vegf 165 (Boster Bio)

Boster Bio vegf 165
Vegf 165, supplied by Boster Bio, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/endothelial+mitogen/pmc04238164-33-8-10?v=Boster+Bio
Average 90 stars, based on 1 article reviews

vegf 165 - by Bioz Stars, 2026-08

90/100 stars

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endothelial mitogen (Merck KGaA)

Merck KGaA endothelial mitogen
Endothelial Mitogen, supplied by Merck KGaA, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/endothelial+mitogen/pmc06148290-352-45-47?v=Merck+KGaA
Average 90 stars, based on 1 article reviews

endothelial mitogen - by Bioz Stars, 2026-08

90/100 stars

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bovine brain endothelial cell mitogen (Serotech Inc)

Serotech Inc bovine brain endothelial cell mitogen
$Pitstop and dynasore inhibit VEGFR2 internalization in <t>endothelial</t> cells. A–F, shown is an antibody feeding assay. Cell surface VEGFR2 was labeled in HUVECs with a VEGFR2 extracellular domain-specific antibody for 30 min at 4 °C. Cells were then either fixed directly or shifted to 37 °C for 30 min and then fixed. Fixed cells were stained with a fluorescently tagged secondary antibody to detect anti-VEGFR2 (VR2) antibody (green) and co-stained for the endosomal marker EEA1 (red). A, localization of anti-VEGFR2 antibody in cells after labeling was performed in the presence of vehicle for 30 min at 4 °C. B, localization of anti-VEGFR2 antibody after labeling in the presence of vehicle for 30 min at 4 °C followed by warming to 37 °C for 30 min in the presence of vehicle is shown. C, localization of anti-VEGFR2 antibody after labeling in the presence of vehicle for 30 min at 4 °C followed by warming to 37 °C for 30 min in the presence of VEGF and vehicle is shown. D, localization of anti-VEGFR2 antibody after labeling in the presence of 10 μm pitstop for 30 min at 4 °C followed by warming to 37 °C for 30 min in the presence of VEGF and 10 μm pitstop is shown. E, localization of anti-VEGFR2 antibody after labeling in the presence of 80 μm dynasore for 30 min at 4 °C followed by warming to 37 °C for 30 min in the presence of VEGF and 80 μm dynasore is shown. F, quantification of VEGFR2 internalization in endothelial cells treated as indicated (same conditions as shown in panels B–E) is shown. The graph shows the number of intracellular structures labeling dual positive for VEGFR2 and EEA1 per cell ± S.E. Quantification of 20 cells from 2 independent experiments was used to generate each data point. *, p < 0.05; **, p < 0.001. Scale bar = 5 μm. G, cell surface biotinylation is shown. HUVECs were treated as follows; vehicle for 45 min (lane 1), vehicle for 30 min followed by VEGF and vehicle for 15 min (lane 2), 10 μm pitstop for 30 min followed by VEGF and 10 μm pitstop for 15 min (lane 3), or 80 μm dynasore for 30 min followed by VEGF and 80 μm dynasore for 15 min (lane 4). Cells were then surface-biotinylated and lysed, and the biotinylated fraction was immunoprecipitated (IP) and probed for VEGFR2. IB, immunoblot. In panels A–E arrowheads indicate VEGFR2-positive endosomes. Arrows indicate VEGFR2 membrane staining.$
Bovine Brain Endothelial Cell Mitogen, supplied by Serotech Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/endothelial+mitogen/pmc03597788-52-9-16?v=Serotech+Inc
Average 90 stars, based on 1 article reviews

bovine brain endothelial cell mitogen - by Bioz Stars, 2026-08

90/100 stars

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endothelial mitogen (Serotech Inc)

Serotech Inc endothelial mitogen
$Pitstop and dynasore inhibit VEGFR2 internalization in <t>endothelial</t> cells. A–F, shown is an antibody feeding assay. Cell surface VEGFR2 was labeled in HUVECs with a VEGFR2 extracellular domain-specific antibody for 30 min at 4 °C. Cells were then either fixed directly or shifted to 37 °C for 30 min and then fixed. Fixed cells were stained with a fluorescently tagged secondary antibody to detect anti-VEGFR2 (VR2) antibody (green) and co-stained for the endosomal marker EEA1 (red). A, localization of anti-VEGFR2 antibody in cells after labeling was performed in the presence of vehicle for 30 min at 4 °C. B, localization of anti-VEGFR2 antibody after labeling in the presence of vehicle for 30 min at 4 °C followed by warming to 37 °C for 30 min in the presence of vehicle is shown. C, localization of anti-VEGFR2 antibody after labeling in the presence of vehicle for 30 min at 4 °C followed by warming to 37 °C for 30 min in the presence of VEGF and vehicle is shown. D, localization of anti-VEGFR2 antibody after labeling in the presence of 10 μm pitstop for 30 min at 4 °C followed by warming to 37 °C for 30 min in the presence of VEGF and 10 μm pitstop is shown. E, localization of anti-VEGFR2 antibody after labeling in the presence of 80 μm dynasore for 30 min at 4 °C followed by warming to 37 °C for 30 min in the presence of VEGF and 80 μm dynasore is shown. F, quantification of VEGFR2 internalization in endothelial cells treated as indicated (same conditions as shown in panels B–E) is shown. The graph shows the number of intracellular structures labeling dual positive for VEGFR2 and EEA1 per cell ± S.E. Quantification of 20 cells from 2 independent experiments was used to generate each data point. *, p < 0.05; **, p < 0.001. Scale bar = 5 μm. G, cell surface biotinylation is shown. HUVECs were treated as follows; vehicle for 45 min (lane 1), vehicle for 30 min followed by VEGF and vehicle for 15 min (lane 2), 10 μm pitstop for 30 min followed by VEGF and 10 μm pitstop for 15 min (lane 3), or 80 μm dynasore for 30 min followed by VEGF and 80 μm dynasore for 15 min (lane 4). Cells were then surface-biotinylated and lysed, and the biotinylated fraction was immunoprecipitated (IP) and probed for VEGFR2. IB, immunoblot. In panels A–E arrowheads indicate VEGFR2-positive endosomes. Arrows indicate VEGFR2 membrane staining.$
Endothelial Mitogen, supplied by Serotech Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/endothelial+mitogen/pmc02928983-204-40-43?v=Serotech+Inc
Average 90 stars, based on 1 article reviews

endothelial mitogen - by Bioz Stars, 2026-08

90/100 stars

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endothelial cell mitogen (Adamis corporation)

Adamis corporation endothelial cell mitogen
$Pitstop and dynasore inhibit VEGFR2 internalization in <t>endothelial</t> cells. A–F, shown is an antibody feeding assay. Cell surface VEGFR2 was labeled in HUVECs with a VEGFR2 extracellular domain-specific antibody for 30 min at 4 °C. Cells were then either fixed directly or shifted to 37 °C for 30 min and then fixed. Fixed cells were stained with a fluorescently tagged secondary antibody to detect anti-VEGFR2 (VR2) antibody (green) and co-stained for the endosomal marker EEA1 (red). A, localization of anti-VEGFR2 antibody in cells after labeling was performed in the presence of vehicle for 30 min at 4 °C. B, localization of anti-VEGFR2 antibody after labeling in the presence of vehicle for 30 min at 4 °C followed by warming to 37 °C for 30 min in the presence of vehicle is shown. C, localization of anti-VEGFR2 antibody after labeling in the presence of vehicle for 30 min at 4 °C followed by warming to 37 °C for 30 min in the presence of VEGF and vehicle is shown. D, localization of anti-VEGFR2 antibody after labeling in the presence of 10 μm pitstop for 30 min at 4 °C followed by warming to 37 °C for 30 min in the presence of VEGF and 10 μm pitstop is shown. E, localization of anti-VEGFR2 antibody after labeling in the presence of 80 μm dynasore for 30 min at 4 °C followed by warming to 37 °C for 30 min in the presence of VEGF and 80 μm dynasore is shown. F, quantification of VEGFR2 internalization in endothelial cells treated as indicated (same conditions as shown in panels B–E) is shown. The graph shows the number of intracellular structures labeling dual positive for VEGFR2 and EEA1 per cell ± S.E. Quantification of 20 cells from 2 independent experiments was used to generate each data point. *, p < 0.05; **, p < 0.001. Scale bar = 5 μm. G, cell surface biotinylation is shown. HUVECs were treated as follows; vehicle for 45 min (lane 1), vehicle for 30 min followed by VEGF and vehicle for 15 min (lane 2), 10 μm pitstop for 30 min followed by VEGF and 10 μm pitstop for 15 min (lane 3), or 80 μm dynasore for 30 min followed by VEGF and 80 μm dynasore for 15 min (lane 4). Cells were then surface-biotinylated and lysed, and the biotinylated fraction was immunoprecipitated (IP) and probed for VEGFR2. IB, immunoblot. In panels A–E arrowheads indicate VEGFR2-positive endosomes. Arrows indicate VEGFR2 membrane staining.$
Endothelial Cell Mitogen, supplied by Adamis corporation, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/endothelial+mitogen/pmc04992630-424-5-22?v=Adamis+corporation
Average 90 stars, based on 1 article reviews

endothelial cell mitogen - by Bioz Stars, 2026-08

90/100 stars

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endothelial mitogen (Biomedical Technologies)

Biomedical Technologies endothelial mitogen
$Pitstop and dynasore inhibit VEGFR2 internalization in <t>endothelial</t> cells. A–F, shown is an antibody feeding assay. Cell surface VEGFR2 was labeled in HUVECs with a VEGFR2 extracellular domain-specific antibody for 30 min at 4 °C. Cells were then either fixed directly or shifted to 37 °C for 30 min and then fixed. Fixed cells were stained with a fluorescently tagged secondary antibody to detect anti-VEGFR2 (VR2) antibody (green) and co-stained for the endosomal marker EEA1 (red). A, localization of anti-VEGFR2 antibody in cells after labeling was performed in the presence of vehicle for 30 min at 4 °C. B, localization of anti-VEGFR2 antibody after labeling in the presence of vehicle for 30 min at 4 °C followed by warming to 37 °C for 30 min in the presence of vehicle is shown. C, localization of anti-VEGFR2 antibody after labeling in the presence of vehicle for 30 min at 4 °C followed by warming to 37 °C for 30 min in the presence of VEGF and vehicle is shown. D, localization of anti-VEGFR2 antibody after labeling in the presence of 10 μm pitstop for 30 min at 4 °C followed by warming to 37 °C for 30 min in the presence of VEGF and 10 μm pitstop is shown. E, localization of anti-VEGFR2 antibody after labeling in the presence of 80 μm dynasore for 30 min at 4 °C followed by warming to 37 °C for 30 min in the presence of VEGF and 80 μm dynasore is shown. F, quantification of VEGFR2 internalization in endothelial cells treated as indicated (same conditions as shown in panels B–E) is shown. The graph shows the number of intracellular structures labeling dual positive for VEGFR2 and EEA1 per cell ± S.E. Quantification of 20 cells from 2 independent experiments was used to generate each data point. *, p < 0.05; **, p < 0.001. Scale bar = 5 μm. G, cell surface biotinylation is shown. HUVECs were treated as follows; vehicle for 45 min (lane 1), vehicle for 30 min followed by VEGF and vehicle for 15 min (lane 2), 10 μm pitstop for 30 min followed by VEGF and 10 μm pitstop for 15 min (lane 3), or 80 μm dynasore for 30 min followed by VEGF and 80 μm dynasore for 15 min (lane 4). Cells were then surface-biotinylated and lysed, and the biotinylated fraction was immunoprecipitated (IP) and probed for VEGFR2. IB, immunoblot. In panels A–E arrowheads indicate VEGFR2-positive endosomes. Arrows indicate VEGFR2 membrane staining.$
Endothelial Mitogen, supplied by Biomedical Technologies, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/endothelial+mitogen/pmc12587490-55-0-3?v=Biomedical+Technologies
Average 86 stars, based on 1 article reviews

endothelial mitogen - by Bioz Stars, 2026-08

86/100 stars

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endothelial mitogen bovine (RayBiotech)

N/A

Endothelial Mitogen Bovine; 20 mg

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endothelial mitogen bovine (Angio-Proteomie)

N/A

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ecgs bovine - bovine endothelial mitogen (Aviva Systems)

N/A

bECGS; Bovine Endothelial Mitogen; Bovine Endothelial Mitogen

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endothelial mitogen (Valiant Co Ltd)

N/A

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$Pitstop and dynasore inhibit VEGFR2 internalization in endothelial cells. A–F, shown is an antibody feeding assay. Cell surface VEGFR2 was labeled in HUVECs with a VEGFR2 extracellular domain-specific antibody for 30 min at 4 °C. Cells were then either fixed directly or shifted to 37 °C for 30 min and then fixed. Fixed cells were stained with a fluorescently tagged secondary antibody to detect anti-VEGFR2 (VR2) antibody (green) and co-stained for the endosomal marker EEA1 (red). A, localization of anti-VEGFR2 antibody in cells after labeling was performed in the presence of vehicle for 30 min at 4 °C. B, localization of anti-VEGFR2 antibody after labeling in the presence of vehicle for 30 min at 4 °C followed by warming to 37 °C for 30 min in the presence of vehicle is shown. C, localization of anti-VEGFR2 antibody after labeling in the presence of vehicle for 30 min at 4 °C followed by warming to 37 °C for 30 min in the presence of VEGF and vehicle is shown. D, localization of anti-VEGFR2 antibody after labeling in the presence of 10 μm pitstop for 30 min at 4 °C followed by warming to 37 °C for 30 min in the presence of VEGF and 10 μm pitstop is shown. E, localization of anti-VEGFR2 antibody after labeling in the presence of 80 μm dynasore for 30 min at 4 °C followed by warming to 37 °C for 30 min in the presence of VEGF and 80 μm dynasore is shown. F, quantification of VEGFR2 internalization in endothelial cells treated as indicated (same conditions as shown in panels B–E) is shown. The graph shows the number of intracellular structures labeling dual positive for VEGFR2 and EEA1 per cell ± S.E. Quantification of 20 cells from 2 independent experiments was used to generate each data point. *, p < 0.05; **, p < 0.001. Scale bar = 5 μm. G, cell surface biotinylation is shown. HUVECs were treated as follows; vehicle for 45 min (lane 1), vehicle for 30 min followed by VEGF and vehicle for 15 min (lane 2), 10 μm pitstop for 30 min followed by VEGF and 10 μm pitstop for 15 min (lane 3), or 80 μm dynasore for 30 min followed by VEGF and 80 μm dynasore for 15 min (lane 4). Cells were then surface-biotinylated and lysed, and the biotinylated fraction was immunoprecipitated (IP) and probed for VEGFR2. IB, immunoblot. In panels A–E arrowheads indicate VEGFR2-positive endosomes. Arrows indicate VEGFR2 membrane staining.$

Journal: The Journal of Biological Chemistry

Article Title: Essential Role for Endocytosis in the Growth Factor-stimulated Activation of ERK1/2 in Endothelial Cells *

doi: 10.1074/jbc.M112.446401

Figure Lengend Snippet: Pitstop and dynasore inhibit VEGFR2 internalization in endothelial cells. A–F, shown is an antibody feeding assay. Cell surface VEGFR2 was labeled in HUVECs with a VEGFR2 extracellular domain-specific antibody for 30 min at 4 °C. Cells were then either fixed directly or shifted to 37 °C for 30 min and then fixed. Fixed cells were stained with a fluorescently tagged secondary antibody to detect anti-VEGFR2 (VR2) antibody (green) and co-stained for the endosomal marker EEA1 (red). A, localization of anti-VEGFR2 antibody in cells after labeling was performed in the presence of vehicle for 30 min at 4 °C. B, localization of anti-VEGFR2 antibody after labeling in the presence of vehicle for 30 min at 4 °C followed by warming to 37 °C for 30 min in the presence of vehicle is shown. C, localization of anti-VEGFR2 antibody after labeling in the presence of vehicle for 30 min at 4 °C followed by warming to 37 °C for 30 min in the presence of VEGF and vehicle is shown. D, localization of anti-VEGFR2 antibody after labeling in the presence of 10 μm pitstop for 30 min at 4 °C followed by warming to 37 °C for 30 min in the presence of VEGF and 10 μm pitstop is shown. E, localization of anti-VEGFR2 antibody after labeling in the presence of 80 μm dynasore for 30 min at 4 °C followed by warming to 37 °C for 30 min in the presence of VEGF and 80 μm dynasore is shown. F, quantification of VEGFR2 internalization in endothelial cells treated as indicated (same conditions as shown in panels B–E) is shown. The graph shows the number of intracellular structures labeling dual positive for VEGFR2 and EEA1 per cell ± S.E. Quantification of 20 cells from 2 independent experiments was used to generate each data point. *, p < 0.05; **, p < 0.001. Scale bar = 5 μm. G, cell surface biotinylation is shown. HUVECs were treated as follows; vehicle for 45 min (lane 1), vehicle for 30 min followed by VEGF and vehicle for 15 min (lane 2), 10 μm pitstop for 30 min followed by VEGF and 10 μm pitstop for 15 min (lane 3), or 80 μm dynasore for 30 min followed by VEGF and 80 μm dynasore for 15 min (lane 4). Cells were then surface-biotinylated and lysed, and the biotinylated fraction was immunoprecipitated (IP) and probed for VEGFR2. IB, immunoblot. In panels A–E arrowheads indicate VEGFR2-positive endosomes. Arrows indicate VEGFR2 membrane staining.

Article Snippet: Reagents Fetal calf serum (FCS) was from Invitrogen, and bovine brain endothelial cell mitogen was from Serotech (Kidlington, Oxfordshire, UK).

Techniques: Feeding Assay, Labeling, Staining, Marker, Immunoprecipitation, Western Blot, Membrane

Activation of MEK1/2 and ERK1/2 in VEGF-stimulated endothelial cells is abrogated by pitstop. A, HUVECs were pretreated with vehicle or 10 μm pitstop for 15 min and then stimulated for the times indicated with 50 ng/ml VEGF. Cell lysates were analyzed by Western blotting for phosphorylated (Tyr(P)-1175) and total VEGFR2, phosphorylated (Tyr(P)-341) and total C-Raf, phosphorylated (Ser(P)-217/Ser(P)-221) and total MEK1/2, phosphorylated (Thr(P)-202/Tyr(P)-204) and total ERK1/2. B–E, quantification of phosphorylation is shown. White bars represent vehicle, gray bars represent pitstop. n = 3 independent experiments. *, p < 0.05; **, p < 0.01; ***, p < 0.001, ns = no significant difference. F, HUVECs were pretreated with the indicated concentrations of pitstop for 15 min and then stimulated with 50 ng/ml VEGF for 10 min. Lysates were analyzed by Western blot for phosphorylated (Thr(P)-202/Tyr(P)-204) and total ERK1/2.

Journal: The Journal of Biological Chemistry

Article Title: Essential Role for Endocytosis in the Growth Factor-stimulated Activation of ERK1/2 in Endothelial Cells *

doi: 10.1074/jbc.M112.446401

Figure Lengend Snippet: Activation of MEK1/2 and ERK1/2 in VEGF-stimulated endothelial cells is abrogated by pitstop. A, HUVECs were pretreated with vehicle or 10 μm pitstop for 15 min and then stimulated for the times indicated with 50 ng/ml VEGF. Cell lysates were analyzed by Western blotting for phosphorylated (Tyr(P)-1175) and total VEGFR2, phosphorylated (Tyr(P)-341) and total C-Raf, phosphorylated (Ser(P)-217/Ser(P)-221) and total MEK1/2, phosphorylated (Thr(P)-202/Tyr(P)-204) and total ERK1/2. B–E, quantification of phosphorylation is shown. White bars represent vehicle, gray bars represent pitstop. n = 3 independent experiments. *, p < 0.05; **, p < 0.01; ***, p < 0.001, ns = no significant difference. F, HUVECs were pretreated with the indicated concentrations of pitstop for 15 min and then stimulated with 50 ng/ml VEGF for 10 min. Lysates were analyzed by Western blot for phosphorylated (Thr(P)-202/Tyr(P)-204) and total ERK1/2.

Article Snippet: Reagents Fetal calf serum (FCS) was from Invitrogen, and bovine brain endothelial cell mitogen was from Serotech (Kidlington, Oxfordshire, UK).

Techniques: Activation Assay, Western Blot, Phospho-proteomics

Activation of MEK1/2 and ERK1/2 in VEGF-stimulated endothelial cells is abrogated by dynasore. A, HUVECs were pretreated with vehicle or 10 μm dynasore for 30 min and then stimulated for the times indicated with 50 ng/ml VEGF. Lysates were analyzed by Western blotting for phosphorylated (Tyr(P)-1175) and total VEGFR2, phosphorylated (Tyr(P)-341) and total C-Raf, phosphorylated (Ser(P)-217/Ser(P)-221) and total MEK1/2, and phosphorylated (Thr(P)-202/Tyr(P)-204) and total ERK1/2. B–E, quantification of phosphorylation is shown. White bars represent vehicle, gray bars represent dynasore. n = 3 independent experiments. *, p < 0.05; **, p < 0.01; ***, p < 0.001; ns = no significant difference. F, HUVECs were pretreated with the indicated concentrations of dynasore for 30 min and then stimulated with 50 ng/ml VEGF for 10 min. Lysates were analyzed by Western blot for phosphorylated (Thr(P)-202/Tyr(P)-204) and total ERK1/2.

Journal: The Journal of Biological Chemistry

Article Title: Essential Role for Endocytosis in the Growth Factor-stimulated Activation of ERK1/2 in Endothelial Cells *

doi: 10.1074/jbc.M112.446401

Figure Lengend Snippet: Activation of MEK1/2 and ERK1/2 in VEGF-stimulated endothelial cells is abrogated by dynasore. A, HUVECs were pretreated with vehicle or 10 μm dynasore for 30 min and then stimulated for the times indicated with 50 ng/ml VEGF. Lysates were analyzed by Western blotting for phosphorylated (Tyr(P)-1175) and total VEGFR2, phosphorylated (Tyr(P)-341) and total C-Raf, phosphorylated (Ser(P)-217/Ser(P)-221) and total MEK1/2, and phosphorylated (Thr(P)-202/Tyr(P)-204) and total ERK1/2. B–E, quantification of phosphorylation is shown. White bars represent vehicle, gray bars represent dynasore. n = 3 independent experiments. *, p < 0.05; **, p < 0.01; ***, p < 0.001; ns = no significant difference. F, HUVECs were pretreated with the indicated concentrations of dynasore for 30 min and then stimulated with 50 ng/ml VEGF for 10 min. Lysates were analyzed by Western blot for phosphorylated (Thr(P)-202/Tyr(P)-204) and total ERK1/2.

Article Snippet: Reagents Fetal calf serum (FCS) was from Invitrogen, and bovine brain endothelial cell mitogen was from Serotech (Kidlington, Oxfordshire, UK).

Techniques: Activation Assay, Western Blot, Phospho-proteomics

Activation of ERK1/2 in VEGF-stimulated endothelial cells is suppressed by clathrin or dynamin II knockdown. A–F, HUVECs infected with lentivirus encoding either control non-targeting, clathrin targeting, or dynamin II (dyn II) targeting shRNA oligos were stimulated for the indicated times with 50 ng/ml VEGF. Cell lysates were analyzed by Western blotting (A and D) for phosphorylated (Thr(P)-202/Tyr(P)-204) ERK1/2, total ERK1/2, and clathrin or dynamin II. B and E, shown is quantification of ERK1/2 phosphorylation. n = 3 independent experiments. C and F, shown is quantification of clathrin or dynamin expression. n = 3 independent experiments. *, p < 0.05.

Journal: The Journal of Biological Chemistry

Article Title: Essential Role for Endocytosis in the Growth Factor-stimulated Activation of ERK1/2 in Endothelial Cells *

doi: 10.1074/jbc.M112.446401

Figure Lengend Snippet: Activation of ERK1/2 in VEGF-stimulated endothelial cells is suppressed by clathrin or dynamin II knockdown. A–F, HUVECs infected with lentivirus encoding either control non-targeting, clathrin targeting, or dynamin II (dyn II) targeting shRNA oligos were stimulated for the indicated times with 50 ng/ml VEGF. Cell lysates were analyzed by Western blotting (A and D) for phosphorylated (Thr(P)-202/Tyr(P)-204) ERK1/2, total ERK1/2, and clathrin or dynamin II. B and E, shown is quantification of ERK1/2 phosphorylation. n = 3 independent experiments. C and F, shown is quantification of clathrin or dynamin expression. n = 3 independent experiments. *, p < 0.05.

Article Snippet: Reagents Fetal calf serum (FCS) was from Invitrogen, and bovine brain endothelial cell mitogen was from Serotech (Kidlington, Oxfordshire, UK).

Techniques: Activation Assay, Knockdown, Infection, Control, shRNA, Western Blot, Phospho-proteomics, Expressing

Activation of ERK1/2 in endothelial cells by FGF2 and HGF is abrogated by pitstop and dynasore, whereas activation of ERK1/2 by FCS or TPA is unimpeded. A–C, HUVECs were pretreated with vehicle, 10 μm pitstop, or 80 μm dynasore and then stimulated for the times indicated with 50 ng/ml FGF2 (A), 10 ng/ml HGF (B), or 10% FCS (C). Cell lysates were analyzed by Western blotting for phosphorylated (Thr(P)-202/Tyr(P)-204) and total ERK1/2. D, HUVECs were pretreated with vehicle, 10 μm pitstop, or 80 μm dynasore and then stimulated for 15 min with 10 μm TPA. Cell lysates were analyzed by Western blotting for phosphorylated (Thr(P)-202/Tyr(P)-204) and total ERK1/2.

Journal: The Journal of Biological Chemistry

Article Title: Essential Role for Endocytosis in the Growth Factor-stimulated Activation of ERK1/2 in Endothelial Cells *

doi: 10.1074/jbc.M112.446401

Figure Lengend Snippet: Activation of ERK1/2 in endothelial cells by FGF2 and HGF is abrogated by pitstop and dynasore, whereas activation of ERK1/2 by FCS or TPA is unimpeded. A–C, HUVECs were pretreated with vehicle, 10 μm pitstop, or 80 μm dynasore and then stimulated for the times indicated with 50 ng/ml FGF2 (A), 10 ng/ml HGF (B), or 10% FCS (C). Cell lysates were analyzed by Western blotting for phosphorylated (Thr(P)-202/Tyr(P)-204) and total ERK1/2. D, HUVECs were pretreated with vehicle, 10 μm pitstop, or 80 μm dynasore and then stimulated for 15 min with 10 μm TPA. Cell lysates were analyzed by Western blotting for phosphorylated (Thr(P)-202/Tyr(P)-204) and total ERK1/2.

Article Snippet: Reagents Fetal calf serum (FCS) was from Invitrogen, and bovine brain endothelial cell mitogen was from Serotech (Kidlington, Oxfordshire, UK).

Techniques: Activation Assay, Western Blot

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