anti phosphor extracellular signal regulated kinase p erk  (Cell Signaling Technology Inc)

 
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    Cell Signaling Technology Inc anti phosphor extracellular signal regulated kinase p erk
    Anti Phosphor Extracellular Signal Regulated Kinase P Erk, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 93/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti phosphor extracellular signal regulated kinase p erk/product/Cell Signaling Technology Inc
    Average 93 stars, based on 3 article reviews
    Price from $9.99 to $1999.99
    anti phosphor extracellular signal regulated kinase p erk - by Bioz Stars, 2020-09
    93/100 stars

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    Article Title: Preventive Effect of Garlic Oil and Its Organosulfur Component Diallyl-Disulfide on Cigarette Smoke-Induced Airway Inflammation in Mice
    Article Snippet: The primary antibodies used were as follows: anti-β-actin (Cell Signaling, Danvers, MA, USA), anti-MMP-9 (Abcam), anti-phosphor-extracellular signal-regulated kinase (p-ERK) (Cell Signaling) and anti-ERK (Cell Signaling).

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    Cell Signaling Technology Inc antibodies against phosphorylation erk1 2
    <t>ERK1/2,</t> JNK and PI3K are involved in the protective effects of lean ATCM against H 2 O 2 induced neurotoxicity. ( a ) Adipose tissue conditioned media (ATCM) from lean subjects was applied to SH-SY5Y neuronal cells for 1 h and the phosphorylation of JNK, Akt at threonine 308, and ERK1/2 was measured by western blotting. Phosphorylated signaling proteins are expressed relative to respective total protein and the ATCM condition was compared to vehicle (veh) treated well and ( b ) Adipose tissue conditioned media (ATCM) from lean subjects was applied to SH-SY5Y neuronal cells for 24 h in the presence of 800 µM H 2 O 2 . Chemical inhibition of JNK with SP600125 (5 µM), PI3-K with LY29400 (20 µM) and ERK with PD98059 (25 µM) partially inhibited the neuroprotective effects of ATCM in SH-SY5Y cells under oxidative stress conditions. Representative western blots are shown to the right of the quantified data in panel A. All cell culture experiments were repeated on two separate passages of cells with ATCM from three different subjects ( n = 6). * p
    Antibodies Against Phosphorylation Erk1 2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 89/100, based on 174 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/antibodies against phosphorylation erk1 2/product/Cell Signaling Technology Inc
    Average 89 stars, based on 174 article reviews
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    Cell Signaling Technology Inc anti phospho mek
    Effect of miR-1246 on <t>MEK-ERK</t> signaling. A375P/Mdr cells were transiently transfected with a miR-1246 mimic or control RNA for 24 hours. Cell lysates were then prepared after treatment with the indicated concentrations of PLX4720 for 24 hours. The phosphorylated forms of MEK and ERK were detected by immunoblotting using anti–p-MEK and anti–p-ERK antibodies. The same blots were stripped and reprobed with anti-MEK and anti-ERK antibodies to confirm similar expression levels of MEK and ERK proteins in all lanes. The numbers listed below each band indicate the phosphorylated protein/total protein ratios determined using the Image Lab software. Data are representative of at least three independent experiments.
    Anti Phospho Mek, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 90/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti phospho mek/product/Cell Signaling Technology Inc
    Average 90 stars, based on 8 article reviews
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    ERK1/2, JNK and PI3K are involved in the protective effects of lean ATCM against H 2 O 2 induced neurotoxicity. ( a ) Adipose tissue conditioned media (ATCM) from lean subjects was applied to SH-SY5Y neuronal cells for 1 h and the phosphorylation of JNK, Akt at threonine 308, and ERK1/2 was measured by western blotting. Phosphorylated signaling proteins are expressed relative to respective total protein and the ATCM condition was compared to vehicle (veh) treated well and ( b ) Adipose tissue conditioned media (ATCM) from lean subjects was applied to SH-SY5Y neuronal cells for 24 h in the presence of 800 µM H 2 O 2 . Chemical inhibition of JNK with SP600125 (5 µM), PI3-K with LY29400 (20 µM) and ERK with PD98059 (25 µM) partially inhibited the neuroprotective effects of ATCM in SH-SY5Y cells under oxidative stress conditions. Representative western blots are shown to the right of the quantified data in panel A. All cell culture experiments were repeated on two separate passages of cells with ATCM from three different subjects ( n = 6). * p

    Journal: International Journal of Molecular Sciences

    Article Title: Human Adipose Tissue Conditioned Media from Lean Subjects Is Protective against H2O2 Induced Neurotoxicity in Human SH-SY5Y Neuronal Cells

    doi: 10.3390/ijms16011221

    Figure Lengend Snippet: ERK1/2, JNK and PI3K are involved in the protective effects of lean ATCM against H 2 O 2 induced neurotoxicity. ( a ) Adipose tissue conditioned media (ATCM) from lean subjects was applied to SH-SY5Y neuronal cells for 1 h and the phosphorylation of JNK, Akt at threonine 308, and ERK1/2 was measured by western blotting. Phosphorylated signaling proteins are expressed relative to respective total protein and the ATCM condition was compared to vehicle (veh) treated well and ( b ) Adipose tissue conditioned media (ATCM) from lean subjects was applied to SH-SY5Y neuronal cells for 24 h in the presence of 800 µM H 2 O 2 . Chemical inhibition of JNK with SP600125 (5 µM), PI3-K with LY29400 (20 µM) and ERK with PD98059 (25 µM) partially inhibited the neuroprotective effects of ATCM in SH-SY5Y cells under oxidative stress conditions. Representative western blots are shown to the right of the quantified data in panel A. All cell culture experiments were repeated on two separate passages of cells with ATCM from three different subjects ( n = 6). * p

    Article Snippet: Antibodies against phosphorylation-ERK1/2 (p-ERK1/2) (cat#4370), p-JNK (cat#4668), p-Akt serine473 (cat#4060), ERK1/2 (cat#4695), JNK (cat#9258), Akt (cat#4691), and beta-actin (cat#4970), protease/phosphatase inhibitor cocktail (100X) (cat#5872S), phenylmethylsulfonyl fluoride (PMSF; cat#8553), SignalFire ECL Reagent (cat#6883S) and cell lysis buffer (cat#9803) were from Cell Signaling (Danvers, MA, USA).

    Techniques: Western Blot, Inhibition, Cell Culture

    Inhibition of µ-opioid or EGF-induced ERK phosphorylation in immortalized astrocytes. (a) Cells were transfected with MOR cDNA, serum-starved, and treated with 1 µM morphine (Morph) or DAMGO, followed by EGF (50 ng/mL, 3 min) and ERK1/2 phosphorylation was assayed. In these and following figures of ERK assays, gels shown are representative immunoblots showing phosphorylated and total ERK1/2. EGF stimulated ERK1/2 [15 ± 1.6 fold over controls ( n = 6)]. ERK1/2 phosphorylation was assayed. EGF stimulation of ERK was 10–15 fold over controls at concentrations of 10, 20, 50, and 100 ng/mL in immortalized astrocytes. * p

    Journal: Journal of neurochemistry

    Article Title: Inhibition of EGF-induced ERK/MAP kinase-mediated astrocyte proliferation by µ opioids: integration of G protein and β-arrestin 2-dependent pathways

    doi: 10.1111/j.1471-4159.2009.06156.x

    Figure Lengend Snippet: Inhibition of µ-opioid or EGF-induced ERK phosphorylation in immortalized astrocytes. (a) Cells were transfected with MOR cDNA, serum-starved, and treated with 1 µM morphine (Morph) or DAMGO, followed by EGF (50 ng/mL, 3 min) and ERK1/2 phosphorylation was assayed. In these and following figures of ERK assays, gels shown are representative immunoblots showing phosphorylated and total ERK1/2. EGF stimulated ERK1/2 [15 ± 1.6 fold over controls ( n = 6)]. ERK1/2 phosphorylation was assayed. EGF stimulation of ERK was 10–15 fold over controls at concentrations of 10, 20, 50, and 100 ng/mL in immortalized astrocytes. * p

    Article Snippet: Chemicals were purchased from Sigma Chemical Co. (St. Louis, MO, USA) with the following exceptions: CTAP, DAMGO, morphine, and norbinaltorphimine were obtained from NIDA Drug Supply (Research Triangle, NC, USA); Protein G plus/Protein A-Agarose beads, EGF, AG1478, and W-7 were obtained from Calbiochem (San Diego, CA, USA); trypsin-EDTA solution was obtained from Gibco (Carlsbad, CA, USA); PTX was obtained from List Biological Laboratories, Inc. (Campbell, CA, USA); Dulbecco’s modified Eagle’s medium (DMEM) and fetal bovine serum (FBS) were obtained from ATCC (Manassas, VA, USA); anti-phospho-ERK1/2 (p-ERK; directed against phospho Thr202/Tyr204) antibody (Ab), anti-EGFR Abs for immunoprecipitation and immunoblotting, and antiphosphoTyr Ab were obtained from Cell Signaling Technology (Beverly, MA, USA); anti-glial fibrillary acidic protein (GFAP) Ab was obtained from ImmunoStar, Inc. (Catalog #:22522; Hudson, WI, USA); anti-β-arrestin2 and anti-ERK Ab were obtained from Santa Cruz Biotechnology (Santa Cruz, CA, USA); anti-TuJ 1 Ab was obtained from Neuromics (Edina, MN, USA); FuGENE 6, 5′-bromo-2′-deoxy-uridine (BrdU), and the Abs for its detection from the BrdU Labeling and Detection Kit I was obtained from Roche (Basel, Switzerland), Alexa Fluor-labeled secondary Abs and horse serum were obtained from Invitrogen (Carlsbad, CA, USA) or Molecular Probes (Eugene, OR, USA); and Vectashield Mounting Medium was obtained from Vector Laboratories, Inc. (Burlingame, CA, USA).

    Techniques: Inhibition, Transfection, Western Blot

    Cellular regulation of 14-3-3 binding of IRS2, CCDC6, ZNRF2, SASH1, PRAS40, VASP, and LSR. HA-IRS2, HA-CCDC6, HA-ZNRF2 (wild type and S19A mutant), HA-SASH1 (wild type and S90A mutant), HA-PRAS40, HA-VASP, and HA-LSR (wild type and S493A mutant) were isolated from transfected HEK293 cells that were stimulated as indicated, and anti-HA immunoprecipitates ( IP ) were analyzed by 14-3-3 overlay and Western blotting. Note that at higher exposures and in other experiments it was clear that 14-3-3 binding is not completely abolished with the ZNRF2 S19A mutation. As controls for the efficacy of stimuli and inhibitors, lysates were analyzed with antibodies against phospho-Thr 308 and phospho-Ser 473 of PKB/Akt, total PKB/Akt, phospho-Erk1/2 ( pErk ), and total Erk1/2. PI3 , PI-103; BID , BI-D1870.

    Journal: Molecular & Cellular Proteomics : MCP

    Article Title: Differential 14-3-3 Affinity Capture Reveals New Downstream Targets of Phosphatidylinositol 3-Kinase Signaling *

    doi: 10.1074/mcp.M800544-MCP200

    Figure Lengend Snippet: Cellular regulation of 14-3-3 binding of IRS2, CCDC6, ZNRF2, SASH1, PRAS40, VASP, and LSR. HA-IRS2, HA-CCDC6, HA-ZNRF2 (wild type and S19A mutant), HA-SASH1 (wild type and S90A mutant), HA-PRAS40, HA-VASP, and HA-LSR (wild type and S493A mutant) were isolated from transfected HEK293 cells that were stimulated as indicated, and anti-HA immunoprecipitates ( IP ) were analyzed by 14-3-3 overlay and Western blotting. Note that at higher exposures and in other experiments it was clear that 14-3-3 binding is not completely abolished with the ZNRF2 S19A mutation. As controls for the efficacy of stimuli and inhibitors, lysates were analyzed with antibodies against phospho-Thr 308 and phospho-Ser 473 of PKB/Akt, total PKB/Akt, phospho-Erk1/2 ( pErk ), and total Erk1/2. PI3 , PI-103; BID , BI-D1870.

    Article Snippet: Anti-phospho-Erk1/2 (Thr(P)202 /Tyr(P)204 ), anti-phospho-Thr308 PKB, and anti-PKB/Akt were from Cell Signaling Technology.

    Techniques: Binding Assay, Mutagenesis, Isolation, Transfection, Western Blot

    Effect of miR-1246 on MEK-ERK signaling. A375P/Mdr cells were transiently transfected with a miR-1246 mimic or control RNA for 24 hours. Cell lysates were then prepared after treatment with the indicated concentrations of PLX4720 for 24 hours. The phosphorylated forms of MEK and ERK were detected by immunoblotting using anti–p-MEK and anti–p-ERK antibodies. The same blots were stripped and reprobed with anti-MEK and anti-ERK antibodies to confirm similar expression levels of MEK and ERK proteins in all lanes. The numbers listed below each band indicate the phosphorylated protein/total protein ratios determined using the Image Lab software. Data are representative of at least three independent experiments.

    Journal: Cancer Research and Treatment : Official Journal of Korean Cancer Association

    Article Title: Upregulation of MicroRNA-1246 Is Associated with BRAF Inhibitor Resistance in Melanoma Cells with Mutant BRAF

    doi: 10.4143/crt.2016.280

    Figure Lengend Snippet: Effect of miR-1246 on MEK-ERK signaling. A375P/Mdr cells were transiently transfected with a miR-1246 mimic or control RNA for 24 hours. Cell lysates were then prepared after treatment with the indicated concentrations of PLX4720 for 24 hours. The phosphorylated forms of MEK and ERK were detected by immunoblotting using anti–p-MEK and anti–p-ERK antibodies. The same blots were stripped and reprobed with anti-MEK and anti-ERK antibodies to confirm similar expression levels of MEK and ERK proteins in all lanes. The numbers listed below each band indicate the phosphorylated protein/total protein ratios determined using the Image Lab software. Data are representative of at least three independent experiments.

    Article Snippet: Rabbit polyclonal anti-MEK, anti-ERK, anti-p21Cip1 , and anti-p27Kip1 antibodies were acquired from Santa Cruz Biotechnology (Santa Cruz, CA), whereas anti–phospho-MEK (anti–p-MEK Ser217/221) and anti–phospho-ERK (anti–p-ERK, Thr202/Tyr204) antibodies were purchased from Cell Signaling Technology (Danvers, MA).

    Techniques: Transfection, Expressing, Software