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    Name:
    EGF
    Description:
    53 amino acid human EGF protein 500 µg 6 2 kDa biologically active protein purified from bacterial lysates biological activity determined by dose dependent proliferation of murine M NFS 60 indicator cells ED50 2 0 ng ml
    Catalog Number:
    SC-4552
    Price:
    None
    Category:
    Antibodies Primary Antibodies and ImmunoCruz Conjugates Growth Factors and Hormones EGF Antibodies EGF hBA 53
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    Structured Review

    Santa Cruz Biotechnology p egfr
    Pra-B suppressed epidermal growth factor receptor <t>(EGFR)–MEK–ERK</t> activation in 786-O and ACHN cells. ( A ) 786-O and ACHN cells were treated with various concentrations of Pra-B (0, 10, 20, and 30 μM) for 24 h, after which the cells were harvested to detect MAPKs-related proteins (p-ERK, t-ERK, p-JNK, t-JNK, p-p38, t-p38) and ( B ) the p-EGFR, t-EGFR, p-MEK, t-MEK, p-ERK, t-ERK protein expression levels through immunoblotting. The histogram represents the densitometric analysis of protein expression. β-actin was used as the loading control. * p
    53 amino acid human EGF protein 500 µg 6 2 kDa biologically active protein purified from bacterial lysates biological activity determined by dose dependent proliferation of murine M NFS 60 indicator cells ED50 2 0 ng ml
    https://www.bioz.com/result/p egfr/product/Santa Cruz Biotechnology
    Average 96 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    p egfr - by Bioz Stars, 2021-05
    96/100 stars

    Images

    1) Product Images from "Praeruptorin B Mitigates the Metastatic Ability of Human Renal Carcinoma Cells through Targeting CTSC and CTSV Expression"

    Article Title: Praeruptorin B Mitigates the Metastatic Ability of Human Renal Carcinoma Cells through Targeting CTSC and CTSV Expression

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms21082919

    Pra-B suppressed epidermal growth factor receptor (EGFR)–MEK–ERK activation in 786-O and ACHN cells. ( A ) 786-O and ACHN cells were treated with various concentrations of Pra-B (0, 10, 20, and 30 μM) for 24 h, after which the cells were harvested to detect MAPKs-related proteins (p-ERK, t-ERK, p-JNK, t-JNK, p-p38, t-p38) and ( B ) the p-EGFR, t-EGFR, p-MEK, t-MEK, p-ERK, t-ERK protein expression levels through immunoblotting. The histogram represents the densitometric analysis of protein expression. β-actin was used as the loading control. * p
    Figure Legend Snippet: Pra-B suppressed epidermal growth factor receptor (EGFR)–MEK–ERK activation in 786-O and ACHN cells. ( A ) 786-O and ACHN cells were treated with various concentrations of Pra-B (0, 10, 20, and 30 μM) for 24 h, after which the cells were harvested to detect MAPKs-related proteins (p-ERK, t-ERK, p-JNK, t-JNK, p-p38, t-p38) and ( B ) the p-EGFR, t-EGFR, p-MEK, t-MEK, p-ERK, t-ERK protein expression levels through immunoblotting. The histogram represents the densitometric analysis of protein expression. β-actin was used as the loading control. * p

    Techniques Used: Activation Assay, Expressing

    Pra-B attenuated epidermal growth factor-induced migration ability through the EGFR signaling pathway. The cells were pretreated with EGF (20 ng/mL) for 2 h and then incubated with various concentrations of Pra-B (0, 10, 20, and 30 μM) for 24 h. ( A ) Cell migration and invasion were measured using an in vitro migration and Matrigel-based invasion assay. Quantification of migrating cells presented in terms of percentage of control (0 μM) is shown as a histogram. ( B ) Cells were harvested to detect the p-EGFR, t-EGFR, p-MEK, t-MEK, p-ERK, t-ERK, CTSC, and CTSV protein expression levels through immunoblotting. β-actin was used as the loading control. The expression of these proteins was detected by densitometry as an average relative ratio compared to β-actin from three different experiments. ** p
    Figure Legend Snippet: Pra-B attenuated epidermal growth factor-induced migration ability through the EGFR signaling pathway. The cells were pretreated with EGF (20 ng/mL) for 2 h and then incubated with various concentrations of Pra-B (0, 10, 20, and 30 μM) for 24 h. ( A ) Cell migration and invasion were measured using an in vitro migration and Matrigel-based invasion assay. Quantification of migrating cells presented in terms of percentage of control (0 μM) is shown as a histogram. ( B ) Cells were harvested to detect the p-EGFR, t-EGFR, p-MEK, t-MEK, p-ERK, t-ERK, CTSC, and CTSV protein expression levels through immunoblotting. β-actin was used as the loading control. The expression of these proteins was detected by densitometry as an average relative ratio compared to β-actin from three different experiments. ** p

    Techniques Used: Migration, Incubation, In Vitro, Invasion Assay, Expressing

    Illustration of how Pra-B inhibits the migration and invasion of human RCC cells through suppressing EGFR–MEK–ERK activation depending on CTSC and CTSV expression.
    Figure Legend Snippet: Illustration of how Pra-B inhibits the migration and invasion of human RCC cells through suppressing EGFR–MEK–ERK activation depending on CTSC and CTSV expression.

    Techniques Used: Migration, Activation Assay, Expressing

    2) Product Images from "Involvement of NF-κB/miR-448 regulatory feedback loop in chemotherapy-induced epithelial-mesenchymal transition of breast cancer cells"

    Article Title: Involvement of NF-κB/miR-448 regulatory feedback loop in chemotherapy-induced epithelial-mesenchymal transition of breast cancer cells

    Journal: Cell Death and Differentiation

    doi: 10.1038/cdd.2010.103

    Identification of AR–EGFR axis as downstream pathway of SATB1. ( a ) Adriamycin-treated MCF7 cells were processed for ChIP using an antibody against SATB1. DNA was interrogated with primers specific for AR promoter. ‘−' and ‘+'
    Figure Legend Snippet: Identification of AR–EGFR axis as downstream pathway of SATB1. ( a ) Adriamycin-treated MCF7 cells were processed for ChIP using an antibody against SATB1. DNA was interrogated with primers specific for AR promoter. ‘−' and ‘+'

    Techniques Used: Chromatin Immunoprecipitation

    3) Product Images from "S5, a Withanolide Isolated from Physalis Pubescens L., Induces G2/M Cell Cycle Arrest via the EGFR/P38 Pathway in Human Melanoma A375 Cells"

    Article Title: S5, a Withanolide Isolated from Physalis Pubescens L., Induces G2/M Cell Cycle Arrest via the EGFR/P38 Pathway in Human Melanoma A375 Cells

    Journal: Molecules

    doi: 10.3390/molecules23123175

    EGFR/P38 signaling pathway was involved in S5-induced cell G2/M arrest. The cells cultured with 40 μM of S5 for 36 h in the absence or presence of 5 μM of SB203580, 40 μg/mL of cetuximab or 5 μM of PD98059. ( A ) The percentage of cells in G2/M phase of the cell cycle was represented using a bar diagram. Data from a representative experiment are shown. n = 3, mean ± SD. * p
    Figure Legend Snippet: EGFR/P38 signaling pathway was involved in S5-induced cell G2/M arrest. The cells cultured with 40 μM of S5 for 36 h in the absence or presence of 5 μM of SB203580, 40 μg/mL of cetuximab or 5 μM of PD98059. ( A ) The percentage of cells in G2/M phase of the cell cycle was represented using a bar diagram. Data from a representative experiment are shown. n = 3, mean ± SD. * p

    Techniques Used: Cell Culture

    ERK, P38 and EGFR are involved in the anti-proliferation of S5 on A375 cells. ( A ) The cells were pretreated with 1.25 μM of SP600125, 5 μM of PD98059, and 5 μM of SB203580 or 40 μg/mL cetuximab for 1 h and then incubated with 40 μM of S5 for 24 h. The death rate of cells was measured using an MTT assay. ( B ) S5 affects the expression of MAPKs and EGFR proteins. The cells were lysed for protein extraction. Samples (25 μg) were subjected to 10% SDS-PAGE and western blotting for the detection of specific proteins. Results presented are the mean from three parallel experiments, n = 3, mean ± SD. * p
    Figure Legend Snippet: ERK, P38 and EGFR are involved in the anti-proliferation of S5 on A375 cells. ( A ) The cells were pretreated with 1.25 μM of SP600125, 5 μM of PD98059, and 5 μM of SB203580 or 40 μg/mL cetuximab for 1 h and then incubated with 40 μM of S5 for 24 h. The death rate of cells was measured using an MTT assay. ( B ) S5 affects the expression of MAPKs and EGFR proteins. The cells were lysed for protein extraction. Samples (25 μg) were subjected to 10% SDS-PAGE and western blotting for the detection of specific proteins. Results presented are the mean from three parallel experiments, n = 3, mean ± SD. * p

    Techniques Used: Incubation, MTT Assay, Expressing, Protein Extraction, SDS Page, Western Blot

    4) Product Images from "EGFR inhibition attenuates diabetic nephropathy through decreasing ROS and endoplasmic reticulum stress"

    Article Title: EGFR inhibition attenuates diabetic nephropathy through decreasing ROS and endoplasmic reticulum stress

    Journal: Oncotarget

    doi: 10.18632/oncotarget.15948

    AG1478 and NAC attenuate HG-induced EGFR signaling activation, ROS generation, endoplasmic reticulum stress, cell firosis and apoptosis in SV40 cells SV40 cells pretreated with AG1478 (10 μM) or NAC (10 mM) for 1 h were incubated with HG (33 mM) for 1 h. Then cells were lysed and the extracted total proteins were processed for the detection of p-EGFR and p-AKT using Western blot; and statistic figure was shown, data were presented as mean ± SDs. (Six mice in each group were used for above analysis ( A ). ( B ) AG1478 and NAC inhibit high glucose-induced ROS generation. SV40 cells pretreated with AG1478 (10 μM) or NAC (10mM) for 1h were incubated with HG (33 mM) for 2h. DCFH-DA probes were loaded and the ROS positive cells were detected using the fluorescence microscope. Also, after loading with the probes, cells were processed to flow cytometry analysis for O2 level, and mean fluorescence intensity (MFI) value was determined. Data were presented as mean ± SDs. ( n = 3 for each experiment. ** P
    Figure Legend Snippet: AG1478 and NAC attenuate HG-induced EGFR signaling activation, ROS generation, endoplasmic reticulum stress, cell firosis and apoptosis in SV40 cells SV40 cells pretreated with AG1478 (10 μM) or NAC (10 mM) for 1 h were incubated with HG (33 mM) for 1 h. Then cells were lysed and the extracted total proteins were processed for the detection of p-EGFR and p-AKT using Western blot; and statistic figure was shown, data were presented as mean ± SDs. (Six mice in each group were used for above analysis ( A ). ( B ) AG1478 and NAC inhibit high glucose-induced ROS generation. SV40 cells pretreated with AG1478 (10 μM) or NAC (10mM) for 1h were incubated with HG (33 mM) for 2h. DCFH-DA probes were loaded and the ROS positive cells were detected using the fluorescence microscope. Also, after loading with the probes, cells were processed to flow cytometry analysis for O2 level, and mean fluorescence intensity (MFI) value was determined. Data were presented as mean ± SDs. ( n = 3 for each experiment. ** P

    Techniques Used: Activation Assay, Incubation, Western Blot, Mouse Assay, Fluorescence, Microscopy, Flow Cytometry, Cytometry

    Scheme for EGFR/AKT/ROS/ER stress signaling pathway in preventing DN Inhibition of EGFR by AG1478 eliminated AKT phosphorylation, sequentially reduced oxidative stress and ER stress, decreased diabetes-induced renal.
    Figure Legend Snippet: Scheme for EGFR/AKT/ROS/ER stress signaling pathway in preventing DN Inhibition of EGFR by AG1478 eliminated AKT phosphorylation, sequentially reduced oxidative stress and ER stress, decreased diabetes-induced renal.

    Techniques Used: Inhibition

    AG1478 attenuate diabetes-induced EGFR signaling activation in diabetic kidney ( A ) Representative images for the histochemical staining for p-EGFR and EGFR expression in the formalin-fixed renal tissues (200× magnification). ( B ) Western blot analysis for the expression of p-EGFR in renal tissue. And statistic figure was shown, data were presented as mean ± SDs. ( C ) Representative images for the histochemical staining for p-AKT and AKT expression in the formalin-fixed renal tissues (200× magnification). (Eight mice in each group were used for above analysis. ** P
    Figure Legend Snippet: AG1478 attenuate diabetes-induced EGFR signaling activation in diabetic kidney ( A ) Representative images for the histochemical staining for p-EGFR and EGFR expression in the formalin-fixed renal tissues (200× magnification). ( B ) Western blot analysis for the expression of p-EGFR in renal tissue. And statistic figure was shown, data were presented as mean ± SDs. ( C ) Representative images for the histochemical staining for p-AKT and AKT expression in the formalin-fixed renal tissues (200× magnification). (Eight mice in each group were used for above analysis. ** P

    Techniques Used: Activation Assay, Staining, Expressing, Western Blot, Mouse Assay

    EGFR and AKT mediate HG-induced ER stress and cell damage in SV40 MES 13 cells ( A ) SV40 cells were transfected with EGFR siRNA or control siRNA for 48 h, the expression of EGFR was detected by Western blot analysis. ( B ) EGFR silencing by siRNA reduced HG-induced ER stress, fibrosis and apoptosis. ( C ) SV40 cells were transfected with AKT siRNA or control siRNA for 48 h, the expression of AKT was detected by Western blot analysis. ( D ) AKT silencing by siRNA reduced HG-induced ER stress, fibrosis and apoptosis. Data were obtained from three independent experiments.
    Figure Legend Snippet: EGFR and AKT mediate HG-induced ER stress and cell damage in SV40 MES 13 cells ( A ) SV40 cells were transfected with EGFR siRNA or control siRNA for 48 h, the expression of EGFR was detected by Western blot analysis. ( B ) EGFR silencing by siRNA reduced HG-induced ER stress, fibrosis and apoptosis. ( C ) SV40 cells were transfected with AKT siRNA or control siRNA for 48 h, the expression of AKT was detected by Western blot analysis. ( D ) AKT silencing by siRNA reduced HG-induced ER stress, fibrosis and apoptosis. Data were obtained from three independent experiments.

    Techniques Used: Transfection, Expressing, Western Blot

    5) Product Images from "AUY922 Effectively Overcomes MET- and AXL-Mediated Resistance to EGFR-TKI in Lung Cancer Cells"

    Article Title: AUY922 Effectively Overcomes MET- and AXL-Mediated Resistance to EGFR-TKI in Lung Cancer Cells

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0119832

    Suppression of MET and AXL by AUY922 in resistant cell lines. A , Cells were treated with the indicated doses of AUY922 for 72 hours in medium containing 1% FBS. Attached cells were stained with trypan blue solution (top). Cell viability based on cell counting is also shown (bottom). Bars represent the mean ±SD of three wells. B , Cells treated with AUY922, similar to panel A. After 48 hours, cells were harvested and EGFR-related signaling molecules were evaluated using western blotting. C , LK2 cells were treated with vector-containing wild-type EGFR, del E746-E750, MET, or AXL and the indicated doses of AUY922 for 12 hours.
    Figure Legend Snippet: Suppression of MET and AXL by AUY922 in resistant cell lines. A , Cells were treated with the indicated doses of AUY922 for 72 hours in medium containing 1% FBS. Attached cells were stained with trypan blue solution (top). Cell viability based on cell counting is also shown (bottom). Bars represent the mean ±SD of three wells. B , Cells treated with AUY922, similar to panel A. After 48 hours, cells were harvested and EGFR-related signaling molecules were evaluated using western blotting. C , LK2 cells were treated with vector-containing wild-type EGFR, del E746-E750, MET, or AXL and the indicated doses of AUY922 for 12 hours.

    Techniques Used: Staining, Cell Counting, Western Blot, Plasmid Preparation

    6) Product Images from "Multiple signaling pathways are responsible for prostaglandin E2-induced murine keratinocyte proliferation"

    Article Title: Multiple signaling pathways are responsible for prostaglandin E2-induced murine keratinocyte proliferation

    Journal: Molecular cancer research : MCR

    doi: 10.1158/1541-7786.MCR-07-2144

    PGE 2 -induces activation of CREB, AP-1 and NF-κB transcription factors in PMKs. PMKs were incubated with vehicle (control, lane 2) or with PGE 2 (10 µM) (lanes 3–7) for 15 min. To demonstrate the effect of phamacological inhibitors on PGE 2 -induced transcription factor-binding, PMKs were treated with PD98059, AG1478, H-89 or wortmannin for 30 min prior to PGE 2 treatment. Nuclear extracts were subjected to electrophoretic mobility shift assay analysis, as described in experimental procedures. A. PGE 2 -induced CREB activation in PMKs. The arrow indicates the specific binding of CREB to its consensus oligonucleotide. B. PGE 2 -induced AP-1 activation in PMKs. The arrow indicates the specific binding of AP-1 to its consensus oligonucleotide. C. PGE 2 -induced NF-κB activation in PMKs. The arrows indicate the specific binding of NF-κB to its consensus oligonucleotide ( upper arrow ) and non-specific (ns) binding ( lower arrow ). D. EGFR, ERK1/2, PKA/CREB and PI3-K/Akt signaling cascades are involved in PGE 2 -stimulated cell proliferation. PMKs were treated with various kinase inhibitors 30 min prior to PGE 2 (10 µM) treatment for 20 h and pulsed with ( 3 H)-thymidine 2 h before harvest. The ( 3 H)-thymidine incorporated by PMKs was measured in triplicate samples and normalized to protein concentration as described in experimental procedures. Representative data from at least 2 independent experiments are presented as the means ± SD. *p
    Figure Legend Snippet: PGE 2 -induces activation of CREB, AP-1 and NF-κB transcription factors in PMKs. PMKs were incubated with vehicle (control, lane 2) or with PGE 2 (10 µM) (lanes 3–7) for 15 min. To demonstrate the effect of phamacological inhibitors on PGE 2 -induced transcription factor-binding, PMKs were treated with PD98059, AG1478, H-89 or wortmannin for 30 min prior to PGE 2 treatment. Nuclear extracts were subjected to electrophoretic mobility shift assay analysis, as described in experimental procedures. A. PGE 2 -induced CREB activation in PMKs. The arrow indicates the specific binding of CREB to its consensus oligonucleotide. B. PGE 2 -induced AP-1 activation in PMKs. The arrow indicates the specific binding of AP-1 to its consensus oligonucleotide. C. PGE 2 -induced NF-κB activation in PMKs. The arrows indicate the specific binding of NF-κB to its consensus oligonucleotide ( upper arrow ) and non-specific (ns) binding ( lower arrow ). D. EGFR, ERK1/2, PKA/CREB and PI3-K/Akt signaling cascades are involved in PGE 2 -stimulated cell proliferation. PMKs were treated with various kinase inhibitors 30 min prior to PGE 2 (10 µM) treatment for 20 h and pulsed with ( 3 H)-thymidine 2 h before harvest. The ( 3 H)-thymidine incorporated by PMKs was measured in triplicate samples and normalized to protein concentration as described in experimental procedures. Representative data from at least 2 independent experiments are presented as the means ± SD. *p

    Techniques Used: Activation Assay, Incubation, Binding Assay, Electrophoretic Mobility Shift Assay, Protein Concentration

    Effect of pharmacological inhibitors on PGE 2 -induced cAMP production and EGFR, c-src, ERK1/2, Akt and PKA/ CREB signaling pathways in PMKs. PMKs were serum starved for 24 h prior to treating with vehicle or PGE 2 (10 µM) for 5 min. Pathway-specific inhibitors were added 30 min before PGE 2 treatment. Western blots of proteins from whole cell lysates were performed with antibodies to the proteins indicated. A. Akt and EGFR inhibitors inhibit PGE 2 -induced Akt activation. Both AG1478 (EGFR inhibitor) and wortmannin (Akt inhibitor) blocked PGE 2 -stimulated phosphorylation of Akt (ser 473 ). B. Effect of MEK, EGFR, and Akt inhibitors on ERK1/2 activation. PD98059 (MEK/ERK inhibitor) completely blocked PGE 2 -stimulated ERK1/2 phosphorylation, while AG1478 and wortmannin were only partially effective. C. Effect of EGFR, c-src, and PKA inhibitors on EGFR activation. AG1478 as expected blocked PGE 2 -stimulated EGFR phosphorylation (tyr 1173 ), while PP2 (c-src inhibitor) and H-89 (PKA inhibitor) had little or no effect. D. EGFR and c-src inhibitors block PGE 2 -induced c-src activation. Both AG1478 and PP2 completely inhibit PGE 2 -stimulated phosphorylation of c-src (tyr 416 ). E. PGE 2 induces cAMP production. Serum-starved PMKs were treated with PGE 2 (0–30 µM) for 30 min with or without a 20 min pretreatment with SQ 22,536 (10 µM), an adenylate cyclase inhibitor. The mean (±SD) levels of cAMP from triplicate samples are expressed as pmol/mg protein. *p
    Figure Legend Snippet: Effect of pharmacological inhibitors on PGE 2 -induced cAMP production and EGFR, c-src, ERK1/2, Akt and PKA/ CREB signaling pathways in PMKs. PMKs were serum starved for 24 h prior to treating with vehicle or PGE 2 (10 µM) for 5 min. Pathway-specific inhibitors were added 30 min before PGE 2 treatment. Western blots of proteins from whole cell lysates were performed with antibodies to the proteins indicated. A. Akt and EGFR inhibitors inhibit PGE 2 -induced Akt activation. Both AG1478 (EGFR inhibitor) and wortmannin (Akt inhibitor) blocked PGE 2 -stimulated phosphorylation of Akt (ser 473 ). B. Effect of MEK, EGFR, and Akt inhibitors on ERK1/2 activation. PD98059 (MEK/ERK inhibitor) completely blocked PGE 2 -stimulated ERK1/2 phosphorylation, while AG1478 and wortmannin were only partially effective. C. Effect of EGFR, c-src, and PKA inhibitors on EGFR activation. AG1478 as expected blocked PGE 2 -stimulated EGFR phosphorylation (tyr 1173 ), while PP2 (c-src inhibitor) and H-89 (PKA inhibitor) had little or no effect. D. EGFR and c-src inhibitors block PGE 2 -induced c-src activation. Both AG1478 and PP2 completely inhibit PGE 2 -stimulated phosphorylation of c-src (tyr 416 ). E. PGE 2 induces cAMP production. Serum-starved PMKs were treated with PGE 2 (0–30 µM) for 30 min with or without a 20 min pretreatment with SQ 22,536 (10 µM), an adenylate cyclase inhibitor. The mean (±SD) levels of cAMP from triplicate samples are expressed as pmol/mg protein. *p

    Techniques Used: Western Blot, Activation Assay, Blocking Assay

    Effect of PGE 2 on keratinocyte proliferation and EGFR, Ras- ERK1/2, and Akt signaling pathways in primary mouse keratinocytes (PMKs). A . PGE 2 increases keratinocyte proliferation in a dose-dependent manner. PMKs from WT mice were treated with PGE 2 (10–30 µM) for 20 h and pulsed with ( 3 H)-thymidine for 2 h before harvest. The ( 3 H)-thymidine incorporated by PMKs was measured and normalized to protein concentration. Data are presented as fold induction of specific activity. At least 2 independent experiments were done, with triplicates for each treatment group; data from a representative experiment are shown as means±SD. *p
    Figure Legend Snippet: Effect of PGE 2 on keratinocyte proliferation and EGFR, Ras- ERK1/2, and Akt signaling pathways in primary mouse keratinocytes (PMKs). A . PGE 2 increases keratinocyte proliferation in a dose-dependent manner. PMKs from WT mice were treated with PGE 2 (10–30 µM) for 20 h and pulsed with ( 3 H)-thymidine for 2 h before harvest. The ( 3 H)-thymidine incorporated by PMKs was measured and normalized to protein concentration. Data are presented as fold induction of specific activity. At least 2 independent experiments were done, with triplicates for each treatment group; data from a representative experiment are shown as means±SD. *p

    Techniques Used: Mouse Assay, Protein Concentration, Activity Assay

    7) Product Images from "Hypoxia Changes the Expression of the Epidermal Growth Factor (EGF) System in Human Hearts and Cultured Cardiomyocytes"

    Article Title: Hypoxia Changes the Expression of the Epidermal Growth Factor (EGF) System in Human Hearts and Cultured Cardiomyocytes

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0040243

    mRNA expressions of the EGF receptors EGFR, HER2, HER3, and the JM-b isoform of HER4 in human biopsies. Samples were obtained from a normoxic part of the heart and compared to another sample from the hypoxic part of the same heart. Expressions of mRNA are adjusted by division with the expression of beta-actin. Normoxic tissue expressions are depicted with circular points and hypoxic expression with squares. Each paired sample is connected with a grey dashed line. Data is represented with means and SEM. EGFR shows significant up-regulation from a mean value of 1.0 (normoxic) to a mean value of 2.6 (mean of hypoxic) ( P = 0.03 ). HER2 shows significant down-regulation from 15.0 ((mean of normoxic) to 5.8 ((mean of hypoxic) ( P = 0.0005 ). The differences in HER3 and HER4/JM-b are non-significant ( P = 0.5 and P = 0.4, respectively).
    Figure Legend Snippet: mRNA expressions of the EGF receptors EGFR, HER2, HER3, and the JM-b isoform of HER4 in human biopsies. Samples were obtained from a normoxic part of the heart and compared to another sample from the hypoxic part of the same heart. Expressions of mRNA are adjusted by division with the expression of beta-actin. Normoxic tissue expressions are depicted with circular points and hypoxic expression with squares. Each paired sample is connected with a grey dashed line. Data is represented with means and SEM. EGFR shows significant up-regulation from a mean value of 1.0 (normoxic) to a mean value of 2.6 (mean of hypoxic) ( P = 0.03 ). HER2 shows significant down-regulation from 15.0 ((mean of normoxic) to 5.8 ((mean of hypoxic) ( P = 0.0005 ). The differences in HER3 and HER4/JM-b are non-significant ( P = 0.5 and P = 0.4, respectively).

    Techniques Used: Expressing

    Western Blot showing HL-1 cardiomyocytes exposed to 1% oxygen with or without treatment with trastuzumab. Influence of HB-EGF. Mouse HL-1 cardiomyocytes kept at 1% oxygen were treated either with or without 20 nM trastuzumab for 1 hour followed by treatment with 10 nM HB-EGF for 10 minutes. Whole cell lysates were investigated for phosphorylated and total amounts of the receptors EGFR, HER2, HER3, and HER4. Also examined was the phosphorylation and total amounts of the down-stream signaling molecules MAPK and Akt. Actin was used a loading control. This experiment was repeated twice giving similar results.
    Figure Legend Snippet: Western Blot showing HL-1 cardiomyocytes exposed to 1% oxygen with or without treatment with trastuzumab. Influence of HB-EGF. Mouse HL-1 cardiomyocytes kept at 1% oxygen were treated either with or without 20 nM trastuzumab for 1 hour followed by treatment with 10 nM HB-EGF for 10 minutes. Whole cell lysates were investigated for phosphorylated and total amounts of the receptors EGFR, HER2, HER3, and HER4. Also examined was the phosphorylation and total amounts of the down-stream signaling molecules MAPK and Akt. Actin was used a loading control. This experiment was repeated twice giving similar results.

    Techniques Used: Western Blot

    Regional expression of HB-EGF, EGFR, and HER2 in normal pig hearts. Tissue mRNA expressions are all depicted with circular points. Each paired sample is connected with a grey dashed line. Samples were obtained from the left atrium, the posterior wall of the left ventricle, or the anterior wall of the left ventricle. Data is represented with means and SEM as the ratio between the reference gene GAPDH. HB-EGF, EGFR and HER2 showed no significant regional variation in mRNA expression (all P > 0.05 ).
    Figure Legend Snippet: Regional expression of HB-EGF, EGFR, and HER2 in normal pig hearts. Tissue mRNA expressions are all depicted with circular points. Each paired sample is connected with a grey dashed line. Samples were obtained from the left atrium, the posterior wall of the left ventricle, or the anterior wall of the left ventricle. Data is represented with means and SEM as the ratio between the reference gene GAPDH. HB-EGF, EGFR and HER2 showed no significant regional variation in mRNA expression (all P > 0.05 ).

    Techniques Used: Expressing

    8) Product Images from "Requirement for Metalloproteinase-dependent ERK and AKT Activation in UVB-induced G1-S Cell Cycle Progression of Human Keratinocytes"

    Article Title: Requirement for Metalloproteinase-dependent ERK and AKT Activation in UVB-induced G1-S Cell Cycle Progression of Human Keratinocytes

    Journal: Photochemistry and photobiology

    doi: 10.1111/j.1751-1097.2008.00531.x

    Inhibition of EGFR pathway blocked ERK/AKT/cyclin D1 pathways and cell cycle progression induced by UVB exposure. (A) Cells were incubated with or without AG1478 (1 µ M ), an EGFR kinase inhibitor, and then exposed to UVB radiation (10 mJ cm −2
    Figure Legend Snippet: Inhibition of EGFR pathway blocked ERK/AKT/cyclin D1 pathways and cell cycle progression induced by UVB exposure. (A) Cells were incubated with or without AG1478 (1 µ M ), an EGFR kinase inhibitor, and then exposed to UVB radiation (10 mJ cm −2

    Techniques Used: Inhibition, Incubation

    Cells were exposed to UVB as in . Cells were harvested at 1.5, 3 or 6 h following UVB radiation for Western blot analysis using specific antibodies against cyclin D1, p-AKT, AKT, p-ERK, ERK, p-EGFR, EGFR and beta-actin (an equal loading control)
    Figure Legend Snippet: Cells were exposed to UVB as in . Cells were harvested at 1.5, 3 or 6 h following UVB radiation for Western blot analysis using specific antibodies against cyclin D1, p-AKT, AKT, p-ERK, ERK, p-EGFR, EGFR and beta-actin (an equal loading control)

    Techniques Used: Western Blot

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    Article Title: Involvement of NF-κB/miR-448 regulatory feedback loop in chemotherapy-induced epithelial-mesenchymal transition of breast cancer cells
    Article Snippet: Total protein was extracted from cells using RIPA lysis buffer (Santa Cruz Biotechnology, Santa Cruz, CA, USA). .. Protein extract (50 μ g/lane) was electrophoresed, transferred to PVDF membranes and incubated overnight with primary antibodies against E-cadherin (sc-8426, Santa Cruz Biotechnology), vimentin (sc-32322, Santa Cruz Biotechnology), SATB1 (PRS4631, Sigma, St. Louis, MO, USA), Twist1 (AV37997, Sigma), p-EGFR (sc-101669, Santa Cruz Biotechnology), EGFR (sc-71034, Santa Cruz Biotechnology), p-MAPK (no. 4695, Cell Signaling Technology), MAPK (no. 4370, Cell Signaling Technology, Danvers, MA, USA), p-Akt (no. 4058, Cell Signaling Technology) and Akt (no. 9272, Cell Signaling Technology), respectively. .. Membranes were then treated with the appropriate HRP-conjugated secondary antibodies (Invitrogen).

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    Santa Cruz Biotechnology p egfr
    Pra-B suppressed epidermal growth factor receptor <t>(EGFR)–MEK–ERK</t> activation in 786-O and ACHN cells. ( A ) 786-O and ACHN cells were treated with various concentrations of Pra-B (0, 10, 20, and 30 μM) for 24 h, after which the cells were harvested to detect MAPKs-related proteins (p-ERK, t-ERK, p-JNK, t-JNK, p-p38, t-p38) and ( B ) the p-EGFR, t-EGFR, p-MEK, t-MEK, p-ERK, t-ERK protein expression levels through immunoblotting. The histogram represents the densitometric analysis of protein expression. β-actin was used as the loading control. * p
    P Egfr, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/p egfr/product/Santa Cruz Biotechnology
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    Santa Cruz Biotechnology phospho egfr
    Proposed mechanisms of RX-induced increase of glutamate transporters. RX activates both nuclear ERs (ER-α/ER-β) and GPR30 leading to activation of MAPK, <t>CREB,</t> <t>EGFR</t> and NF-κB signaling pathways, resulting in upregulation of GLT-1 and GLAST. This leads to enhanced glutamate uptake and ultimately, protection of neurons from glutamate-induced excitotoxicity.
    Phospho Egfr, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Pra-B suppressed epidermal growth factor receptor (EGFR)–MEK–ERK activation in 786-O and ACHN cells. ( A ) 786-O and ACHN cells were treated with various concentrations of Pra-B (0, 10, 20, and 30 μM) for 24 h, after which the cells were harvested to detect MAPKs-related proteins (p-ERK, t-ERK, p-JNK, t-JNK, p-p38, t-p38) and ( B ) the p-EGFR, t-EGFR, p-MEK, t-MEK, p-ERK, t-ERK protein expression levels through immunoblotting. The histogram represents the densitometric analysis of protein expression. β-actin was used as the loading control. * p

    Journal: International Journal of Molecular Sciences

    Article Title: Praeruptorin B Mitigates the Metastatic Ability of Human Renal Carcinoma Cells through Targeting CTSC and CTSV Expression

    doi: 10.3390/ijms21082919

    Figure Lengend Snippet: Pra-B suppressed epidermal growth factor receptor (EGFR)–MEK–ERK activation in 786-O and ACHN cells. ( A ) 786-O and ACHN cells were treated with various concentrations of Pra-B (0, 10, 20, and 30 μM) for 24 h, after which the cells were harvested to detect MAPKs-related proteins (p-ERK, t-ERK, p-JNK, t-JNK, p-p38, t-p38) and ( B ) the p-EGFR, t-EGFR, p-MEK, t-MEK, p-ERK, t-ERK protein expression levels through immunoblotting. The histogram represents the densitometric analysis of protein expression. β-actin was used as the loading control. * p

    Article Snippet: Antibodies for CTSC, CTSV, t-ERK, p-JNK, t-JNK, p-p38, t-p38, p-MEK, t-MEK, p-EGFR, t-EGFR, and β-actin were purchased from Santa Cruz Biotechnology (Santa Cruz, CA, USA).

    Techniques: Activation Assay, Expressing

    Pra-B attenuated epidermal growth factor-induced migration ability through the EGFR signaling pathway. The cells were pretreated with EGF (20 ng/mL) for 2 h and then incubated with various concentrations of Pra-B (0, 10, 20, and 30 μM) for 24 h. ( A ) Cell migration and invasion were measured using an in vitro migration and Matrigel-based invasion assay. Quantification of migrating cells presented in terms of percentage of control (0 μM) is shown as a histogram. ( B ) Cells were harvested to detect the p-EGFR, t-EGFR, p-MEK, t-MEK, p-ERK, t-ERK, CTSC, and CTSV protein expression levels through immunoblotting. β-actin was used as the loading control. The expression of these proteins was detected by densitometry as an average relative ratio compared to β-actin from three different experiments. ** p

    Journal: International Journal of Molecular Sciences

    Article Title: Praeruptorin B Mitigates the Metastatic Ability of Human Renal Carcinoma Cells through Targeting CTSC and CTSV Expression

    doi: 10.3390/ijms21082919

    Figure Lengend Snippet: Pra-B attenuated epidermal growth factor-induced migration ability through the EGFR signaling pathway. The cells were pretreated with EGF (20 ng/mL) for 2 h and then incubated with various concentrations of Pra-B (0, 10, 20, and 30 μM) for 24 h. ( A ) Cell migration and invasion were measured using an in vitro migration and Matrigel-based invasion assay. Quantification of migrating cells presented in terms of percentage of control (0 μM) is shown as a histogram. ( B ) Cells were harvested to detect the p-EGFR, t-EGFR, p-MEK, t-MEK, p-ERK, t-ERK, CTSC, and CTSV protein expression levels through immunoblotting. β-actin was used as the loading control. The expression of these proteins was detected by densitometry as an average relative ratio compared to β-actin from three different experiments. ** p

    Article Snippet: Antibodies for CTSC, CTSV, t-ERK, p-JNK, t-JNK, p-p38, t-p38, p-MEK, t-MEK, p-EGFR, t-EGFR, and β-actin were purchased from Santa Cruz Biotechnology (Santa Cruz, CA, USA).

    Techniques: Migration, Incubation, In Vitro, Invasion Assay, Expressing

    Illustration of how Pra-B inhibits the migration and invasion of human RCC cells through suppressing EGFR–MEK–ERK activation depending on CTSC and CTSV expression.

    Journal: International Journal of Molecular Sciences

    Article Title: Praeruptorin B Mitigates the Metastatic Ability of Human Renal Carcinoma Cells through Targeting CTSC and CTSV Expression

    doi: 10.3390/ijms21082919

    Figure Lengend Snippet: Illustration of how Pra-B inhibits the migration and invasion of human RCC cells through suppressing EGFR–MEK–ERK activation depending on CTSC and CTSV expression.

    Article Snippet: Antibodies for CTSC, CTSV, t-ERK, p-JNK, t-JNK, p-p38, t-p38, p-MEK, t-MEK, p-EGFR, t-EGFR, and β-actin were purchased from Santa Cruz Biotechnology (Santa Cruz, CA, USA).

    Techniques: Migration, Activation Assay, Expressing

    Identification of AR–EGFR axis as downstream pathway of SATB1. ( a ) Adriamycin-treated MCF7 cells were processed for ChIP using an antibody against SATB1. DNA was interrogated with primers specific for AR promoter. ‘−' and ‘+'

    Journal: Cell Death and Differentiation

    Article Title: Involvement of NF-κB/miR-448 regulatory feedback loop in chemotherapy-induced epithelial-mesenchymal transition of breast cancer cells

    doi: 10.1038/cdd.2010.103

    Figure Lengend Snippet: Identification of AR–EGFR axis as downstream pathway of SATB1. ( a ) Adriamycin-treated MCF7 cells were processed for ChIP using an antibody against SATB1. DNA was interrogated with primers specific for AR promoter. ‘−' and ‘+'

    Article Snippet: Protein extract (50 μ g/lane) was electrophoresed, transferred to PVDF membranes and incubated overnight with primary antibodies against E-cadherin (sc-8426, Santa Cruz Biotechnology), vimentin (sc-32322, Santa Cruz Biotechnology), SATB1 (PRS4631, Sigma, St. Louis, MO, USA), Twist1 (AV37997, Sigma), p-EGFR (sc-101669, Santa Cruz Biotechnology), EGFR (sc-71034, Santa Cruz Biotechnology), p-MAPK (no. 4695, Cell Signaling Technology), MAPK (no. 4370, Cell Signaling Technology, Danvers, MA, USA), p-Akt (no. 4058, Cell Signaling Technology) and Akt (no. 9272, Cell Signaling Technology), respectively.

    Techniques: Chromatin Immunoprecipitation

    Proposed mechanisms of RX-induced increase of glutamate transporters. RX activates both nuclear ERs (ER-α/ER-β) and GPR30 leading to activation of MAPK, CREB, EGFR and NF-κB signaling pathways, resulting in upregulation of GLT-1 and GLAST. This leads to enhanced glutamate uptake and ultimately, protection of neurons from glutamate-induced excitotoxicity.

    Journal: Glia

    Article Title: Mechanism of Raloxifene-induced Upregulation of Glutamate TransporterS in Rat Primary Astrocytes

    doi: 10.1002/glia.22679

    Figure Lengend Snippet: Proposed mechanisms of RX-induced increase of glutamate transporters. RX activates both nuclear ERs (ER-α/ER-β) and GPR30 leading to activation of MAPK, CREB, EGFR and NF-κB signaling pathways, resulting in upregulation of GLT-1 and GLAST. This leads to enhanced glutamate uptake and ultimately, protection of neurons from glutamate-induced excitotoxicity.

    Article Snippet: ERK (sc-135900), phospho-ERK (sc-7383), Akt (sc-55523), phospho-Akt (sc-7985), CREB (sc-186), phospho-CREB (sc-7978), EGFR (sc-120), phospho-EGFR (sc-12357), NF-κB (p65, sc-372 and p50, sc-114), EAAC1 (sc-25658) and β-actin (sc-1616) antibodies were from Santa Cruz Biotechnology (Santa Cruz, CA).

    Techniques: Activation Assay