phospho erk1 2 antibody Search Results


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Sino Biological phospho erk1 2 thr202 tyr204 rabbit mab
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Cell Signaling Technology Inc anti perk 1 2
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Cell Signaling Technology Inc phospho erk1 2 pathway sampler kit
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Boster Bio anti phospho erk1 2 antibodies
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Biorbyt erk1 2
Primary antibodies and lectin used in the present study.
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MedChemExpress phosphoerk1 2 tyr204 tyr187 antibody
Primary antibodies and lectin used in the present study.
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Primary antibodies and lectin used in the present study.
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Boster Bio phospho erk1 2
(A) Ectopic expression of PTEN mRNA in MDA-MB-231/anti-miR-21 cells and MDA-MB-231/control cells were verified by real time RT-PCR assay (p = 0.003). (B, C, D) Protein levels of PTEN, p-AKT, <t>AKT,</t> <t>p-ERK1/2,</t> and ERK1/2 in indicated cells were detected by Western blot analysis, and bands were semi-quantified using ImageJ software. GAPDH was used as loading control. (*indicates p<0.05).
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MedChemExpress phosphorylated erk p erk
(A) Ectopic expression of PTEN mRNA in MDA-MB-231/anti-miR-21 cells and MDA-MB-231/control cells were verified by real time RT-PCR assay (p = 0.003). (B, C, D) Protein levels of PTEN, p-AKT, <t>AKT,</t> <t>p-ERK1/2,</t> and ERK1/2 in indicated cells were detected by Western blot analysis, and bands were semi-quantified using ImageJ software. GAPDH was used as loading control. (*indicates p<0.05).
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Image Search Results


Primary antibodies and lectin used in the present study.

Journal: Cells

Article Title: Blockade of 67-kDa Laminin Receptor Facilitates AQP4 Down-Regulation and BBB Disruption via ERK1/2-and p38 MAPK-Mediated PI3K/AKT Activations

doi: 10.3390/cells9071670

Figure Lengend Snippet: Primary antibodies and lectin used in the present study.

Article Snippet: ERK1/2 (a synthesized peptide derived from human ERK 1/2 around the non-phosphorylation site of Y204) , Rabbit IgG , Biorbyt (Orb160960) , 1:2000 (WB).

Techniques: Sequencing, Purification, Phospho-proteomics, Derivative Assay, Synthesized, Activation Assay, Plasmid Preparation

Densities (mean ± S.D. fold of control IgG-infused animal level) of 67LR, total kinases, phospho (p)-kinases, and AQP4 in the PC of 67LR IgG-infused animals (* ,# p < 0.05 vs. control IgG and vehicle, respectively).

Journal: Cells

Article Title: Blockade of 67-kDa Laminin Receptor Facilitates AQP4 Down-Regulation and BBB Disruption via ERK1/2-and p38 MAPK-Mediated PI3K/AKT Activations

doi: 10.3390/cells9071670

Figure Lengend Snippet: Densities (mean ± S.D. fold of control IgG-infused animal level) of 67LR, total kinases, phospho (p)-kinases, and AQP4 in the PC of 67LR IgG-infused animals (* ,# p < 0.05 vs. control IgG and vehicle, respectively).

Article Snippet: ERK1/2 (a synthesized peptide derived from human ERK 1/2 around the non-phosphorylation site of Y204) , Rabbit IgG , Biorbyt (Orb160960) , 1:2000 (WB).

Techniques: Control

Densities (mean ± S.D. fold of control animal level) of 67LR, total kinases, phospho (p)-kinases, and AQP4 in the PC of SE-induced animals (* ,# p < 0.05 vs. control animal and vehicle, respectively).

Journal: Cells

Article Title: Blockade of 67-kDa Laminin Receptor Facilitates AQP4 Down-Regulation and BBB Disruption via ERK1/2-and p38 MAPK-Mediated PI3K/AKT Activations

doi: 10.3390/cells9071670

Figure Lengend Snippet: Densities (mean ± S.D. fold of control animal level) of 67LR, total kinases, phospho (p)-kinases, and AQP4 in the PC of SE-induced animals (* ,# p < 0.05 vs. control animal and vehicle, respectively).

Article Snippet: ERK1/2 (a synthesized peptide derived from human ERK 1/2 around the non-phosphorylation site of Y204) , Rabbit IgG , Biorbyt (Orb160960) , 1:2000 (WB).

Techniques: Control

(A) Ectopic expression of PTEN mRNA in MDA-MB-231/anti-miR-21 cells and MDA-MB-231/control cells were verified by real time RT-PCR assay (p = 0.003). (B, C, D) Protein levels of PTEN, p-AKT, AKT, p-ERK1/2, and ERK1/2 in indicated cells were detected by Western blot analysis, and bands were semi-quantified using ImageJ software. GAPDH was used as loading control. (*indicates p<0.05).

Journal: PLoS ONE

Article Title: Antagonism of miR-21 Reverses Epithelial-Mesenchymal Transition and Cancer Stem Cell Phenotype through AKT/ERK1/2 Inactivation by Targeting PTEN

doi: 10.1371/journal.pone.0039520

Figure Lengend Snippet: (A) Ectopic expression of PTEN mRNA in MDA-MB-231/anti-miR-21 cells and MDA-MB-231/control cells were verified by real time RT-PCR assay (p = 0.003). (B, C, D) Protein levels of PTEN, p-AKT, AKT, p-ERK1/2, and ERK1/2 in indicated cells were detected by Western blot analysis, and bands were semi-quantified using ImageJ software. GAPDH was used as loading control. (*indicates p<0.05).

Article Snippet: Primary antibodies including rabbit antihuman E-cadherin antibody (No: BS1098; Bioworlde, St. Louis, MO, USA), N-cadherin antibody (No: BS2224; Bioworlde), Vimentin antibody (No: BS1776; Bioworlde), alpha-SMA antibody (No: ab5694; Abcam, Cambridge, UK), ALDH1 antibody (No: ab51028; Abcam), CD44 antibody (No: BA0321; Boster, Wuhan, China), PTEN antibody (No: BS1304; Bioworlde), AKT antibody (No: BS1810; Bioworlde), phospho-AKT (p-AKT) antibody (No: BS4006; Bioworlde), ERK1/2 antibody (No: BS3628; Bioworlde), phospho-ERK1/2 (p-ERK1/2) antibody(No: BS4621; Bioworlde), GAPDH antibody (No: AP0063; Bioworlde) and beta-actin antibody (No: BA2305; Boster), and HRP-conjugated anti-rabbit IgG secondary antibody (No: BA1055; Boster) were used for Western blot analysis.

Techniques: Expressing, Quantitative RT-PCR, Western Blot, Software

Established MDA-MB-231/anti-miR-21 cells were transfected with hsa-miR-21 mimics at a concentration of 40 nmol for 72 h. (A) MDA-MB-231/anti-miR-21 cells were treated with hsa-miR-21 mimics elevated the expression of miR-21, as compared to control groups (n1 = n2 = 3; p = 0.00373), by real-time RT-PCR analysis. (B-F) Protein levels of mesenchymal markers (N-cadherin, Vimentin and alpha-SMA) (B), epithelial marker (E-cadherin) (B), CSC markers (ALDH1 and CD44) (C), PTEN (D), p-AKT and AKT (E), as well as p-ERK1/2 and ERK1/2 (E) in indicated cells were measured by Western blot analysis, and bands were semi-quantified using ImageJ software (F). Beta-actin or GAPDH was used as loading control. (*indicates p<0.05; ★ indicates p<0.001).

Journal: PLoS ONE

Article Title: Antagonism of miR-21 Reverses Epithelial-Mesenchymal Transition and Cancer Stem Cell Phenotype through AKT/ERK1/2 Inactivation by Targeting PTEN

doi: 10.1371/journal.pone.0039520

Figure Lengend Snippet: Established MDA-MB-231/anti-miR-21 cells were transfected with hsa-miR-21 mimics at a concentration of 40 nmol for 72 h. (A) MDA-MB-231/anti-miR-21 cells were treated with hsa-miR-21 mimics elevated the expression of miR-21, as compared to control groups (n1 = n2 = 3; p = 0.00373), by real-time RT-PCR analysis. (B-F) Protein levels of mesenchymal markers (N-cadherin, Vimentin and alpha-SMA) (B), epithelial marker (E-cadherin) (B), CSC markers (ALDH1 and CD44) (C), PTEN (D), p-AKT and AKT (E), as well as p-ERK1/2 and ERK1/2 (E) in indicated cells were measured by Western blot analysis, and bands were semi-quantified using ImageJ software (F). Beta-actin or GAPDH was used as loading control. (*indicates p<0.05; ★ indicates p<0.001).

Article Snippet: Primary antibodies including rabbit antihuman E-cadherin antibody (No: BS1098; Bioworlde, St. Louis, MO, USA), N-cadherin antibody (No: BS2224; Bioworlde), Vimentin antibody (No: BS1776; Bioworlde), alpha-SMA antibody (No: ab5694; Abcam, Cambridge, UK), ALDH1 antibody (No: ab51028; Abcam), CD44 antibody (No: BA0321; Boster, Wuhan, China), PTEN antibody (No: BS1304; Bioworlde), AKT antibody (No: BS1810; Bioworlde), phospho-AKT (p-AKT) antibody (No: BS4006; Bioworlde), ERK1/2 antibody (No: BS3628; Bioworlde), phospho-ERK1/2 (p-ERK1/2) antibody(No: BS4621; Bioworlde), GAPDH antibody (No: AP0063; Bioworlde) and beta-actin antibody (No: BA2305; Boster), and HRP-conjugated anti-rabbit IgG secondary antibody (No: BA1055; Boster) were used for Western blot analysis.

Techniques: Transfection, Concentration Assay, Expressing, Quantitative RT-PCR, Marker, Western Blot, Software

Antagonism of miR-21 could inactivate AKT and ERK1/2 pathways presumably through PTEN up-regulation, and finally reverse EMT and CSC phenotype in MDA-MB-231 cells.

Journal: PLoS ONE

Article Title: Antagonism of miR-21 Reverses Epithelial-Mesenchymal Transition and Cancer Stem Cell Phenotype through AKT/ERK1/2 Inactivation by Targeting PTEN

doi: 10.1371/journal.pone.0039520

Figure Lengend Snippet: Antagonism of miR-21 could inactivate AKT and ERK1/2 pathways presumably through PTEN up-regulation, and finally reverse EMT and CSC phenotype in MDA-MB-231 cells.

Article Snippet: Primary antibodies including rabbit antihuman E-cadherin antibody (No: BS1098; Bioworlde, St. Louis, MO, USA), N-cadherin antibody (No: BS2224; Bioworlde), Vimentin antibody (No: BS1776; Bioworlde), alpha-SMA antibody (No: ab5694; Abcam, Cambridge, UK), ALDH1 antibody (No: ab51028; Abcam), CD44 antibody (No: BA0321; Boster, Wuhan, China), PTEN antibody (No: BS1304; Bioworlde), AKT antibody (No: BS1810; Bioworlde), phospho-AKT (p-AKT) antibody (No: BS4006; Bioworlde), ERK1/2 antibody (No: BS3628; Bioworlde), phospho-ERK1/2 (p-ERK1/2) antibody(No: BS4621; Bioworlde), GAPDH antibody (No: AP0063; Bioworlde) and beta-actin antibody (No: BA2305; Boster), and HRP-conjugated anti-rabbit IgG secondary antibody (No: BA1055; Boster) were used for Western blot analysis.

Techniques: