0124; (E) TRTS (18 h/day) plus 0.5 μM SB203580; (F) TRTS (18 h/day) plus 1.0 μM GW441756; (G) 40 ng/ml BMP4; (H) 40 ng/ml BMP4 plus 2.5 μM U0126; (I) 40 ng/ml BMP4 plus 2.5 μM U0124; (J) 40 ng/ml BMP4 plus 0.5 μM SB203580; (K) 40 ng/ml BMP4 plus 1.0 μM GW441756. Scale bar, 100 μm. (L, M) PC12 cells were treated with TRTS at 39.5°C (18 h/day), 40 ng/ml BMP4, or left untreated for 7 days in the presence of the indicated concentrations of U0126, U0124, SB203580, or GW441756. The percentage of neurite-bearing cells on day 7 was assayed. The data represent the mean ± SD of three replicates. †† P
    U0126, supplied by Merck KGaA, used in various techniques. Bioz Stars score: 93/100, based on 225 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Millipore inactive isoforms
    TRTS-induced changes in PC12 cell differentiation after exposure to various inhibitors. (A–K) PC12 cells in the differentiation medium were treated with TRTS at 39.5°C (18 h/day), 40 ng/ml BMP4, or left untreated for 7 days in the presence or absence of 2.5 μM <t>U0126,</t> 2.5 μM U0124, 0.5 μM SB203580, or 1.0 μM GW441756. (A) Representative phase-contrast images of PC12 cells on day 7 after treatment with no stimulation; (B) TRTS (18 h/day); (C) TRTS (18 h/day) plus 2.5 μM U0126; (D) TRTS (18 h/day) plus 2.5 μM U0124; (E) TRTS (18 h/day) plus 0.5 μM SB203580; (F) TRTS (18 h/day) plus 1.0 μM GW441756; (G) 40 ng/ml BMP4; (H) 40 ng/ml BMP4 plus 2.5 μM U0126; (I) 40 ng/ml BMP4 plus 2.5 μM U0124; (J) 40 ng/ml BMP4 plus 0.5 μM SB203580; (K) 40 ng/ml BMP4 plus 1.0 μM GW441756. Scale bar, 100 μm. (L, M) PC12 cells were treated with TRTS at 39.5°C (18 h/day), 40 ng/ml BMP4, or left untreated for 7 days in the presence of the indicated concentrations of U0126, U0124, SB203580, or GW441756. The percentage of neurite-bearing cells on day 7 was assayed. The data represent the mean ± SD of three replicates. †† P
    Inactive Isoforms, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Millipore mek1 inhibitors
    Erk1/2 MAP kinase activity is required for the upregulation of PV1 as well as for the morphological changes induced by PMA in ECs. PMA activates the Erk1/2 MAP kinase pathway in ECs as demonstrated by immunoblotting with phospho-specific antibodies to components of the pathway such as <t>MEK1,</t> Erk1/2, and Elk-1, a downstream effector of Erk1/2 (F). MEK1, Erk1/2, and β-actin (to show the loading, Actin) were probed on the same membrane. (G) Inhibitors of MEK1 such as U0126 and PD98059 prevent the upregulation of PV1 by PMA in a dose-dependent manner, as shown by immunoblotting with anti-PV1C pAb. U0124, an inactive analog of U0126 is without effect. Immunoblotting with anti β-actin mAb shows the loading (Actin). Same inhibitors of MEK1, U0126 (D), and PD98059 (E), prevent the phenotype change of ECs induced by PMA (A), whereas U0124 has no effect (C). Control ECs (A) treated with 50 nM PMA or (B) without treatment.
    Mek1 Inhibitors, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    Infusion of U0126 but not U0124 in PVA blocks the SNI-induced cardioprotection. a Schematic of experimental design showing the timeline for sham/SNI surgery (D0), intra-PVA infusion of U0126/or U0124 (1.5 mM in 0.3 μL 50% DMSO, D3) and myocardial IR surgery (D5). b Immunohistochemical staining of pERK, an indication of ERK activation, in PVA (outlined by dashed line ) from sham and SNI animals received U0126 or U0124 infusion. Scale bar = 100 μm. Immunofluorescent imaging of pERK ( green ) and NeuN ( red ) in PVA from SNI animal. Scale bar = 50 μm (lower magnification) and 10 μm (higher magnification), respectively. Quantification results of pERK-positive cells in PVA from these animals. c Mechanical responses of hind paws at D0 (basal) and D5, after intra-PVA infusion of U0124 or U0126 (D3). * p

    Journal: Nature Communications

    Article Title: Cardioprotection induced in a mouse model of neuropathic pain via anterior nucleus of paraventricular thalamus

    doi: 10.1038/s41467-017-00891-z

    Figure Lengend Snippet: Infusion of U0126 but not U0124 in PVA blocks the SNI-induced cardioprotection. a Schematic of experimental design showing the timeline for sham/SNI surgery (D0), intra-PVA infusion of U0126/or U0124 (1.5 mM in 0.3 μL 50% DMSO, D3) and myocardial IR surgery (D5). b Immunohistochemical staining of pERK, an indication of ERK activation, in PVA (outlined by dashed line ) from sham and SNI animals received U0126 or U0124 infusion. Scale bar = 100 μm. Immunofluorescent imaging of pERK ( green ) and NeuN ( red ) in PVA from SNI animal. Scale bar = 50 μm (lower magnification) and 10 μm (higher magnification), respectively. Quantification results of pERK-positive cells in PVA from these animals. c Mechanical responses of hind paws at D0 (basal) and D5, after intra-PVA infusion of U0124 or U0126 (D3). * p

    Article Snippet: U0126 and U0124 were purchased from Tocris.

    Techniques: Immunohistochemistry, Staining, Activation Assay, Imaging

    A small molecule MEK1/2 inhibitor U0126 inhibits migration and invasion of human MM cells in vitro. (A) A transwell insert model shows significantly increased migration of the sarcomatoid MO line in comparison to other MM lines. (B) The MEK1/2 inhibitor, U0126, inhibits migration of the MO line. (C) Increased invasion of the MO line using a transwell insert coated with Matrigel. (D) The MEK1/2 inhibitor, U0126 (20 μM) inhibits invasion of MO cells, whereas its inactive analog, U0124 (20 μM) is ineffective. Results are expressed as Mean +/− SEM. *=p

    Journal: International Journal of Cancer. Journal International du Cancer

    Article Title: ERK2 is Essential for the Growth of Human Epithelioid Malignant Mesotheliomas

    doi: 10.1002/ijc.25763

    Figure Lengend Snippet: A small molecule MEK1/2 inhibitor U0126 inhibits migration and invasion of human MM cells in vitro. (A) A transwell insert model shows significantly increased migration of the sarcomatoid MO line in comparison to other MM lines. (B) The MEK1/2 inhibitor, U0126, inhibits migration of the MO line. (C) Increased invasion of the MO line using a transwell insert coated with Matrigel. (D) The MEK1/2 inhibitor, U0126 (20 μM) inhibits invasion of MO cells, whereas its inactive analog, U0124 (20 μM) is ineffective. Results are expressed as Mean +/− SEM. *=p

    Article Snippet: The synthetic MEK1/2 inhibitor, U0126, and its inactive analog, U0124, were obtained from Calbiochem (La Jolla, CA) and added to cells at 10 and 20 μM in medium containing ≤0.1% DMSO.

    Techniques: Migration, In Vitro

    A small molecule MEK1/2 inhibitor, U0126, inhibits the growth of human MM cells in vitro. (A) Growth curves of 5 human MM lines. (B) Growth of MO line. (C) ME-26 line. (D) HMESO line. (E) PPMMill line in the presence of U0126 or U0124, its inactive analog. Results are expressed as Mean +/− SEM. *=p

    Journal: International Journal of Cancer. Journal International du Cancer

    Article Title: ERK2 is Essential for the Growth of Human Epithelioid Malignant Mesotheliomas

    doi: 10.1002/ijc.25763

    Figure Lengend Snippet: A small molecule MEK1/2 inhibitor, U0126, inhibits the growth of human MM cells in vitro. (A) Growth curves of 5 human MM lines. (B) Growth of MO line. (C) ME-26 line. (D) HMESO line. (E) PPMMill line in the presence of U0126 or U0124, its inactive analog. Results are expressed as Mean +/− SEM. *=p

    Article Snippet: The synthetic MEK1/2 inhibitor, U0126, and its inactive analog, U0124, were obtained from Calbiochem (La Jolla, CA) and added to cells at 10 and 20 μM in medium containing ≤0.1% DMSO.

    Techniques: In Vitro

    U0126 application during a specific time-window decreases ERK phosphorylation specifically . A : Diphospho-Erk staining in the trunk of wt 24 hpf embryos. B : U0126 eliminates ERK1/2 phosphorylation (green) in the trunk and tail of 24 hpf zebrafish embryos. Notice that U0126-treated embryos have been overexposed (can be judged by the autofluorescence of the yolk sac extension) and still fail to show specific staining. C : U0124 does not eliminate the p-Erk staining. D : PD98059 also does not eliminate p-Erk staining when given just below the level of lethal toxicity (25 μM). E : Somewhat weaker but still significant p-Erk staining in embryos treated with U0126 starting at 10 hpf. F : Western-blot analysis demonstrated a slight but incomplete reduction in pErk1/2 levels in 10-somite embryos. G : Stage and dose-dependency of U0126 application. There is a dramatic drop in the percentage of affected embryos when treatment is applied after epiboly is completed. H : Washout experiments reveal the necessity of U0126 to be present until at least the 18 somite stage to produce the full phenotype.

    Journal: BMC Developmental Biology

    Article Title: The small molecule Mek1/2 inhibitor U0126 disrupts the chordamesoderm to notochord transition in zebrafish

    doi: 10.1186/1471-213X-8-42

    Figure Lengend Snippet: U0126 application during a specific time-window decreases ERK phosphorylation specifically . A : Diphospho-Erk staining in the trunk of wt 24 hpf embryos. B : U0126 eliminates ERK1/2 phosphorylation (green) in the trunk and tail of 24 hpf zebrafish embryos. Notice that U0126-treated embryos have been overexposed (can be judged by the autofluorescence of the yolk sac extension) and still fail to show specific staining. C : U0124 does not eliminate the p-Erk staining. D : PD98059 also does not eliminate p-Erk staining when given just below the level of lethal toxicity (25 μM). E : Somewhat weaker but still significant p-Erk staining in embryos treated with U0126 starting at 10 hpf. F : Western-blot analysis demonstrated a slight but incomplete reduction in pErk1/2 levels in 10-somite embryos. G : Stage and dose-dependency of U0126 application. There is a dramatic drop in the percentage of affected embryos when treatment is applied after epiboly is completed. H : Washout experiments reveal the necessity of U0126 to be present until at least the 18 somite stage to produce the full phenotype.

    Article Snippet: U0124 was dissolved in 2% DMSO fish water as it precipitated otherwise, the appropriate control was used to ensure no effect of the high DMSO treatment.

    Techniques: Staining, Western Blot

    Effects of intra-amygdala infusion of U0126 on nociceptive behavior. a , Spontaneous nociceptive responses to formalin were not significantly different in U0126- versus vehicle-injected mice ( n = 8–10 animals per treatment). b , Baseline mechanical thresholds (in the absence of inflammation) are not affected by intra-amygdala infusion of vehicle (50% DMSO) or U0126 (1.5 nmol) ( n = 3 mice per treatment). c , d , Five days after cannulation, animals were injected with 5% formalin into the hindpaw. Two hours after the paw injection, the MEK inhibitor U0126, the structural analog control compound U0124, or vehicle was infused into the amygdala. One hour after the amygdala injection, the effects of these treatments on thermal latencies ( c ) or mechanical thresholds ( d ) were analyzed. c , U0126 infusion into the amygdala did not affect formalin-induced thermal hypersensitivity ( n = 4 animals per treatment). d , U0126 infusion significantly reduced formalin-induced mechanical hypersensitivity in both the injected and the noninjected hindpaw ( n = 6–7 animals per treatment; p

    Journal: The Journal of Neuroscience

    Article Title: Activation of the Extracellular Signal-Regulated Kinase in the Amygdala Modulates Pain Perception

    doi: 10.1523/JNEUROSCI.3536-06.2007

    Figure Lengend Snippet: Effects of intra-amygdala infusion of U0126 on nociceptive behavior. a , Spontaneous nociceptive responses to formalin were not significantly different in U0126- versus vehicle-injected mice ( n = 8–10 animals per treatment). b , Baseline mechanical thresholds (in the absence of inflammation) are not affected by intra-amygdala infusion of vehicle (50% DMSO) or U0126 (1.5 nmol) ( n = 3 mice per treatment). c , d , Five days after cannulation, animals were injected with 5% formalin into the hindpaw. Two hours after the paw injection, the MEK inhibitor U0126, the structural analog control compound U0124, or vehicle was infused into the amygdala. One hour after the amygdala injection, the effects of these treatments on thermal latencies ( c ) or mechanical thresholds ( d ) were analyzed. c , U0126 infusion into the amygdala did not affect formalin-induced thermal hypersensitivity ( n = 4 animals per treatment). d , U0126 infusion significantly reduced formalin-induced mechanical hypersensitivity in both the injected and the noninjected hindpaw ( n = 6–7 animals per treatment; p

    Article Snippet: U0126 and U0124 (VWR Scientific Products, Batavia, IL) were dissolved as described previously ( ).

    Techniques: Injection, Mouse Assay

    TRTS-induced changes in PC12 cell differentiation after exposure to various inhibitors. (A–K) PC12 cells in the differentiation medium were treated with TRTS at 39.5°C (18 h/day), 40 ng/ml BMP4, or left untreated for 7 days in the presence or absence of 2.5 μM U0126, 2.5 μM U0124, 0.5 μM SB203580, or 1.0 μM GW441756. (A) Representative phase-contrast images of PC12 cells on day 7 after treatment with no stimulation; (B) TRTS (18 h/day); (C) TRTS (18 h/day) plus 2.5 μM U0126; (D) TRTS (18 h/day) plus 2.5 μM U0124; (E) TRTS (18 h/day) plus 0.5 μM SB203580; (F) TRTS (18 h/day) plus 1.0 μM GW441756; (G) 40 ng/ml BMP4; (H) 40 ng/ml BMP4 plus 2.5 μM U0126; (I) 40 ng/ml BMP4 plus 2.5 μM U0124; (J) 40 ng/ml BMP4 plus 0.5 μM SB203580; (K) 40 ng/ml BMP4 plus 1.0 μM GW441756. Scale bar, 100 μm. (L, M) PC12 cells were treated with TRTS at 39.5°C (18 h/day), 40 ng/ml BMP4, or left untreated for 7 days in the presence of the indicated concentrations of U0126, U0124, SB203580, or GW441756. The percentage of neurite-bearing cells on day 7 was assayed. The data represent the mean ± SD of three replicates. †† P

    Journal: PLoS ONE

    Article Title: Induction of Neurite Outgrowth in PC12 Cells Treated with Temperature-Controlled Repeated Thermal Stimulation

    doi: 10.1371/journal.pone.0124024

    Figure Lengend Snippet: TRTS-induced changes in PC12 cell differentiation after exposure to various inhibitors. (A–K) PC12 cells in the differentiation medium were treated with TRTS at 39.5°C (18 h/day), 40 ng/ml BMP4, or left untreated for 7 days in the presence or absence of 2.5 μM U0126, 2.5 μM U0124, 0.5 μM SB203580, or 1.0 μM GW441756. (A) Representative phase-contrast images of PC12 cells on day 7 after treatment with no stimulation; (B) TRTS (18 h/day); (C) TRTS (18 h/day) plus 2.5 μM U0126; (D) TRTS (18 h/day) plus 2.5 μM U0124; (E) TRTS (18 h/day) plus 0.5 μM SB203580; (F) TRTS (18 h/day) plus 1.0 μM GW441756; (G) 40 ng/ml BMP4; (H) 40 ng/ml BMP4 plus 2.5 μM U0126; (I) 40 ng/ml BMP4 plus 2.5 μM U0124; (J) 40 ng/ml BMP4 plus 0.5 μM SB203580; (K) 40 ng/ml BMP4 plus 1.0 μM GW441756. Scale bar, 100 μm. (L, M) PC12 cells were treated with TRTS at 39.5°C (18 h/day), 40 ng/ml BMP4, or left untreated for 7 days in the presence of the indicated concentrations of U0126, U0124, SB203580, or GW441756. The percentage of neurite-bearing cells on day 7 was assayed. The data represent the mean ± SD of three replicates. †† P

    Article Snippet: The results presented in show that SB203580 and U0126, but not U0124, suppressed more than half of TRTS- or BMP4-induced neuritogenesis in PC12 cells.

    Techniques: Cell Differentiation

    Effects of small molecule inhibitors on the growth of MCF10 cell variants in 3D rBM overlay cultures. Cells were incubated for 9 days in 3D rBM overlay cultures under control (DMSO vehicle) or drug treatment conditions. Inhibitors used were U0126 at 10 μM, U0124 at 10 μM, wortmannin at 200 nM, CI-1040 at 100 nM, and doxorubicin at 1 μM. Phase-contrast images are shown. Scale bar, 100 μm.

    Journal: The Journal of Pharmacology and Experimental Therapeutics

    Article Title: Three-Dimensional Overlay Culture Models of Human Breast Cancer Reveal a Critical Sensitivity to Mitogen-Activated Protein Kinase Kinase Inhibitors S⃞

    doi: 10.1124/jpet.109.160390

    Figure Lengend Snippet: Effects of small molecule inhibitors on the growth of MCF10 cell variants in 3D rBM overlay cultures. Cells were incubated for 9 days in 3D rBM overlay cultures under control (DMSO vehicle) or drug treatment conditions. Inhibitors used were U0126 at 10 μM, U0124 at 10 μM, wortmannin at 200 nM, CI-1040 at 100 nM, and doxorubicin at 1 μM. Phase-contrast images are shown. Scale bar, 100 μm.

    Article Snippet: The MEK inhibitor U0126 and its inactive analog U0124 were purchased from Calbiochem (San Diego, CA).

    Techniques: Incubation

    MEK inhibition decreases NIS protein levels and NIS-mediated RA radioactive iodide uptake in tRA/H-treated MCF-7 human breast cancer cells (A) Western blot analysis showed that MEK inhibitor U0126 (left panel) or recombinant adenovirus carrying dominant negative MEK1 A217/A221 (right panel) decreased NIS protein levels in MCF-7-tRA/H cells. MCF-7 cells treated with tRA/H were cultured in the presence of DMSO, U0126, or inactive analog U0124 for 24 hours, or were infected with recombinant adenovirus carrying LacZ (rAdLacZ) or dominant negative MEK1 (rAdDNMEK1) at a multiplicity of infection (MOI) of 5 for 24 hours prior to western blot analysis. β-actin served as a loading control. The results are representative of at least two independent experiments. (B) Bar graph indicates the densitometry values of NIS protein level normalized with β-actin of cells under various treatments (represented as percentage relative to MCF-7/tRA/H or MCF-7/tRA/H/Lac-Z control). (C) U0126 decreased radioactive iodide uptake in a dose-dependent manner in tRA/H-induced MCF-7 cells. The results are representative of three independent experiments performed in triplicate and the mean ± SD are shown. Asterisk indicates statistically significant difference (P

    Journal: Endocrine-related cancer

    Article Title: MEK Inhibition Leads To Lysosome-Mediated Na+/I- Symporter Protein Degradation In Human Breast Cancer Cells

    doi: 10.1530/ERC-12-0342

    Figure Lengend Snippet: MEK inhibition decreases NIS protein levels and NIS-mediated RA radioactive iodide uptake in tRA/H-treated MCF-7 human breast cancer cells (A) Western blot analysis showed that MEK inhibitor U0126 (left panel) or recombinant adenovirus carrying dominant negative MEK1 A217/A221 (right panel) decreased NIS protein levels in MCF-7-tRA/H cells. MCF-7 cells treated with tRA/H were cultured in the presence of DMSO, U0126, or inactive analog U0124 for 24 hours, or were infected with recombinant adenovirus carrying LacZ (rAdLacZ) or dominant negative MEK1 (rAdDNMEK1) at a multiplicity of infection (MOI) of 5 for 24 hours prior to western blot analysis. β-actin served as a loading control. The results are representative of at least two independent experiments. (B) Bar graph indicates the densitometry values of NIS protein level normalized with β-actin of cells under various treatments (represented as percentage relative to MCF-7/tRA/H or MCF-7/tRA/H/Lac-Z control). (C) U0126 decreased radioactive iodide uptake in a dose-dependent manner in tRA/H-induced MCF-7 cells. The results are representative of three independent experiments performed in triplicate and the mean ± SD are shown. Asterisk indicates statistically significant difference (P

    Article Snippet: U0126 (Promega) and U0124 (Promega) were dissolved in DMSO at 10mM before adding them to the media.

    Techniques: Inhibition, Western Blot, Recombinant, Dominant Negative Mutation, Cell Culture, Infection

    U0126 reduces H 2 O 2 -induced ROS level in PC12 cells. (a) Representative images of the green channel (DCHFDA fluorescence) at 10 min and 2 h after H 2 O 2 addition. The fluorescence intensity is correlated with the amount of ROS in cells. All images are shown with the same intensity scale bar. (b) Quantitative measurements of the fluorescence intensity show that U0126 and U0124 are able to reduce the amount of ROS in PC-12 cells within 10 min of incubation. The ROS level is maintained low at 2 h. Trametinib increases the amount of ROS in PC-12 cells. Images are collated from three sets of individual experiments and the error bars depict ± SD. Scale bar = 100 μm.

    Journal: ACS Chemical Neuroscience

    Article Title: U0126 Protects Cells against Oxidative Stress Independent of Its Function as a MEK Inhibitor

    doi: 10.1021/cn500288n

    Figure Lengend Snippet: U0126 reduces H 2 O 2 -induced ROS level in PC12 cells. (a) Representative images of the green channel (DCHFDA fluorescence) at 10 min and 2 h after H 2 O 2 addition. The fluorescence intensity is correlated with the amount of ROS in cells. All images are shown with the same intensity scale bar. (b) Quantitative measurements of the fluorescence intensity show that U0126 and U0124 are able to reduce the amount of ROS in PC-12 cells within 10 min of incubation. The ROS level is maintained low at 2 h. Trametinib increases the amount of ROS in PC-12 cells. Images are collated from three sets of individual experiments and the error bars depict ± SD. Scale bar = 100 μm.

    Article Snippet: U0124 and trametinib were purchased from Cell Signaling.

    Techniques: Fluorescence, Incubation

    U0126 protects PC12 cells against H 2 O 2 -induced cell death. (a) Chemical structures of U0126, its inactive analogue U0124, and other MEK inhibitors used in the study: trametinib, CI-1040, PD318088, and pimasertib. (b) Representative images of H 2 O 2 -induced dead cells stained by propidium iodide. These are accompanied by bright field images that show all cells. Scale bar = 100 μm. (c) U0126 treatment shows reduced cell death compared with DMSO ( p

    Journal: ACS Chemical Neuroscience

    Article Title: U0126 Protects Cells against Oxidative Stress Independent of Its Function as a MEK Inhibitor

    doi: 10.1021/cn500288n

    Figure Lengend Snippet: U0126 protects PC12 cells against H 2 O 2 -induced cell death. (a) Chemical structures of U0126, its inactive analogue U0124, and other MEK inhibitors used in the study: trametinib, CI-1040, PD318088, and pimasertib. (b) Representative images of H 2 O 2 -induced dead cells stained by propidium iodide. These are accompanied by bright field images that show all cells. Scale bar = 100 μm. (c) U0126 treatment shows reduced cell death compared with DMSO ( p

    Article Snippet: U0124 and trametinib were purchased from Cell Signaling.

    Techniques: Staining

    U0126 protects PC12 cells against different types of oxidative stress inducers. (a) Upon 6 h of blue light illumination at 10 mW/cm 2 , U0126 treatment results in a dramatic decrease in cell death (3.5%) compared to DMSO (42.0%), while trametinib sees a significant increase in cell death (88.9%). U0124, a U0126 analogue, provides some cell protective effects, with a death rate at 17.9%. (b) U0126 protects PC12 cells against oxidative stress induced by 20 mM sodium azide for 24 h. (c) U0126 results in higher cell death than DMSO upon treatment with 5 μM rotenone, but the death rate is still significantly less than that by trametinib. (d) U0126 results in slightly lower cell death than DMSO upon treatment with 2 mM paraquat for 24 h. (e) U0126 results in slightly lower cell death than DMSO upon treatment with 3.3 μM cisplatin for 24 h. For each condition, the cell death data is computed from 75 individual images taken from three different sets of experiments and each image comprises of 150–250 cells. SEM error bars are depicted in the graph.

    Journal: ACS Chemical Neuroscience

    Article Title: U0126 Protects Cells against Oxidative Stress Independent of Its Function as a MEK Inhibitor

    doi: 10.1021/cn500288n

    Figure Lengend Snippet: U0126 protects PC12 cells against different types of oxidative stress inducers. (a) Upon 6 h of blue light illumination at 10 mW/cm 2 , U0126 treatment results in a dramatic decrease in cell death (3.5%) compared to DMSO (42.0%), while trametinib sees a significant increase in cell death (88.9%). U0124, a U0126 analogue, provides some cell protective effects, with a death rate at 17.9%. (b) U0126 protects PC12 cells against oxidative stress induced by 20 mM sodium azide for 24 h. (c) U0126 results in higher cell death than DMSO upon treatment with 5 μM rotenone, but the death rate is still significantly less than that by trametinib. (d) U0126 results in slightly lower cell death than DMSO upon treatment with 2 mM paraquat for 24 h. (e) U0126 results in slightly lower cell death than DMSO upon treatment with 3.3 μM cisplatin for 24 h. For each condition, the cell death data is computed from 75 individual images taken from three different sets of experiments and each image comprises of 150–250 cells. SEM error bars are depicted in the graph.

    Article Snippet: U0124 and trametinib were purchased from Cell Signaling.

    Techniques:

    Dissociation of zenk and behavioral response measures to novel song a day after the infusion procedure. Birds were injected with the non-functional analogue U0124 prior to training on one song, and then tested a day later with a different (novel) song. Birds had significantly shorter response latency on testing day than on training day (n = 4, p

    Journal: Genes, brain, and behavior

    Article Title: Partial Dissociation of Molecular and Behavioral Measures of Song Habituation in Adult Zebra Finches

    doi: 10.1111/j.1601-183X.2008.00423.x

    Figure Lengend Snippet: Dissociation of zenk and behavioral response measures to novel song a day after the infusion procedure. Birds were injected with the non-functional analogue U0124 prior to training on one song, and then tested a day later with a different (novel) song. Birds had significantly shorter response latency on testing day than on training day (n = 4, p

    Article Snippet: The control group was injected with the nonfunctional analog U0124 (10 μg/μl in DMSO; Cell Signaling Technology).

    Techniques: Injection, Functional Assay

    Blocking ERK pathway during training inhibits zenk habituation. a, Representative in situ hybridization images of zenk expression in AL. Arrows point to the cannula tips. Left: 30 min after familiar song stimulation, U0126-injected brain; Right: 30 min after familiar song stimulation, U0124-injected brain. b, Mean zenk -positive cell density in AL from birds exposed to 30 min of familiar song; n = 5 each group. The birds infused with U0126 on training day had statistically significant higher zenk mRNA level in AL than U0124-injected birds (p

    Journal: Genes, brain, and behavior

    Article Title: Partial Dissociation of Molecular and Behavioral Measures of Song Habituation in Adult Zebra Finches

    doi: 10.1111/j.1601-183X.2008.00423.x

    Figure Lengend Snippet: Blocking ERK pathway during training inhibits zenk habituation. a, Representative in situ hybridization images of zenk expression in AL. Arrows point to the cannula tips. Left: 30 min after familiar song stimulation, U0126-injected brain; Right: 30 min after familiar song stimulation, U0124-injected brain. b, Mean zenk -positive cell density in AL from birds exposed to 30 min of familiar song; n = 5 each group. The birds infused with U0126 on training day had statistically significant higher zenk mRNA level in AL than U0124-injected birds (p

    Article Snippet: The control group was injected with the nonfunctional analog U0124 (10 μg/μl in DMSO; Cell Signaling Technology).

    Techniques: Blocking Assay, In Situ Hybridization, Expressing, Injection

    Erk 1,2 mediates enhanced c-Met expression through MITF (a) WM1341D and WM1552C/MCSP transfected cells were incubated with 2.4 μM U0126 or control compound U0124 overnight in serum free medium. Lysates were evaluated by western blot using the indicated antibodies. (b) WM1552C/MCSP cells were transfected with MITF specific or control siRNA for 48 hours and assayed for expression of C-Met, MITF, and pErk 1, 2 by western blot. (c) WM1552C/MCSP cells were transfected with c-Met specific or control siRNA for 48 hours and assayed for expression of C-Met, MITF and pErk 1,2 and MCSP by western blot.

    Journal: Cancer research

    Article Title: Melanoma Proteoglycan Modifies Gene Expression to Stimulate Tumor Cell Motility, Growth and Epithelial to Mesenchymal Transition

    doi: 10.1158/0008-5472.CAN-08-4626

    Figure Lengend Snippet: Erk 1,2 mediates enhanced c-Met expression through MITF (a) WM1341D and WM1552C/MCSP transfected cells were incubated with 2.4 μM U0126 or control compound U0124 overnight in serum free medium. Lysates were evaluated by western blot using the indicated antibodies. (b) WM1552C/MCSP cells were transfected with MITF specific or control siRNA for 48 hours and assayed for expression of C-Met, MITF, and pErk 1, 2 by western blot. (c) WM1552C/MCSP cells were transfected with c-Met specific or control siRNA for 48 hours and assayed for expression of C-Met, MITF and pErk 1,2 and MCSP by western blot.

    Article Snippet: Other antibodies and reagents were purchased from the indicated companies: Anti-tubulin from Oncogene Research Products (Pasadena, CA); anti-phospho p44/42 MAPK (pErk 1,2), anti-p44/42 MAPK (Erk1,2), anti-c-Met and phospho c-Met (pc-Met), Mek inhibitor U0126 and control compound U0124 from Cell Signaling Technology, Inc (Boston, MA); anti-GST from Abcam, Inc (Boston, MA); anti-E-Cadherin from BD Transduction Labs (Lexington, KY); anti-MITF from Santa Cruz Biotech.

    Techniques: Expressing, Transfection, Incubation, Western Blot

    Inhibition of MEK1/2 could reverse NRG1-induced microgliosis and mechanical and cold pain-related hypersensitivity. NRG1 was administered intrathecally (4 ng given daily for 3 days) together with the MEK inhibitor U0126 (10 μg) or the inactive analogue U0124 (10μg). a and b : Dorsal horn of animals treated with NRG1 + U0124 (in a) or NRG1 + U0126 (in b) immunostained with Iba1. Note that U0126 but not U0124 could prevent NRG1 associated increase in numbers of microglia with an effector morphology. In c quantification of this response is shown. In d – k we assessed proliferation (pulse labeling with BrdU) after injections (Iba1 is shown in red, DAPI in blue, BrdU in yellow and in the last panel merged images are shown). d–g: Dorsal horn microglia from a NRG1 + U0124 treated animal. h–k: Dorsal horn microglia from a NRG1 + U0126 treated animal. In ( l ) quantification of all BrdU-positive microglia in the dorsal horn is shown. Again, U0126 but not U0124 prevented NRG1 induced increase in microglial proliferation. Mechanical (shown in m ) and cold (shown in n ) pain related hypersensitivity developed after NRG1 injections which were reversed by U0126 but not by U0124. Scale bars: a and b: 100 μm, d–k: 50 μm. * P

    Journal: Glia

    Article Title: Following Nerve Injury Neuregulin-1 Drives Microglial Proliferation and Neuropathic Pain via the MEK/ERK Pathway

    doi: 10.1002/glia.21124

    Figure Lengend Snippet: Inhibition of MEK1/2 could reverse NRG1-induced microgliosis and mechanical and cold pain-related hypersensitivity. NRG1 was administered intrathecally (4 ng given daily for 3 days) together with the MEK inhibitor U0126 (10 μg) or the inactive analogue U0124 (10μg). a and b : Dorsal horn of animals treated with NRG1 + U0124 (in a) or NRG1 + U0126 (in b) immunostained with Iba1. Note that U0126 but not U0124 could prevent NRG1 associated increase in numbers of microglia with an effector morphology. In c quantification of this response is shown. In d – k we assessed proliferation (pulse labeling with BrdU) after injections (Iba1 is shown in red, DAPI in blue, BrdU in yellow and in the last panel merged images are shown). d–g: Dorsal horn microglia from a NRG1 + U0124 treated animal. h–k: Dorsal horn microglia from a NRG1 + U0126 treated animal. In ( l ) quantification of all BrdU-positive microglia in the dorsal horn is shown. Again, U0126 but not U0124 prevented NRG1 induced increase in microglial proliferation. Mechanical (shown in m ) and cold (shown in n ) pain related hypersensitivity developed after NRG1 injections which were reversed by U0126 but not by U0124. Scale bars: a and b: 100 μm, d–k: 50 μm. * P

    Article Snippet: In another experiment NRG1 was administered to naive animals together with the MEK inhibitor U0126 (Promega) or the inactive analogue U0124 (Merck) which were dissolved in 24% DMSO and saline (as previously described by Zhuang et al., ).

    Techniques: Inhibition, Labeling

    Microgliosis and mechanical and cold hypersensitivity following L5 SNL were significantly reduced by blocking MEK1/2 pathways. Animals underwent L5 SNL and were injected intrathecally daily with a 10 μg dose of the MEK inhibitor U0126 or its inactive analogue U0124. Three days after SNL animals treated with the inactive analogue U0124 demonstrated a dramatic increase in the number of dorsal horn microglia showing an effector morphology compared with naïve animals injected with saline. This microgliosis was significantly reduced when animals received the MEK inhibitor U0126. In ( a ) (SNL + U0124) and ( b ) (SNL + U0126) we show representative sections of the L5 spinal cord of these animals stained with Iba1 to label microglia. In ( c ) we show the quantification ( n = 4 per group, P

    Journal: Glia

    Article Title: Following Nerve Injury Neuregulin-1 Drives Microglial Proliferation and Neuropathic Pain via the MEK/ERK Pathway

    doi: 10.1002/glia.21124

    Figure Lengend Snippet: Microgliosis and mechanical and cold hypersensitivity following L5 SNL were significantly reduced by blocking MEK1/2 pathways. Animals underwent L5 SNL and were injected intrathecally daily with a 10 μg dose of the MEK inhibitor U0126 or its inactive analogue U0124. Three days after SNL animals treated with the inactive analogue U0124 demonstrated a dramatic increase in the number of dorsal horn microglia showing an effector morphology compared with naïve animals injected with saline. This microgliosis was significantly reduced when animals received the MEK inhibitor U0126. In ( a ) (SNL + U0124) and ( b ) (SNL + U0126) we show representative sections of the L5 spinal cord of these animals stained with Iba1 to label microglia. In ( c ) we show the quantification ( n = 4 per group, P

    Article Snippet: In another experiment NRG1 was administered to naive animals together with the MEK inhibitor U0126 (Promega) or the inactive analogue U0124 (Merck) which were dissolved in 24% DMSO and saline (as previously described by Zhuang et al., ).

    Techniques: Blocking Assay, Injection, Staining

    FLNA overexpression is sensitive to MEK-ERK1/2 blockade but insensitive to mTOR blockade (A) Immunoblots for FLNA, S6K1, S6, ERK1/2, and their respective phosphorylated forms from P14 OB of R Tsc1 cHet and R Tsc1 cKO mice (N=3 each). (B) Normalized % changes for pS6/S6, FLNA/ERK1/2, and pERK1/2/ERK1/2 in R Tsc1 cHet (black) and R Tsc1 cKO mice (red) with or without rapamycin treatment in vivo . (C) Immunoblots for FLNA, S6, ERK1/2, and their phosphorylated forms in GFP (control) and Rheb CA -transfected Neuro2a cells treated with vehicle, mTOR (rapamycin and Torin 1) blockers, or MEK-ERK1/2 blockers, PD0325901 (PD, 2 μM) and U0126 (20 μM, n=3 sets of Neuro2a cells). U0124 (20 μM) is the inactive form of U0126. (D) Normalized % changes for pS6/S6, FLNA/ERK, and pERK/ERK in GFP and Rheb CA -transfected cells. (E) .

    Journal: Neuron

    Article Title: MEK-ERK1/2-dependent FLNA overexpression promotes abnormal dendritic patterning in tuberous sclerosis independent of mTOR

    doi: 10.1016/j.neuron.2014.09.009

    Figure Lengend Snippet: FLNA overexpression is sensitive to MEK-ERK1/2 blockade but insensitive to mTOR blockade (A) Immunoblots for FLNA, S6K1, S6, ERK1/2, and their respective phosphorylated forms from P14 OB of R Tsc1 cHet and R Tsc1 cKO mice (N=3 each). (B) Normalized % changes for pS6/S6, FLNA/ERK1/2, and pERK1/2/ERK1/2 in R Tsc1 cHet (black) and R Tsc1 cKO mice (red) with or without rapamycin treatment in vivo . (C) Immunoblots for FLNA, S6, ERK1/2, and their phosphorylated forms in GFP (control) and Rheb CA -transfected Neuro2a cells treated with vehicle, mTOR (rapamycin and Torin 1) blockers, or MEK-ERK1/2 blockers, PD0325901 (PD, 2 μM) and U0126 (20 μM, n=3 sets of Neuro2a cells). U0124 (20 μM) is the inactive form of U0126. (D) Normalized % changes for pS6/S6, FLNA/ERK, and pERK/ERK in GFP and Rheb CA -transfected cells. (E) .

    Article Snippet: Torin 1 and ERK blockers (U0126 and U0124) were from Tocris.

    Techniques: Over Expression, Western Blot, Mouse Assay, In Vivo, Transfection

    TRTS-induced changes in PC12 cell differentiation after exposure to various inhibitors. (A–K) PC12 cells in the differentiation medium were treated with TRTS at 39.5°C (18 h/day), 40 ng/ml BMP4, or left untreated for 7 days in the presence or absence of 2.5 μM U0126, 2.5 μM U0124, 0.5 μM SB203580, or 1.0 μM GW441756. (A) Representative phase-contrast images of PC12 cells on day 7 after treatment with no stimulation; (B) TRTS (18 h/day); (C) TRTS (18 h/day) plus 2.5 μM U0126; (D) TRTS (18 h/day) plus 2.5 μM U0124; (E) TRTS (18 h/day) plus 0.5 μM SB203580; (F) TRTS (18 h/day) plus 1.0 μM GW441756; (G) 40 ng/ml BMP4; (H) 40 ng/ml BMP4 plus 2.5 μM U0126; (I) 40 ng/ml BMP4 plus 2.5 μM U0124; (J) 40 ng/ml BMP4 plus 0.5 μM SB203580; (K) 40 ng/ml BMP4 plus 1.0 μM GW441756. Scale bar, 100 μm. (L, M) PC12 cells were treated with TRTS at 39.5°C (18 h/day), 40 ng/ml BMP4, or left untreated for 7 days in the presence of the indicated concentrations of U0126, U0124, SB203580, or GW441756. The percentage of neurite-bearing cells on day 7 was assayed. The data represent the mean ± SD of three replicates. †† P

    Journal: PLoS ONE

    Article Title: Induction of Neurite Outgrowth in PC12 Cells Treated with Temperature-Controlled Repeated Thermal Stimulation

    doi: 10.1371/journal.pone.0124024

    Figure Lengend Snippet: TRTS-induced changes in PC12 cell differentiation after exposure to various inhibitors. (A–K) PC12 cells in the differentiation medium were treated with TRTS at 39.5°C (18 h/day), 40 ng/ml BMP4, or left untreated for 7 days in the presence or absence of 2.5 μM U0126, 2.5 μM U0124, 0.5 μM SB203580, or 1.0 μM GW441756. (A) Representative phase-contrast images of PC12 cells on day 7 after treatment with no stimulation; (B) TRTS (18 h/day); (C) TRTS (18 h/day) plus 2.5 μM U0126; (D) TRTS (18 h/day) plus 2.5 μM U0124; (E) TRTS (18 h/day) plus 0.5 μM SB203580; (F) TRTS (18 h/day) plus 1.0 μM GW441756; (G) 40 ng/ml BMP4; (H) 40 ng/ml BMP4 plus 2.5 μM U0126; (I) 40 ng/ml BMP4 plus 2.5 μM U0124; (J) 40 ng/ml BMP4 plus 0.5 μM SB203580; (K) 40 ng/ml BMP4 plus 1.0 μM GW441756. Scale bar, 100 μm. (L, M) PC12 cells were treated with TRTS at 39.5°C (18 h/day), 40 ng/ml BMP4, or left untreated for 7 days in the presence of the indicated concentrations of U0126, U0124, SB203580, or GW441756. The percentage of neurite-bearing cells on day 7 was assayed. The data represent the mean ± SD of three replicates. †† P

    Article Snippet: We also scored PC12 cells incubated in the presence of a negative control for U0126 (U0124, 2.5 μM) to assess the inhibition of TRTS-mediated neurite outgrowth.

    Techniques: Cell Differentiation

    Erk1/2 MAP kinase activity is required for the upregulation of PV1 as well as for the morphological changes induced by PMA in ECs. PMA activates the Erk1/2 MAP kinase pathway in ECs as demonstrated by immunoblotting with phospho-specific antibodies to components of the pathway such as MEK1, Erk1/2, and Elk-1, a downstream effector of Erk1/2 (F). MEK1, Erk1/2, and β-actin (to show the loading, Actin) were probed on the same membrane. (G) Inhibitors of MEK1 such as U0126 and PD98059 prevent the upregulation of PV1 by PMA in a dose-dependent manner, as shown by immunoblotting with anti-PV1C pAb. U0124, an inactive analog of U0126 is without effect. Immunoblotting with anti β-actin mAb shows the loading (Actin). Same inhibitors of MEK1, U0126 (D), and PD98059 (E), prevent the phenotype change of ECs induced by PMA (A), whereas U0124 has no effect (C). Control ECs (A) treated with 50 nM PMA or (B) without treatment.

    Journal: Molecular Biology of the Cell

    Article Title: PV1 Is a Key Structural Component for the Formation of the Stomatal and Fenestral Diaphragms

    doi: 10.1091/mbc.E03-08-0593

    Figure Lengend Snippet: Erk1/2 MAP kinase activity is required for the upregulation of PV1 as well as for the morphological changes induced by PMA in ECs. PMA activates the Erk1/2 MAP kinase pathway in ECs as demonstrated by immunoblotting with phospho-specific antibodies to components of the pathway such as MEK1, Erk1/2, and Elk-1, a downstream effector of Erk1/2 (F). MEK1, Erk1/2, and β-actin (to show the loading, Actin) were probed on the same membrane. (G) Inhibitors of MEK1 such as U0126 and PD98059 prevent the upregulation of PV1 by PMA in a dose-dependent manner, as shown by immunoblotting with anti-PV1C pAb. U0124, an inactive analog of U0126 is without effect. Immunoblotting with anti β-actin mAb shows the loading (Actin). Same inhibitors of MEK1, U0126 (D), and PD98059 (E), prevent the phenotype change of ECs induced by PMA (A), whereas U0124 has no effect (C). Control ECs (A) treated with 50 nM PMA or (B) without treatment.

    Article Snippet: Protein kinase C (PKC) inhibitors (staurosporine, calphostin C, Go9068, and bis-indolilmaleimide I) and MEK1 Inhibitors (PD98059, U0126 and its negative control U0124) were from Calbiochem (San Diego, CA).

    Techniques: Activity Assay