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recombinant rat vegf  (R&D Systems)


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    Structured Review

    R&D Systems recombinant rat vegf
    Microdialysis relative recovery enhancement of cytokines using heparin-immobilized microspheres as affinity agents as compared to control at three different flow rates
    Recombinant Rat Vegf, supplied by R&D Systems, used in various techniques. Bioz Stars score: 90/100, based on 36 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/564-RV/Recombinant+Rat+VEGF+164+Protein%2C+CF/pmc03864007-113-0-10
    Average 90 stars, based on 36 article reviews
    recombinant rat vegf - by Bioz Stars, 2026-11
    90/100 stars

    Images

    1) Product Images from "In vitro and in vivo affinity microdialysis sampling of cytokines using heparin-immobilized microspheres"

    Article Title: In vitro and in vivo affinity microdialysis sampling of cytokines using heparin-immobilized microspheres

    Journal: Analytical and bioanalytical chemistry

    doi: 10.1007/s00216-010-4333-0

    Microdialysis relative recovery enhancement of cytokines using heparin-immobilized microspheres as affinity agents as compared to control at three different flow rates
    Figure Legend Snippet: Microdialysis relative recovery enhancement of cytokines using heparin-immobilized microspheres as affinity agents as compared to control at three different flow rates

    Techniques Used: Control

    Related Articles

    Binding Assay:

    Article Title: Pharmacodynamic and Antitumor Activity of BI 836880, a Dual Vascular Endothelial Growth Factor and Angiopoietin 2 Inhibitor, Alone and Combined with Programmed Cell Death Protein-1 Inhibition.
    Article Snippet: Other reagents were RMP1-14 (murine anti–PD-1 antibody; BioXCell; BE0146) and the corresponding isotype InVivoMAb Rat IgG2a (BioXCell; BE0089), bevacizumab (anti-VEGF antibody; Roche), and vatalanib [small-molecule tyrosine kinase inhibitor of VEGF receptor (VEGFR); MedChemExpress; HY-12018]. .. For the binding assays, the following commercial recombinant proteins were used: human VEGF165 (R&D Systems; 293-VE/CF), human VEGF121 (R&D Systems; 298-VERSUS/CF), rat VEGF164 (R&D Systems; 564-RV/CF), mouse VEGF164 (R&D Systems; 493- MV/CF), human VEGF-B (R&D Systems; 751-VE), human VEGF-C (R&D Systems; 2179-VC/CF), human VEGF-D (R&D Systems; 622- VD/CF), human placental growth factor (R&D Systems; 264-PG/CF), FLAG-tagged human ANG1 (Alexis Biochemicals), FLAG-tagged human ANG2 (Alexis Biochemicals), human TIE2-Fc (R&D Systems; 313-TI), and recombinant human ANG2 (R&D Systems; 623-AN). .. Also used were recombinant proteins produced by Boehringer Ingelheim: mouse, rat, and cynomolgus ANG2-fibrinogen-like domain (FLD) fragments, as well as monomeric ANG2-FLD, which consists of the C-terminal FLD domain of ANG2 and contains the key amino acid residues involved in its interaction with the receptor TIE2.

    Recombinant:

    Article Title: Pharmacodynamic and Antitumor Activity of BI 836880, a Dual Vascular Endothelial Growth Factor and Angiopoietin 2 Inhibitor, Alone and Combined with Programmed Cell Death Protein-1 Inhibition.
    Article Snippet: Other reagents were RMP1-14 (murine anti–PD-1 antibody; BioXCell; BE0146) and the corresponding isotype InVivoMAb Rat IgG2a (BioXCell; BE0089), bevacizumab (anti-VEGF antibody; Roche), and vatalanib [small-molecule tyrosine kinase inhibitor of VEGF receptor (VEGFR); MedChemExpress; HY-12018]. .. For the binding assays, the following commercial recombinant proteins were used: human VEGF165 (R&D Systems; 293-VE/CF), human VEGF121 (R&D Systems; 298-VERSUS/CF), rat VEGF164 (R&D Systems; 564-RV/CF), mouse VEGF164 (R&D Systems; 493- MV/CF), human VEGF-B (R&D Systems; 751-VE), human VEGF-C (R&D Systems; 2179-VC/CF), human VEGF-D (R&D Systems; 622- VD/CF), human placental growth factor (R&D Systems; 264-PG/CF), FLAG-tagged human ANG1 (Alexis Biochemicals), FLAG-tagged human ANG2 (Alexis Biochemicals), human TIE2-Fc (R&D Systems; 313-TI), and recombinant human ANG2 (R&D Systems; 623-AN). .. Also used were recombinant proteins produced by Boehringer Ingelheim: mouse, rat, and cynomolgus ANG2-fibrinogen-like domain (FLD) fragments, as well as monomeric ANG2-FLD, which consists of the C-terminal FLD domain of ANG2 and contains the key amino acid residues involved in its interaction with the receptor TIE2.

    Article Title: AMP-activated protein kinase is a key regulator of acute neurovascular permeability
    Article Snippet: .. Recombinant rat VEGF-A (165) was purchased from R&D Systems (Abingdon, United Kingdom). .. Bradykinin, sulforhodamine B, Evans Blue, SU-1498, SB203580, compound C, STO-609, L-N G -nitroarginine methyl ester (L-NAME), BAPTA-AM, 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR), A769662, diethylammonium (Z)-1-(N,N-diethylamino)diazen-1-ium-1,2-diolate (DEANO) and 1H-[1,2,4]-oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) were purchased from MERCK (Dorset, United Kingdom).



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    R&D Systems recombinant human vegf
    Figure 4. Induction of <t>VEGF</t> (A,B), angiogenic factors (C) or pro-inflammatory factors (D) in cultured cells in vitro. RAW264.7 cells, NIH3T3 cells or U937 cells were cultured in hypoxic condition (5% or 0.5%) for 8 h (A,C,D) or indicated time period (B). The induction of Vegf (A), angiogenic factors (C) or pro-inflammatory factors (D) was then examined by RT-PCR analyses (A,C,D, n = 6) and the secretion of VEGF by ELISA (B, n = 6). Data represents as Mean and S.E.M. Statistical analysis was done by a non-parametric Mann–Whitney test or by a Kruskal–Wallis test followed by a Steel test. *p < 0.05, **p < 0.01.
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    Image Search Results


    Figure 6. Cultured retinal progenitor cell groups with Top2b overexpression (OE) and knockdown (KD) illustrate altered expression of select chemotactic receptors compared to wildtype cell groups with no Top2b manipulation (WT). Cell groups illustrated significant differences in the expression of selected chemotactic receptors: vascular endothelial growth factor receptor (VEGFR1), fibroblast growth factor receptor (FGFR1), and c-x-c chemokine receptor 4 (CXCR4, receptor for the stromal cell-derived factor 1, SDF-1a, ligand). Statistical significance across the cell groups is denoted by p-value: * < 0.05, ** < 0.01, **** < 0.0001 as via two-way ANOVA tests followed by Dunnett’s post-hoc test

    Journal: Exploration of BioMat-X

    Article Title: Top2b regulates morphological and migratory properties of retinal progenitor cells in vivo and upon transplantable matrix substrates

    doi: 10.37349/ebmx.2025.101335

    Figure Lengend Snippet: Figure 6. Cultured retinal progenitor cell groups with Top2b overexpression (OE) and knockdown (KD) illustrate altered expression of select chemotactic receptors compared to wildtype cell groups with no Top2b manipulation (WT). Cell groups illustrated significant differences in the expression of selected chemotactic receptors: vascular endothelial growth factor receptor (VEGFR1), fibroblast growth factor receptor (FGFR1), and c-x-c chemokine receptor 4 (CXCR4, receptor for the stromal cell-derived factor 1, SDF-1a, ligand). Statistical significance across the cell groups is denoted by p-value: * < 0.05, ** < 0.01, **** < 0.0001 as via two-way ANOVA tests followed by Dunnett’s post-hoc test

    Article Snippet: Approximately 600 μL of each growth factor vascular endothelial growth factor (VEGF; R&D Systems, Minneapolis, MN, USA, 564-RV), fibroblast growth factor-8 (FGF-8; Invitrogen, Carlsbad, CA, USA, PHG0184), and stromal derived factor 1-a (SDF-1a; Sigma Aldrich, St. Louis, MO, USA, SRP3276) was added to the bottom of separate transwell assays.

    Techniques: Cell Culture, Over Expression, Knockdown, Expressing, Derivative Assay

    Figure 4. Induction of VEGF (A,B), angiogenic factors (C) or pro-inflammatory factors (D) in cultured cells in vitro. RAW264.7 cells, NIH3T3 cells or U937 cells were cultured in hypoxic condition (5% or 0.5%) for 8 h (A,C,D) or indicated time period (B). The induction of Vegf (A), angiogenic factors (C) or pro-inflammatory factors (D) was then examined by RT-PCR analyses (A,C,D, n = 6) and the secretion of VEGF by ELISA (B, n = 6). Data represents as Mean and S.E.M. Statistical analysis was done by a non-parametric Mann–Whitney test or by a Kruskal–Wallis test followed by a Steel test. *p < 0.05, **p < 0.01.

    Journal: Scientific reports

    Article Title: Hypoxic microenvironment as a crucial factor triggering events leading to rupture of intracranial aneurysm.

    doi: 10.1038/s41598-023-32001-z

    Figure Lengend Snippet: Figure 4. Induction of VEGF (A,B), angiogenic factors (C) or pro-inflammatory factors (D) in cultured cells in vitro. RAW264.7 cells, NIH3T3 cells or U937 cells were cultured in hypoxic condition (5% or 0.5%) for 8 h (A,C,D) or indicated time period (B). The induction of Vegf (A), angiogenic factors (C) or pro-inflammatory factors (D) was then examined by RT-PCR analyses (A,C,D, n = 6) and the secretion of VEGF by ELISA (B, n = 6). Data represents as Mean and S.E.M. Statistical analysis was done by a non-parametric Mann–Whitney test or by a Kruskal–Wallis test followed by a Steel test. *p < 0.05, **p < 0.01.

    Article Snippet: :(0123456789) Scientific Reports | (2023) 13:5545 | https://doi.org/10.1038/s41598-023-32001-z slow-release of VEGF was placed on the brain surface (MedGel II from Nitta-gelatin (♯PI9, Osaka Japan) and recombinant human VEGF (1 μg/head, #564-RV-010/CF, lot #CWC0620081) from R&D systems, Inc. (Minneapolis, MN) resolved in phosphate buffered saline containing 0.1% human serum albumin (#A1653-5G, lot #SLBG2676V, Sigma)).

    Techniques: Cell Culture, In Vitro, Reverse Transcription Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay, MANN-WHITNEY

    Figure 5. Expression of VEGF in rupture-prone intracranial aneurysm (IA) lesions induced in rats. The images of immunofluorescent staining of IA lesions for VEGF (green), the marker for macrophages, CD68 (red), the marker for smooth muscle cell, α-smooth muscle actin (SMA, gray), nuclear staining by DAPI (blue), and merged images are shown. The images from immunohistochemistry without a primary antibody were served as a negative control. Magnified images corresponding to the square in the upper panels are shown in the lower panels. Scale bar: 50 μm.

    Journal: Scientific reports

    Article Title: Hypoxic microenvironment as a crucial factor triggering events leading to rupture of intracranial aneurysm.

    doi: 10.1038/s41598-023-32001-z

    Figure Lengend Snippet: Figure 5. Expression of VEGF in rupture-prone intracranial aneurysm (IA) lesions induced in rats. The images of immunofluorescent staining of IA lesions for VEGF (green), the marker for macrophages, CD68 (red), the marker for smooth muscle cell, α-smooth muscle actin (SMA, gray), nuclear staining by DAPI (blue), and merged images are shown. The images from immunohistochemistry without a primary antibody were served as a negative control. Magnified images corresponding to the square in the upper panels are shown in the lower panels. Scale bar: 50 μm.

    Article Snippet: :(0123456789) Scientific Reports | (2023) 13:5545 | https://doi.org/10.1038/s41598-023-32001-z slow-release of VEGF was placed on the brain surface (MedGel II from Nitta-gelatin (♯PI9, Osaka Japan) and recombinant human VEGF (1 μg/head, #564-RV-010/CF, lot #CWC0620081) from R&D systems, Inc. (Minneapolis, MN) resolved in phosphate buffered saline containing 0.1% human serum albumin (#A1653-5G, lot #SLBG2676V, Sigma)).

    Techniques: Expressing, Staining, Marker, Immunohistochemistry, Negative Control

    Figure 6. Expression of VEGF in human unruptured intracranial aneurysm (IA) lesions. The images of immunofluorescent staining of IA lesions for VEGF (green), nuclear staining by DAPI (blue), and merged images are shown. The images from immunohistochemistry without a primary antibody were served as a negative control. Scale bar: 50 μm.

    Journal: Scientific reports

    Article Title: Hypoxic microenvironment as a crucial factor triggering events leading to rupture of intracranial aneurysm.

    doi: 10.1038/s41598-023-32001-z

    Figure Lengend Snippet: Figure 6. Expression of VEGF in human unruptured intracranial aneurysm (IA) lesions. The images of immunofluorescent staining of IA lesions for VEGF (green), nuclear staining by DAPI (blue), and merged images are shown. The images from immunohistochemistry without a primary antibody were served as a negative control. Scale bar: 50 μm.

    Article Snippet: :(0123456789) Scientific Reports | (2023) 13:5545 | https://doi.org/10.1038/s41598-023-32001-z slow-release of VEGF was placed on the brain surface (MedGel II from Nitta-gelatin (♯PI9, Osaka Japan) and recombinant human VEGF (1 μg/head, #564-RV-010/CF, lot #CWC0620081) from R&D systems, Inc. (Minneapolis, MN) resolved in phosphate buffered saline containing 0.1% human serum albumin (#A1653-5G, lot #SLBG2676V, Sigma)).

    Techniques: Expressing, Staining, Immunohistochemistry, Negative Control

    Figure 7. VEGF-mediated induction of neovessels in subarachnoid space. The sheet for slow-release of VEGF or vehicle was placed on the right or the left of brain surface in the same rat (A) and the induction of vasa vasorum in subarachnoid space was examined. Asterisks indicate the sheets placed on brain surface. Scale bar: 1 mm. The macroscopic image of the brain surface (B) and the histopathological images from hematoxylin– eosin staining from specimen of vehicle- or VEGF-treated side (C) are shown. Dotted circles in (B) indicate the region where the sheet was placed. Noted the reddish appearance only in the VEGF-treated side indicating the induction of neovessels. Magnified images corresponding to the square in the left panels in (C) are shown on the right. Arrows indicate the neovessels induced in subarachnoid space. Scale bar: 50 μm. The images of immunofluorescent staining for the marker for smooth muscle cell, α-smooth muscle actin (SMA, red), nuclear staining by DAPI (blue), and merged images are shown in (D). Magnified images corresponding to the squares in the left panels are shown on the right. Scale bar: 100 μm.

    Journal: Scientific reports

    Article Title: Hypoxic microenvironment as a crucial factor triggering events leading to rupture of intracranial aneurysm.

    doi: 10.1038/s41598-023-32001-z

    Figure Lengend Snippet: Figure 7. VEGF-mediated induction of neovessels in subarachnoid space. The sheet for slow-release of VEGF or vehicle was placed on the right or the left of brain surface in the same rat (A) and the induction of vasa vasorum in subarachnoid space was examined. Asterisks indicate the sheets placed on brain surface. Scale bar: 1 mm. The macroscopic image of the brain surface (B) and the histopathological images from hematoxylin– eosin staining from specimen of vehicle- or VEGF-treated side (C) are shown. Dotted circles in (B) indicate the region where the sheet was placed. Noted the reddish appearance only in the VEGF-treated side indicating the induction of neovessels. Magnified images corresponding to the square in the left panels in (C) are shown on the right. Arrows indicate the neovessels induced in subarachnoid space. Scale bar: 50 μm. The images of immunofluorescent staining for the marker for smooth muscle cell, α-smooth muscle actin (SMA, red), nuclear staining by DAPI (blue), and merged images are shown in (D). Magnified images corresponding to the squares in the left panels are shown on the right. Scale bar: 100 μm.

    Article Snippet: :(0123456789) Scientific Reports | (2023) 13:5545 | https://doi.org/10.1038/s41598-023-32001-z slow-release of VEGF was placed on the brain surface (MedGel II from Nitta-gelatin (♯PI9, Osaka Japan) and recombinant human VEGF (1 μg/head, #564-RV-010/CF, lot #CWC0620081) from R&D systems, Inc. (Minneapolis, MN) resolved in phosphate buffered saline containing 0.1% human serum albumin (#A1653-5G, lot #SLBG2676V, Sigma)).

    Techniques: Staining, Marker