Structured Review

R&D Systems vegfr 2 kdr
Representative flow cytometric density plots demonstrating the gating protocol used to identify angiogenic cells: A) PBMCs stained with PE-conjugated and APC-conjugated mouse IgG (isotype controls) for non-specific fluorescent signals; B) PBMCs stained with antibodies against human CD133 (AC133) (PE-conjugated) and <t>VEGFR-2</t> (KDR) (APC-conjugated) for AC133 + /KDR + PBMCs; A1, B1) FSC-SSC density dot plots of Ficoll-isolated PBMCs and R1 was gated for monocytes; A2, B2) FL2 (PE)-FL4 (APC) density dot plots of R1-gated monocytes. Angiogenic cells = cells in B2 upper-right quadrant – cells in A2 upper-right quadrant.
Vegfr 2 Kdr, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Increased Carotid Intima-Media Thickness and Reduced Distensibility in Human Class III Obesity: Independent and Differential Influences of Adiposity and Blood Pressure on the Vasculature"

Article Title: Increased Carotid Intima-Media Thickness and Reduced Distensibility in Human Class III Obesity: Independent and Differential Influences of Adiposity and Blood Pressure on the Vasculature

Journal: PLoS ONE

doi: 10.1371/journal.pone.0053972

Representative flow cytometric density plots demonstrating the gating protocol used to identify angiogenic cells: A) PBMCs stained with PE-conjugated and APC-conjugated mouse IgG (isotype controls) for non-specific fluorescent signals; B) PBMCs stained with antibodies against human CD133 (AC133) (PE-conjugated) and VEGFR-2 (KDR) (APC-conjugated) for AC133 + /KDR + PBMCs; A1, B1) FSC-SSC density dot plots of Ficoll-isolated PBMCs and R1 was gated for monocytes; A2, B2) FL2 (PE)-FL4 (APC) density dot plots of R1-gated monocytes. Angiogenic cells = cells in B2 upper-right quadrant – cells in A2 upper-right quadrant.
Figure Legend Snippet: Representative flow cytometric density plots demonstrating the gating protocol used to identify angiogenic cells: A) PBMCs stained with PE-conjugated and APC-conjugated mouse IgG (isotype controls) for non-specific fluorescent signals; B) PBMCs stained with antibodies against human CD133 (AC133) (PE-conjugated) and VEGFR-2 (KDR) (APC-conjugated) for AC133 + /KDR + PBMCs; A1, B1) FSC-SSC density dot plots of Ficoll-isolated PBMCs and R1 was gated for monocytes; A2, B2) FL2 (PE)-FL4 (APC) density dot plots of R1-gated monocytes. Angiogenic cells = cells in B2 upper-right quadrant – cells in A2 upper-right quadrant.

Techniques Used: Staining, Isolation


Structured Review

R&D Systems vegfr 2
Inhibition of <t>VEGFR-2</t> RTK autophosphorylation by ABP 215, bevacizumab (US), and bevacizumab (EU).
Vegfr 2, supplied by R&D Systems, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Analytical and functional similarity of Amgen biosimilar ABP 215 to bevacizumab"

Article Title: Analytical and functional similarity of Amgen biosimilar ABP 215 to bevacizumab

Journal: mAbs

doi: 10.1080/19420862.2018.1452580

Inhibition of VEGFR-2 RTK autophosphorylation by ABP 215, bevacizumab (US), and bevacizumab (EU).
Figure Legend Snippet: Inhibition of VEGFR-2 RTK autophosphorylation by ABP 215, bevacizumab (US), and bevacizumab (EU).

Techniques Used: Inhibition


Structured Review

R&D Systems kdr vegfr 2 pe
Kdr Vegfr 2 Pe, supplied by R&D Systems, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Structured Review

R&D Systems pe conjugated vegfr 2
Pe Conjugated Vegfr 2, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Structured Review

R&D Systems mouse anti human vegfr 2
A , Prostatic LEC tube length at 4.5 hours post VEGF-C treatment was quantified using ImageJ. VEGF-C significantly increased the number of tubes formed compared to vehicle control. Data expressed as mean±s.e.m., n = 3, *** P <0.001 using One-way ANOVA, Bonferroni post-analysis. B , Western blotting analysis of <t>VEGFR-2</t> and VEGFR-3 expression in lung, neonatal dermis and prostate LECs. β-tubulin was used as a loading control.
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1) Product Images from "Vascular Endothelial Growth Factor Receptor-3 Directly Interacts with Phosphatidylinositol 3-Kinase to Regulate Lymphangiogenesis"

Article Title: Vascular Endothelial Growth Factor Receptor-3 Directly Interacts with Phosphatidylinositol 3-Kinase to Regulate Lymphangiogenesis

Journal: PLoS ONE

doi: 10.1371/journal.pone.0039558

A , Prostatic LEC tube length at 4.5 hours post VEGF-C treatment was quantified using ImageJ. VEGF-C significantly increased the number of tubes formed compared to vehicle control. Data expressed as mean±s.e.m., n = 3, *** P <0.001 using One-way ANOVA, Bonferroni post-analysis. B , Western blotting analysis of VEGFR-2 and VEGFR-3 expression in lung, neonatal dermis and prostate LECs. β-tubulin was used as a loading control.
Figure Legend Snippet: A , Prostatic LEC tube length at 4.5 hours post VEGF-C treatment was quantified using ImageJ. VEGF-C significantly increased the number of tubes formed compared to vehicle control. Data expressed as mean±s.e.m., n = 3, *** P <0.001 using One-way ANOVA, Bonferroni post-analysis. B , Western blotting analysis of VEGFR-2 and VEGFR-3 expression in lung, neonatal dermis and prostate LECs. β-tubulin was used as a loading control.

Techniques Used: Western Blot, Expressing

. A , Western blotting analysis of phosphorylated Akt (S473) in prostatic LECs following a 15 minute ligand stimulation: VEGF-A (100 ng/ml), VEGF-C (100 ng/ml), VEGF-C156S (250 ng/ml), VEGF-D (250 ng/ml) and VEGF-E (100 ng/ml). B , Time course for Akt phosphorylation (S473) in LECs after VEGF-C (100 ng/ml) stimulation. C , Concentration-dependent phosphorylation of LEC Akt (S473) following 15 minute stimulation with VEGF-C or VEGF-C156S. D , Effect of inhibition of VEGFR-3 (hF4-3C5), VEGFR-2 (IMC-1121b) or VEGFR-1 (IMC-18F1) on LEC Akt (S473) phosphorylation in response to VEGF-C (100 ng/ml). E , Effect of inhibition of PI3K (AS252424, LY294002) or Raf/MEK (PD98059) on Akt (S473) phosphorylation in LECs in response to VEGF-C (100 ng/ml). Serum-free vehicle treated LEC lysate is indicated by ‘0′ in all blots. n = 3. Densitometry analysis is shown for each blot either italicized or graphed; where integrated intensity of phosphorylated molecules was firstly compared to that of the total target protein for each sample, and then expressed as fold increase in integrated density compared to VEGF-C treated control samples. P value calculated using one-way ANOVA. For panels A-B data is compared to time-point zero; panels D-E data is compared to VEGF-C treated control, except where indicated for serum free/VEGF-C treatment comparison. Columns: mean; bars: s.e.m.; P<0.05 (*), P<0.01 (**); P<0.001 (***).
Figure Legend Snippet: . A , Western blotting analysis of phosphorylated Akt (S473) in prostatic LECs following a 15 minute ligand stimulation: VEGF-A (100 ng/ml), VEGF-C (100 ng/ml), VEGF-C156S (250 ng/ml), VEGF-D (250 ng/ml) and VEGF-E (100 ng/ml). B , Time course for Akt phosphorylation (S473) in LECs after VEGF-C (100 ng/ml) stimulation. C , Concentration-dependent phosphorylation of LEC Akt (S473) following 15 minute stimulation with VEGF-C or VEGF-C156S. D , Effect of inhibition of VEGFR-3 (hF4-3C5), VEGFR-2 (IMC-1121b) or VEGFR-1 (IMC-18F1) on LEC Akt (S473) phosphorylation in response to VEGF-C (100 ng/ml). E , Effect of inhibition of PI3K (AS252424, LY294002) or Raf/MEK (PD98059) on Akt (S473) phosphorylation in LECs in response to VEGF-C (100 ng/ml). Serum-free vehicle treated LEC lysate is indicated by ‘0′ in all blots. n = 3. Densitometry analysis is shown for each blot either italicized or graphed; where integrated intensity of phosphorylated molecules was firstly compared to that of the total target protein for each sample, and then expressed as fold increase in integrated density compared to VEGF-C treated control samples. P value calculated using one-way ANOVA. For panels A-B data is compared to time-point zero; panels D-E data is compared to VEGF-C treated control, except where indicated for serum free/VEGF-C treatment comparison. Columns: mean; bars: s.e.m.; P<0.05 (*), P<0.01 (**); P<0.001 (***).

Techniques Used: Western Blot, Concentration Assay, Inhibition

Western blotting analysis of phosphorylated P70S6K ( A, top left ) and eNOS (S1177) ( B, top left ) in prostatic LECs following 15 minute stimulation with ligand: VEGF-C (100 ng/ml), VEGF-A (100 ng/ml), VEGF-C156S (250 ng/ml), VEGF-D (250 ng/ml) and VEGF-E (100 ng/ml). Time- and concentration-dependent phosphorylation of P70S6K ( A, top right ), eNOS (S1177) ( B, top right ), and PLCγ1 (Tyr783) ( C, top left ) in LECs in response to VEGF-C. The effect of inhibition of VEGFR-3 (hF4-3C5), VEGFR-2 (IMC-1121b) or VEGFR-1 (IMC-18F1) on phosphorylation of P70S6K ( A, bottom left ), eNOS (S1177) ( B, bottom left ); and VEGFR-3 (hF4-3C5) on PLCγ1 (Tyr783) ( C, bottom right ) on LEC response to VEGF-C (100 ng/ml). The effect of AS252424, LY294002, PD98059, and U-73122 on phosphorylation of P70S6K ( A, top right ), eNOS (S1177) ( B, bottom right ), and PLCγ1 (Tyr783) ( C, bottom right ) on LECs in response to VEGF-C. The effect of VEGF-C on phosphorylation of PLCγ2 (Tyr759, Tyr1217) in LECs ( C, bottom left ). Control serum-free vehicle treated LEC lysate is indicated by ‘0′ in all blots. n = 3. Densitometry analysis is shown under each blot in italics; where integrated intensity of phosphorylated molecules was firstly compared to that of the total target protein for each sample, and then expressed as fold change in integrated density compared to either serum-free (A, top left and right panels ; B, top left and right panels ; C, top and bottom left panels ) or VEGF-C treated control samples (A, bottom left and right panels ; B, bottom left and right panels ; C, bottom and bottom left panels ).
Figure Legend Snippet: Western blotting analysis of phosphorylated P70S6K ( A, top left ) and eNOS (S1177) ( B, top left ) in prostatic LECs following 15 minute stimulation with ligand: VEGF-C (100 ng/ml), VEGF-A (100 ng/ml), VEGF-C156S (250 ng/ml), VEGF-D (250 ng/ml) and VEGF-E (100 ng/ml). Time- and concentration-dependent phosphorylation of P70S6K ( A, top right ), eNOS (S1177) ( B, top right ), and PLCγ1 (Tyr783) ( C, top left ) in LECs in response to VEGF-C. The effect of inhibition of VEGFR-3 (hF4-3C5), VEGFR-2 (IMC-1121b) or VEGFR-1 (IMC-18F1) on phosphorylation of P70S6K ( A, bottom left ), eNOS (S1177) ( B, bottom left ); and VEGFR-3 (hF4-3C5) on PLCγ1 (Tyr783) ( C, bottom right ) on LEC response to VEGF-C (100 ng/ml). The effect of AS252424, LY294002, PD98059, and U-73122 on phosphorylation of P70S6K ( A, top right ), eNOS (S1177) ( B, bottom right ), and PLCγ1 (Tyr783) ( C, bottom right ) on LECs in response to VEGF-C. The effect of VEGF-C on phosphorylation of PLCγ2 (Tyr759, Tyr1217) in LECs ( C, bottom left ). Control serum-free vehicle treated LEC lysate is indicated by ‘0′ in all blots. n = 3. Densitometry analysis is shown under each blot in italics; where integrated intensity of phosphorylated molecules was firstly compared to that of the total target protein for each sample, and then expressed as fold change in integrated density compared to either serum-free (A, top left and right panels ; B, top left and right panels ; C, top and bottom left panels ) or VEGF-C treated control samples (A, bottom left and right panels ; B, bottom left and right panels ; C, bottom and bottom left panels ).

Techniques Used: Western Blot, Concentration Assay, Inhibition


Structured Review

R&D Systems vegfr 2 antibody
A : Western blot analysis of VEGFR-1 and <t>VEGFR-2</t> from gestational age-matched normal pregnant women (NP, 1–5) and preeclamptic women (PE, 6–10). B : Maternal plasma concentration of VEGFR1, VEGFR2 and Eng (mean±SE, pg/ml) at inclusion (Incl), delivery (day 0, D 0) and during post partum (day 1 to day 5, D 1 to D 5). PE: severe preeclampsia (plain line), NP: normal pregnancies (dashed line).
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1) Product Images from "Differential Expression of Vegfr-2 and Its Soluble Form in Preeclampsia"

Article Title: Differential Expression of Vegfr-2 and Its Soluble Form in Preeclampsia

Journal: PLoS ONE

doi: 10.1371/journal.pone.0033475

A : Western blot analysis of VEGFR-1 and VEGFR-2 from gestational age-matched normal pregnant women (NP, 1–5) and preeclamptic women (PE, 6–10). B : Maternal plasma concentration of VEGFR1, VEGFR2 and Eng (mean±SE, pg/ml) at inclusion (Incl), delivery (day 0, D 0) and during post partum (day 1 to day 5, D 1 to D 5). PE: severe preeclampsia (plain line), NP: normal pregnancies (dashed line).
Figure Legend Snippet: A : Western blot analysis of VEGFR-1 and VEGFR-2 from gestational age-matched normal pregnant women (NP, 1–5) and preeclamptic women (PE, 6–10). B : Maternal plasma concentration of VEGFR1, VEGFR2 and Eng (mean±SE, pg/ml) at inclusion (Incl), delivery (day 0, D 0) and during post partum (day 1 to day 5, D 1 to D 5). PE: severe preeclampsia (plain line), NP: normal pregnancies (dashed line).

Techniques Used: Western Blot, Concentration Assay

A : Schematic representation of pre-mRNA exon-intron structure of VEGFR-2 (central shadowed box not at scale) with primers used to discriminate membrane bound VEGFR-2 mRNA (upper box, exon 13-exon 16; 634 bp) and soluble VEGFR-2 mRNA (lower box, exon 13-intron 13; 278 bp). B : Relative mRNA levels are expressed as arbitrary units (A.U.). NP: normal pregnancies, PE: severe preeclampsia. ** P <0.001 compared to NP group; ns: non-significant compared to NP group.
Figure Legend Snippet: A : Schematic representation of pre-mRNA exon-intron structure of VEGFR-2 (central shadowed box not at scale) with primers used to discriminate membrane bound VEGFR-2 mRNA (upper box, exon 13-exon 16; 634 bp) and soluble VEGFR-2 mRNA (lower box, exon 13-intron 13; 278 bp). B : Relative mRNA levels are expressed as arbitrary units (A.U.). NP: normal pregnancies, PE: severe preeclampsia. ** P <0.001 compared to NP group; ns: non-significant compared to NP group.

Techniques Used:

Placental villi from a normal pregnant women (A, C, E and F) and from a preeclamptic women (B–D): VEGFR-1 is expressed in the cytotrophoblasts, syncytiotrophoblasts (arrow) and also in some endothelial cells (white arrow head). VEGFR-2 is mainly localized in vascular endothelial cells (arrows) in placentas of both groups as identified by serial section immunostaining with CD31.
Figure Legend Snippet: Placental villi from a normal pregnant women (A, C, E and F) and from a preeclamptic women (B–D): VEGFR-1 is expressed in the cytotrophoblasts, syncytiotrophoblasts (arrow) and also in some endothelial cells (white arrow head). VEGFR-2 is mainly localized in vascular endothelial cells (arrows) in placentas of both groups as identified by serial section immunostaining with CD31.

Techniques Used: Immunostaining


Structured Review

R&D Systems mouse vegfr 2 elisa kit
The level of soluble <t>VEGFR-2</t> was evaluated in serum of SCID mice that were sacrificed on day 21 after injection of the OSC-19 cells. Rapamycin treatment significantly increased the level of soluble VEGFR-2 in serum of SCID mice (p = 0.0001; t-test). Serum samples from 9 control mice and 10 rapamycin-treated mice were evaluated.
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1) Product Images from "Anti-lymphangiogenic properties of mTOR inhibitors in head and neck squamous cell carcinoma experimental models"

Article Title: Anti-lymphangiogenic properties of mTOR inhibitors in head and neck squamous cell carcinoma experimental models

Journal: BMC Cancer

doi: 10.1186/1471-2407-13-320

The level of soluble VEGFR-2 was evaluated in serum of SCID mice that were sacrificed on day 21 after injection of the OSC-19 cells. Rapamycin treatment significantly increased the level of soluble VEGFR-2 in serum of SCID mice (p = 0.0001; t-test). Serum samples from 9 control mice and 10 rapamycin-treated mice were evaluated.
Figure Legend Snippet: The level of soluble VEGFR-2 was evaluated in serum of SCID mice that were sacrificed on day 21 after injection of the OSC-19 cells. Rapamycin treatment significantly increased the level of soluble VEGFR-2 in serum of SCID mice (p = 0.0001; t-test). Serum samples from 9 control mice and 10 rapamycin-treated mice were evaluated.

Techniques Used: Injection


Structured Review

R&D Systems vegfr 2
(a) The time-dependent phosphorylation of VEGFR-1 and <t>VEGFR-2</t> in keratinocytes induced by 10 J/cm 2 UVA. Cells were harvested 0, 2, 4, 8, 12, 24 h after irradiation. (b) The densitometric analysis of (a). (c) Top panel: The phosphorylation of VEGFR-1 in keratinocytes 12 h after treatmet of 10 J/cm 2 UVA with or without pre-incubation of VEGFR-1 neutralizing antibody (A-VEGFR-1, 5 µg/ml) for 1 h. Bottom panel: The phosphorylation of VEGFR-2 in keratinocytes 12 h after treatmet of 10 J/cm 2 UVA with or without pre-incubation of VEGFR-2 neutralizing antibody (A-VEGFR-2, 5 µg/ml) for 1 h. (d) The densitometric analysis of P-VEGFR-1 and P-VEGFR-2 in (c). The relative protein expression was normalized to the endogenous control GAPDH. NA, neutralizing antibody; P-VEGFR-1, phospho-VEGFR-1 (Y1213); P-VEGFR-2, phospho-VEGFR-2 (Tyr1175); UVA: UVA; * P <0.05; # P <0.01.
Vegfr 2, supplied by R&D Systems, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Role of VEGF Receptors in Normal and Psoriatic Human Keratinocytes: Evidence from Irradiation with Different UV Sources"

Article Title: Role of VEGF Receptors in Normal and Psoriatic Human Keratinocytes: Evidence from Irradiation with Different UV Sources

Journal: PLoS ONE

doi: 10.1371/journal.pone.0055463

(a) The time-dependent phosphorylation of VEGFR-1 and VEGFR-2 in keratinocytes induced by 10 J/cm 2 UVA. Cells were harvested 0, 2, 4, 8, 12, 24 h after irradiation. (b) The densitometric analysis of (a). (c) Top panel: The phosphorylation of VEGFR-1 in keratinocytes 12 h after treatmet of 10 J/cm 2 UVA with or without pre-incubation of VEGFR-1 neutralizing antibody (A-VEGFR-1, 5 µg/ml) for 1 h. Bottom panel: The phosphorylation of VEGFR-2 in keratinocytes 12 h after treatmet of 10 J/cm 2 UVA with or without pre-incubation of VEGFR-2 neutralizing antibody (A-VEGFR-2, 5 µg/ml) for 1 h. (d) The densitometric analysis of P-VEGFR-1 and P-VEGFR-2 in (c). The relative protein expression was normalized to the endogenous control GAPDH. NA, neutralizing antibody; P-VEGFR-1, phospho-VEGFR-1 (Y1213); P-VEGFR-2, phospho-VEGFR-2 (Tyr1175); UVA: UVA; * P <0.05; # P <0.01.
Figure Legend Snippet: (a) The time-dependent phosphorylation of VEGFR-1 and VEGFR-2 in keratinocytes induced by 10 J/cm 2 UVA. Cells were harvested 0, 2, 4, 8, 12, 24 h after irradiation. (b) The densitometric analysis of (a). (c) Top panel: The phosphorylation of VEGFR-1 in keratinocytes 12 h after treatmet of 10 J/cm 2 UVA with or without pre-incubation of VEGFR-1 neutralizing antibody (A-VEGFR-1, 5 µg/ml) for 1 h. Bottom panel: The phosphorylation of VEGFR-2 in keratinocytes 12 h after treatmet of 10 J/cm 2 UVA with or without pre-incubation of VEGFR-2 neutralizing antibody (A-VEGFR-2, 5 µg/ml) for 1 h. (d) The densitometric analysis of P-VEGFR-1 and P-VEGFR-2 in (c). The relative protein expression was normalized to the endogenous control GAPDH. NA, neutralizing antibody; P-VEGFR-1, phospho-VEGFR-1 (Y1213); P-VEGFR-2, phospho-VEGFR-2 (Tyr1175); UVA: UVA; * P <0.05; # P <0.01.

Techniques Used: Irradiation, Incubation, Expressing

(a) Expression and localization of VEGF165, VEGFR-1, VEGFR-2, NRP-1 and P-VEGFR-2 by immunofluorescence regulated by UVA in normal human epidermis. (b) The fluorescence density analysis of (a). Skin samples from 5 independent individuals were used for quantification. Biopsies were taken 24 h after treatment of 0, one MED, and three MEDs of UVA respectively. The presence of VEGF165 and VEGFRs was indicated by red fluorescence. The presence of P-VEGFR-2 was indicated by green fluorescence. The cellular nuclei were counterstained with DAPI (blue nuclear signal). P-VEGFR-2, phospho-VEGFR-2 (Tyr1175); UVA: UVA; MED, minimal erythema dose; NC, negative controls, which were incubated with non-immune mouse IgG. Bars: 50 µm; Asterisk, epidermis; Yellow triangle, dermis; * P <0.05; # P <0.01.
Figure Legend Snippet: (a) Expression and localization of VEGF165, VEGFR-1, VEGFR-2, NRP-1 and P-VEGFR-2 by immunofluorescence regulated by UVA in normal human epidermis. (b) The fluorescence density analysis of (a). Skin samples from 5 independent individuals were used for quantification. Biopsies were taken 24 h after treatment of 0, one MED, and three MEDs of UVA respectively. The presence of VEGF165 and VEGFRs was indicated by red fluorescence. The presence of P-VEGFR-2 was indicated by green fluorescence. The cellular nuclei were counterstained with DAPI (blue nuclear signal). P-VEGFR-2, phospho-VEGFR-2 (Tyr1175); UVA: UVA; MED, minimal erythema dose; NC, negative controls, which were incubated with non-immune mouse IgG. Bars: 50 µm; Asterisk, epidermis; Yellow triangle, dermis; * P <0.05; # P <0.01.

Techniques Used: Expressing, Immunofluorescence, Fluorescence, Incubation

(a) Western blotting detection of P-VEGFR-1 and P-VEGFR-2 in keratinocytes 12 h after treatment of 10 J/cm 2 UVA with or without pre-incubation of Go6976 (0.5 µM), or rottlerin (5.0 µM) for 1 h. (b) The densitometric analysis of P-VEGFR-1 and P-VEGFR-2 in UVA-treated groups in (a). (c) Western blotting detection of P-VEGFR-1 and P-VEGFR-2 in keratinocytes 12 h after treatment of 0 or 10 J/cm 2 UVA with or without 1 h pre-incubation of GF109203X (3 µM). (d) The densitometric analysis of P-VEGFR-1 and P-VEGFR-2 in UVA-treated groups in (c). (e) Western blotting detection of P-VEGFR-1 and P-VEGFR-2 in keratinocytes 12 h after treatment of 0 or 10 J/cm 2 UVA with or without 1 h pre-incubation of PP2 (10 µM). (f) The densitometric analysis of P-VEGFR-1 and P-VEGFR-2 in UVA-treated groups in (e). The relative expression was normalized to the endogenous control GAPDH. P-VEGFR-1, phospho-VEGFR-1 (Y1213); P-VEGFR-2, phospho-VEGFR-2 (Tyr1175); UVA: UVA; * P <0.05; # P <0.01.
Figure Legend Snippet: (a) Western blotting detection of P-VEGFR-1 and P-VEGFR-2 in keratinocytes 12 h after treatment of 10 J/cm 2 UVA with or without pre-incubation of Go6976 (0.5 µM), or rottlerin (5.0 µM) for 1 h. (b) The densitometric analysis of P-VEGFR-1 and P-VEGFR-2 in UVA-treated groups in (a). (c) Western blotting detection of P-VEGFR-1 and P-VEGFR-2 in keratinocytes 12 h after treatment of 0 or 10 J/cm 2 UVA with or without 1 h pre-incubation of GF109203X (3 µM). (d) The densitometric analysis of P-VEGFR-1 and P-VEGFR-2 in UVA-treated groups in (c). (e) Western blotting detection of P-VEGFR-1 and P-VEGFR-2 in keratinocytes 12 h after treatment of 0 or 10 J/cm 2 UVA with or without 1 h pre-incubation of PP2 (10 µM). (f) The densitometric analysis of P-VEGFR-1 and P-VEGFR-2 in UVA-treated groups in (e). The relative expression was normalized to the endogenous control GAPDH. P-VEGFR-1, phospho-VEGFR-1 (Y1213); P-VEGFR-2, phospho-VEGFR-2 (Tyr1175); UVA: UVA; * P <0.05; # P <0.01.

Techniques Used: Western Blot, Incubation, Expressing

(a) Keratinocytes were incubated with or without neutralizing antibodies against VEGFR-1 (A-VEGFR-1, 5 µg/ml) and VEGFR-2 (AVEGFR-2, 5 µg/ml) 24 h after treatment of 0 or 10 J/cm 2 UVA, and cell apoptosis rate was examined by flow cytometry. (b) Keratinocytes were incubated with neutralizing antibodies against VEGFR-1 (A-VEGFR-1, 5 µg/ml) and/or VEGFR-2 (A-VEGFR-2, 5 µg/ml) 24 h after treatment of 0 or 10 J/cm 2 UVA, and cell survival was determined by MTT assay. (c) Western blotting detection of cleaved-caspase-3 and Bcl-2 in keratinocytes treated by 10 J/cm2 UVA with or without incubation of VEGFR-1 neutralizing antibody (A-VEGFR-1, 5 µg/ml) or VEGFR-2 neutralizing antibody (A-VEGFR-2, 5 µg/ml) for 24 h. (d) Western blotting detection of phospho-ERK1/2 and phospho-Akt in keratinocytes 12 h after treatment of 10 J/cm 2 UVA with or without pre-incubation of VEGFR-1 neutralizing antibody (A-VEGFR-1, 5 µg/ml) or VEGFR-2 neutralizing antibody (A-VEGFR-2, 5 µg/ml) for 1 h. GAPDH was served as loading control for protein normalization, UVA: UVA; * P <0.05; # P <0.01.
Figure Legend Snippet: (a) Keratinocytes were incubated with or without neutralizing antibodies against VEGFR-1 (A-VEGFR-1, 5 µg/ml) and VEGFR-2 (AVEGFR-2, 5 µg/ml) 24 h after treatment of 0 or 10 J/cm 2 UVA, and cell apoptosis rate was examined by flow cytometry. (b) Keratinocytes were incubated with neutralizing antibodies against VEGFR-1 (A-VEGFR-1, 5 µg/ml) and/or VEGFR-2 (A-VEGFR-2, 5 µg/ml) 24 h after treatment of 0 or 10 J/cm 2 UVA, and cell survival was determined by MTT assay. (c) Western blotting detection of cleaved-caspase-3 and Bcl-2 in keratinocytes treated by 10 J/cm2 UVA with or without incubation of VEGFR-1 neutralizing antibody (A-VEGFR-1, 5 µg/ml) or VEGFR-2 neutralizing antibody (A-VEGFR-2, 5 µg/ml) for 24 h. (d) Western blotting detection of phospho-ERK1/2 and phospho-Akt in keratinocytes 12 h after treatment of 10 J/cm 2 UVA with or without pre-incubation of VEGFR-1 neutralizing antibody (A-VEGFR-1, 5 µg/ml) or VEGFR-2 neutralizing antibody (A-VEGFR-2, 5 µg/ml) for 1 h. GAPDH was served as loading control for protein normalization, UVA: UVA; * P <0.05; # P <0.01.

Techniques Used: Incubation, Flow Cytometry, MTT Assay, Western Blot

The times of phototherapy in relation to during and after therapy were 11.2±2.2 and 26.3±3.9, and the days of halomethasone treatment in relation to during and after therapy were 12.7±2.9 and 36.0±8.0. Biopsies were taken before, during, and after phototherapy respectively. The presence of VEGF165 and VEGFRs was indicated red. The presence of P-VEGFR-2 was indicated green. The cellular nuclei were counterstained with DAPI (blue nuclear signal). P-VEGFR-2, phospho-VEGFR-2 (Tyr1175); UVB, narrowband UVB therapy; HMS, topical halomethasone monohydrate 0.05% cream; NC, negative controls, which were incubated with non-immune mouse IgG. Bars: 100 µm; Asterisk, epidermis; Yellow triangle, dermis.
Figure Legend Snippet: The times of phototherapy in relation to during and after therapy were 11.2±2.2 and 26.3±3.9, and the days of halomethasone treatment in relation to during and after therapy were 12.7±2.9 and 36.0±8.0. Biopsies were taken before, during, and after phototherapy respectively. The presence of VEGF165 and VEGFRs was indicated red. The presence of P-VEGFR-2 was indicated green. The cellular nuclei were counterstained with DAPI (blue nuclear signal). P-VEGFR-2, phospho-VEGFR-2 (Tyr1175); UVB, narrowband UVB therapy; HMS, topical halomethasone monohydrate 0.05% cream; NC, negative controls, which were incubated with non-immune mouse IgG. Bars: 100 µm; Asterisk, epidermis; Yellow triangle, dermis.

Techniques Used: Incubation


Structured Review

R&D Systems vegfr 2
(a) The time-dependent phosphorylation of VEGFR-1 and <t>VEGFR-2</t> in keratinocytes induced by 10 J/cm 2 UVA. Cells were harvested 0, 2, 4, 8, 12, 24 h after irradiation. (b) The densitometric analysis of (a). (c) Top panel: The phosphorylation of VEGFR-1 in keratinocytes 12 h after treatmet of 10 J/cm 2 UVA with or without pre-incubation of VEGFR-1 neutralizing antibody (A-VEGFR-1, 5 µg/ml) for 1 h. Bottom panel: The phosphorylation of VEGFR-2 in keratinocytes 12 h after treatmet of 10 J/cm 2 UVA with or without pre-incubation of VEGFR-2 neutralizing antibody (A-VEGFR-2, 5 µg/ml) for 1 h. (d) The densitometric analysis of P-VEGFR-1 and P-VEGFR-2 in (c). The relative protein expression was normalized to the endogenous control GAPDH. NA, neutralizing antibody; P-VEGFR-1, phospho-VEGFR-1 (Y1213); P-VEGFR-2, phospho-VEGFR-2 (Tyr1175); UVA: UVA; * P <0.05; # P <0.01.
Vegfr 2, supplied by R&D Systems, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Images

1) Product Images from "Role of VEGF Receptors in Normal and Psoriatic Human Keratinocytes: Evidence from Irradiation with Different UV Sources"

Article Title: Role of VEGF Receptors in Normal and Psoriatic Human Keratinocytes: Evidence from Irradiation with Different UV Sources

Journal: PLoS ONE

doi: 10.1371/journal.pone.0055463

(a) The time-dependent phosphorylation of VEGFR-1 and VEGFR-2 in keratinocytes induced by 10 J/cm 2 UVA. Cells were harvested 0, 2, 4, 8, 12, 24 h after irradiation. (b) The densitometric analysis of (a). (c) Top panel: The phosphorylation of VEGFR-1 in keratinocytes 12 h after treatmet of 10 J/cm 2 UVA with or without pre-incubation of VEGFR-1 neutralizing antibody (A-VEGFR-1, 5 µg/ml) for 1 h. Bottom panel: The phosphorylation of VEGFR-2 in keratinocytes 12 h after treatmet of 10 J/cm 2 UVA with or without pre-incubation of VEGFR-2 neutralizing antibody (A-VEGFR-2, 5 µg/ml) for 1 h. (d) The densitometric analysis of P-VEGFR-1 and P-VEGFR-2 in (c). The relative protein expression was normalized to the endogenous control GAPDH. NA, neutralizing antibody; P-VEGFR-1, phospho-VEGFR-1 (Y1213); P-VEGFR-2, phospho-VEGFR-2 (Tyr1175); UVA: UVA; * P <0.05; # P <0.01.
Figure Legend Snippet: (a) The time-dependent phosphorylation of VEGFR-1 and VEGFR-2 in keratinocytes induced by 10 J/cm 2 UVA. Cells were harvested 0, 2, 4, 8, 12, 24 h after irradiation. (b) The densitometric analysis of (a). (c) Top panel: The phosphorylation of VEGFR-1 in keratinocytes 12 h after treatmet of 10 J/cm 2 UVA with or without pre-incubation of VEGFR-1 neutralizing antibody (A-VEGFR-1, 5 µg/ml) for 1 h. Bottom panel: The phosphorylation of VEGFR-2 in keratinocytes 12 h after treatmet of 10 J/cm 2 UVA with or without pre-incubation of VEGFR-2 neutralizing antibody (A-VEGFR-2, 5 µg/ml) for 1 h. (d) The densitometric analysis of P-VEGFR-1 and P-VEGFR-2 in (c). The relative protein expression was normalized to the endogenous control GAPDH. NA, neutralizing antibody; P-VEGFR-1, phospho-VEGFR-1 (Y1213); P-VEGFR-2, phospho-VEGFR-2 (Tyr1175); UVA: UVA; * P <0.05; # P <0.01.

Techniques Used: Irradiation, Incubation, Expressing

(a) Expression and localization of VEGF165, VEGFR-1, VEGFR-2, NRP-1 and P-VEGFR-2 by immunofluorescence regulated by UVA in normal human epidermis. (b) The fluorescence density analysis of (a). Skin samples from 5 independent individuals were used for quantification. Biopsies were taken 24 h after treatment of 0, one MED, and three MEDs of UVA respectively. The presence of VEGF165 and VEGFRs was indicated by red fluorescence. The presence of P-VEGFR-2 was indicated by green fluorescence. The cellular nuclei were counterstained with DAPI (blue nuclear signal). P-VEGFR-2, phospho-VEGFR-2 (Tyr1175); UVA: UVA; MED, minimal erythema dose; NC, negative controls, which were incubated with non-immune mouse IgG. Bars: 50 µm; Asterisk, epidermis; Yellow triangle, dermis; * P <0.05; # P <0.01.
Figure Legend Snippet: (a) Expression and localization of VEGF165, VEGFR-1, VEGFR-2, NRP-1 and P-VEGFR-2 by immunofluorescence regulated by UVA in normal human epidermis. (b) The fluorescence density analysis of (a). Skin samples from 5 independent individuals were used for quantification. Biopsies were taken 24 h after treatment of 0, one MED, and three MEDs of UVA respectively. The presence of VEGF165 and VEGFRs was indicated by red fluorescence. The presence of P-VEGFR-2 was indicated by green fluorescence. The cellular nuclei were counterstained with DAPI (blue nuclear signal). P-VEGFR-2, phospho-VEGFR-2 (Tyr1175); UVA: UVA; MED, minimal erythema dose; NC, negative controls, which were incubated with non-immune mouse IgG. Bars: 50 µm; Asterisk, epidermis; Yellow triangle, dermis; * P <0.05; # P <0.01.

Techniques Used: Expressing, Immunofluorescence, Fluorescence, Incubation

(a) Western blotting detection of P-VEGFR-1 and P-VEGFR-2 in keratinocytes 12 h after treatment of 10 J/cm 2 UVA with or without pre-incubation of Go6976 (0.5 µM), or rottlerin (5.0 µM) for 1 h. (b) The densitometric analysis of P-VEGFR-1 and P-VEGFR-2 in UVA-treated groups in (a). (c) Western blotting detection of P-VEGFR-1 and P-VEGFR-2 in keratinocytes 12 h after treatment of 0 or 10 J/cm 2 UVA with or without 1 h pre-incubation of GF109203X (3 µM). (d) The densitometric analysis of P-VEGFR-1 and P-VEGFR-2 in UVA-treated groups in (c). (e) Western blotting detection of P-VEGFR-1 and P-VEGFR-2 in keratinocytes 12 h after treatment of 0 or 10 J/cm 2 UVA with or without 1 h pre-incubation of PP2 (10 µM). (f) The densitometric analysis of P-VEGFR-1 and P-VEGFR-2 in UVA-treated groups in (e). The relative expression was normalized to the endogenous control GAPDH. P-VEGFR-1, phospho-VEGFR-1 (Y1213); P-VEGFR-2, phospho-VEGFR-2 (Tyr1175); UVA: UVA; * P <0.05; # P <0.01.
Figure Legend Snippet: (a) Western blotting detection of P-VEGFR-1 and P-VEGFR-2 in keratinocytes 12 h after treatment of 10 J/cm 2 UVA with or without pre-incubation of Go6976 (0.5 µM), or rottlerin (5.0 µM) for 1 h. (b) The densitometric analysis of P-VEGFR-1 and P-VEGFR-2 in UVA-treated groups in (a). (c) Western blotting detection of P-VEGFR-1 and P-VEGFR-2 in keratinocytes 12 h after treatment of 0 or 10 J/cm 2 UVA with or without 1 h pre-incubation of GF109203X (3 µM). (d) The densitometric analysis of P-VEGFR-1 and P-VEGFR-2 in UVA-treated groups in (c). (e) Western blotting detection of P-VEGFR-1 and P-VEGFR-2 in keratinocytes 12 h after treatment of 0 or 10 J/cm 2 UVA with or without 1 h pre-incubation of PP2 (10 µM). (f) The densitometric analysis of P-VEGFR-1 and P-VEGFR-2 in UVA-treated groups in (e). The relative expression was normalized to the endogenous control GAPDH. P-VEGFR-1, phospho-VEGFR-1 (Y1213); P-VEGFR-2, phospho-VEGFR-2 (Tyr1175); UVA: UVA; * P <0.05; # P <0.01.

Techniques Used: Western Blot, Incubation, Expressing

(a) Keratinocytes were incubated with or without neutralizing antibodies against VEGFR-1 (A-VEGFR-1, 5 µg/ml) and VEGFR-2 (AVEGFR-2, 5 µg/ml) 24 h after treatment of 0 or 10 J/cm 2 UVA, and cell apoptosis rate was examined by flow cytometry. (b) Keratinocytes were incubated with neutralizing antibodies against VEGFR-1 (A-VEGFR-1, 5 µg/ml) and/or VEGFR-2 (A-VEGFR-2, 5 µg/ml) 24 h after treatment of 0 or 10 J/cm 2 UVA, and cell survival was determined by MTT assay. (c) Western blotting detection of cleaved-caspase-3 and Bcl-2 in keratinocytes treated by 10 J/cm2 UVA with or without incubation of VEGFR-1 neutralizing antibody (A-VEGFR-1, 5 µg/ml) or VEGFR-2 neutralizing antibody (A-VEGFR-2, 5 µg/ml) for 24 h. (d) Western blotting detection of phospho-ERK1/2 and phospho-Akt in keratinocytes 12 h after treatment of 10 J/cm 2 UVA with or without pre-incubation of VEGFR-1 neutralizing antibody (A-VEGFR-1, 5 µg/ml) or VEGFR-2 neutralizing antibody (A-VEGFR-2, 5 µg/ml) for 1 h. GAPDH was served as loading control for protein normalization, UVA: UVA; * P <0.05; # P <0.01.
Figure Legend Snippet: (a) Keratinocytes were incubated with or without neutralizing antibodies against VEGFR-1 (A-VEGFR-1, 5 µg/ml) and VEGFR-2 (AVEGFR-2, 5 µg/ml) 24 h after treatment of 0 or 10 J/cm 2 UVA, and cell apoptosis rate was examined by flow cytometry. (b) Keratinocytes were incubated with neutralizing antibodies against VEGFR-1 (A-VEGFR-1, 5 µg/ml) and/or VEGFR-2 (A-VEGFR-2, 5 µg/ml) 24 h after treatment of 0 or 10 J/cm 2 UVA, and cell survival was determined by MTT assay. (c) Western blotting detection of cleaved-caspase-3 and Bcl-2 in keratinocytes treated by 10 J/cm2 UVA with or without incubation of VEGFR-1 neutralizing antibody (A-VEGFR-1, 5 µg/ml) or VEGFR-2 neutralizing antibody (A-VEGFR-2, 5 µg/ml) for 24 h. (d) Western blotting detection of phospho-ERK1/2 and phospho-Akt in keratinocytes 12 h after treatment of 10 J/cm 2 UVA with or without pre-incubation of VEGFR-1 neutralizing antibody (A-VEGFR-1, 5 µg/ml) or VEGFR-2 neutralizing antibody (A-VEGFR-2, 5 µg/ml) for 1 h. GAPDH was served as loading control for protein normalization, UVA: UVA; * P <0.05; # P <0.01.

Techniques Used: Incubation, Flow Cytometry, MTT Assay, Western Blot

The times of phototherapy in relation to during and after therapy were 11.2±2.2 and 26.3±3.9, and the days of halomethasone treatment in relation to during and after therapy were 12.7±2.9 and 36.0±8.0. Biopsies were taken before, during, and after phototherapy respectively. The presence of VEGF165 and VEGFRs was indicated red. The presence of P-VEGFR-2 was indicated green. The cellular nuclei were counterstained with DAPI (blue nuclear signal). P-VEGFR-2, phospho-VEGFR-2 (Tyr1175); UVB, narrowband UVB therapy; HMS, topical halomethasone monohydrate 0.05% cream; NC, negative controls, which were incubated with non-immune mouse IgG. Bars: 100 µm; Asterisk, epidermis; Yellow triangle, dermis.
Figure Legend Snippet: The times of phototherapy in relation to during and after therapy were 11.2±2.2 and 26.3±3.9, and the days of halomethasone treatment in relation to during and after therapy were 12.7±2.9 and 36.0±8.0. Biopsies were taken before, during, and after phototherapy respectively. The presence of VEGF165 and VEGFRs was indicated red. The presence of P-VEGFR-2 was indicated green. The cellular nuclei were counterstained with DAPI (blue nuclear signal). P-VEGFR-2, phospho-VEGFR-2 (Tyr1175); UVB, narrowband UVB therapy; HMS, topical halomethasone monohydrate 0.05% cream; NC, negative controls, which were incubated with non-immune mouse IgG. Bars: 100 µm; Asterisk, epidermis; Yellow triangle, dermis.

Techniques Used: Incubation


Structured Review

R&D Systems vegf vegfr 1 vegfr 2
The information of ten studies detecting <t> VEGF </t> level in serum.
Vegf Vegfr 1 Vegfr 2, supplied by R&D Systems, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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vegf vegfr 1 vegfr 2 - by Bioz Stars, 2023-02
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Images

1) Product Images from "Evaluation of Detection Methods and Values of Circulating Vascular Endothelial Growth Factor in Lung Cancer"

Article Title: Evaluation of Detection Methods and Values of Circulating Vascular Endothelial Growth Factor in Lung Cancer

Journal: Journal of Cancer

doi: 10.7150/jca.22020

The information of ten studies detecting  VEGF  level in serum.
Figure Legend Snippet: The information of ten studies detecting VEGF level in serum.

Techniques Used: Enzyme-linked Immunosorbent Assay

The information of sixteen studies detecting  VEGF  level in plasma.
Figure Legend Snippet: The information of sixteen studies detecting VEGF level in plasma.

Techniques Used: Enzyme-linked Immunosorbent Assay

The information of studies detecting  VEGF  level in sputum, MPE, and EBC.
Figure Legend Snippet: The information of studies detecting VEGF level in sputum, MPE, and EBC.

Techniques Used:

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    R&D Systems vegfr 2 kdr
    Representative flow cytometric density plots demonstrating the gating protocol used to identify angiogenic cells: A) PBMCs stained with PE-conjugated and APC-conjugated mouse IgG (isotype controls) for non-specific fluorescent signals; B) PBMCs stained with antibodies against human CD133 (AC133) (PE-conjugated) and <t>VEGFR-2</t> (KDR) (APC-conjugated) for AC133 + /KDR + PBMCs; A1, B1) FSC-SSC density dot plots of Ficoll-isolated PBMCs and R1 was gated for monocytes; A2, B2) FL2 (PE)-FL4 (APC) density dot plots of R1-gated monocytes. Angiogenic cells = cells in B2 upper-right quadrant – cells in A2 upper-right quadrant.
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    Inhibition of <t>VEGFR-2</t> RTK autophosphorylation by ABP 215, bevacizumab (US), and bevacizumab (EU).
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    Inhibition of <t>VEGFR-2</t> RTK autophosphorylation by ABP 215, bevacizumab (US), and bevacizumab (EU).
    Kdr Vegfr 2 Pe, supplied by R&D Systems, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Inhibition of <t>VEGFR-2</t> RTK autophosphorylation by ABP 215, bevacizumab (US), and bevacizumab (EU).
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    R&D Systems mouse anti human vegfr 2
    A , Prostatic LEC tube length at 4.5 hours post VEGF-C treatment was quantified using ImageJ. VEGF-C significantly increased the number of tubes formed compared to vehicle control. Data expressed as mean±s.e.m., n = 3, *** P <0.001 using One-way ANOVA, Bonferroni post-analysis. B , Western blotting analysis of <t>VEGFR-2</t> and VEGFR-3 expression in lung, neonatal dermis and prostate LECs. β-tubulin was used as a loading control.
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    R&D Systems vegfr 2 antibody
    A : Western blot analysis of VEGFR-1 and <t>VEGFR-2</t> from gestational age-matched normal pregnant women (NP, 1–5) and preeclamptic women (PE, 6–10). B : Maternal plasma concentration of VEGFR1, VEGFR2 and Eng (mean±SE, pg/ml) at inclusion (Incl), delivery (day 0, D 0) and during post partum (day 1 to day 5, D 1 to D 5). PE: severe preeclampsia (plain line), NP: normal pregnancies (dashed line).
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    R&D Systems mouse vegfr 2 elisa kit
    The level of soluble <t>VEGFR-2</t> was evaluated in serum of SCID mice that were sacrificed on day 21 after injection of the OSC-19 cells. Rapamycin treatment significantly increased the level of soluble VEGFR-2 in serum of SCID mice (p = 0.0001; t-test). Serum samples from 9 control mice and 10 rapamycin-treated mice were evaluated.
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    The information of ten studies detecting <t> VEGF </t> level in serum.
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    Representative flow cytometric density plots demonstrating the gating protocol used to identify angiogenic cells: A) PBMCs stained with PE-conjugated and APC-conjugated mouse IgG (isotype controls) for non-specific fluorescent signals; B) PBMCs stained with antibodies against human CD133 (AC133) (PE-conjugated) and VEGFR-2 (KDR) (APC-conjugated) for AC133 + /KDR + PBMCs; A1, B1) FSC-SSC density dot plots of Ficoll-isolated PBMCs and R1 was gated for monocytes; A2, B2) FL2 (PE)-FL4 (APC) density dot plots of R1-gated monocytes. Angiogenic cells = cells in B2 upper-right quadrant – cells in A2 upper-right quadrant.

    Journal: PLoS ONE

    Article Title: Increased Carotid Intima-Media Thickness and Reduced Distensibility in Human Class III Obesity: Independent and Differential Influences of Adiposity and Blood Pressure on the Vasculature

    doi: 10.1371/journal.pone.0053972

    Figure Lengend Snippet: Representative flow cytometric density plots demonstrating the gating protocol used to identify angiogenic cells: A) PBMCs stained with PE-conjugated and APC-conjugated mouse IgG (isotype controls) for non-specific fluorescent signals; B) PBMCs stained with antibodies against human CD133 (AC133) (PE-conjugated) and VEGFR-2 (KDR) (APC-conjugated) for AC133 + /KDR + PBMCs; A1, B1) FSC-SSC density dot plots of Ficoll-isolated PBMCs and R1 was gated for monocytes; A2, B2) FL2 (PE)-FL4 (APC) density dot plots of R1-gated monocytes. Angiogenic cells = cells in B2 upper-right quadrant – cells in A2 upper-right quadrant.

    Article Snippet: In brief, 100 µl of PBMCs (1.5×10 7 /ml) was incubated with Fc-γ receptor blocking agent followed by 30 min incubation on ice with antibodies against human CD133 (PE-conjugated, Miltenyi Biotec, Germany) and VEGFR-2 (KDR) (APC-conjugated, R&D Systems, USA).

    Techniques: Staining, Isolation

    Inhibition of VEGFR-2 RTK autophosphorylation by ABP 215, bevacizumab (US), and bevacizumab (EU).

    Journal: mAbs

    Article Title: Analytical and functional similarity of Amgen biosimilar ABP 215 to bevacizumab

    doi: 10.1080/19420862.2018.1452580

    Figure Lengend Snippet: Inhibition of VEGFR-2 RTK autophosphorylation by ABP 215, bevacizumab (US), and bevacizumab (EU).

    Article Snippet: VEGFR-2 was captured from the lysate onto streptavidin-coated Mesoscale Discovery (MSD, Cat. No. L15SA) plates using a biotinylated antibody against the extracellular portion of VEGFR-2 (R&D Systems, Cat. No. 05–321).

    Techniques: Inhibition

    A , Prostatic LEC tube length at 4.5 hours post VEGF-C treatment was quantified using ImageJ. VEGF-C significantly increased the number of tubes formed compared to vehicle control. Data expressed as mean±s.e.m., n = 3, *** P <0.001 using One-way ANOVA, Bonferroni post-analysis. B , Western blotting analysis of VEGFR-2 and VEGFR-3 expression in lung, neonatal dermis and prostate LECs. β-tubulin was used as a loading control.

    Journal: PLoS ONE

    Article Title: Vascular Endothelial Growth Factor Receptor-3 Directly Interacts with Phosphatidylinositol 3-Kinase to Regulate Lymphangiogenesis

    doi: 10.1371/journal.pone.0039558

    Figure Lengend Snippet: A , Prostatic LEC tube length at 4.5 hours post VEGF-C treatment was quantified using ImageJ. VEGF-C significantly increased the number of tubes formed compared to vehicle control. Data expressed as mean±s.e.m., n = 3, *** P <0.001 using One-way ANOVA, Bonferroni post-analysis. B , Western blotting analysis of VEGFR-2 and VEGFR-3 expression in lung, neonatal dermis and prostate LECs. β-tubulin was used as a loading control.

    Article Snippet: The other antibodies used were: anti-phospho PI3K p85 (Tyr458/p55 Tyr199; Cat. no. 4228; Millipore, MA) and total PI3K p85 (Cat. no. 06–19; Millipore); mouse anti-human CD31 (Clone: JC70A, Cat. no. M0823; DAKO, Denmark); mouse anti-human podoplanin (Clone: D2-40, Cat. no. 730-23; Signet Laboratories, MA); mouse anti-human VEGFR-2 (Cat. no. AF357; R&D Systems, MN), goat anti-human VEGFR-3 (Cat. no. AF349; R&D Systems); mouse anti-human pan-actin (Clone: Ab-5, NeoMarkers, CA); Alexa Fluor 488- and 568-conjugated secondary antibodies (Invitrogen, CA), and IRDye700DX conjugated anti-mouse IgG and IRDye800CW conjugated anti-rabbit IgG (Rockland Immunochemicals, PA).

    Techniques: Western Blot, Expressing

    . A , Western blotting analysis of phosphorylated Akt (S473) in prostatic LECs following a 15 minute ligand stimulation: VEGF-A (100 ng/ml), VEGF-C (100 ng/ml), VEGF-C156S (250 ng/ml), VEGF-D (250 ng/ml) and VEGF-E (100 ng/ml). B , Time course for Akt phosphorylation (S473) in LECs after VEGF-C (100 ng/ml) stimulation. C , Concentration-dependent phosphorylation of LEC Akt (S473) following 15 minute stimulation with VEGF-C or VEGF-C156S. D , Effect of inhibition of VEGFR-3 (hF4-3C5), VEGFR-2 (IMC-1121b) or VEGFR-1 (IMC-18F1) on LEC Akt (S473) phosphorylation in response to VEGF-C (100 ng/ml). E , Effect of inhibition of PI3K (AS252424, LY294002) or Raf/MEK (PD98059) on Akt (S473) phosphorylation in LECs in response to VEGF-C (100 ng/ml). Serum-free vehicle treated LEC lysate is indicated by ‘0′ in all blots. n = 3. Densitometry analysis is shown for each blot either italicized or graphed; where integrated intensity of phosphorylated molecules was firstly compared to that of the total target protein for each sample, and then expressed as fold increase in integrated density compared to VEGF-C treated control samples. P value calculated using one-way ANOVA. For panels A-B data is compared to time-point zero; panels D-E data is compared to VEGF-C treated control, except where indicated for serum free/VEGF-C treatment comparison. Columns: mean; bars: s.e.m.; P<0.05 (*), P<0.01 (**); P<0.001 (***).

    Journal: PLoS ONE

    Article Title: Vascular Endothelial Growth Factor Receptor-3 Directly Interacts with Phosphatidylinositol 3-Kinase to Regulate Lymphangiogenesis

    doi: 10.1371/journal.pone.0039558

    Figure Lengend Snippet: . A , Western blotting analysis of phosphorylated Akt (S473) in prostatic LECs following a 15 minute ligand stimulation: VEGF-A (100 ng/ml), VEGF-C (100 ng/ml), VEGF-C156S (250 ng/ml), VEGF-D (250 ng/ml) and VEGF-E (100 ng/ml). B , Time course for Akt phosphorylation (S473) in LECs after VEGF-C (100 ng/ml) stimulation. C , Concentration-dependent phosphorylation of LEC Akt (S473) following 15 minute stimulation with VEGF-C or VEGF-C156S. D , Effect of inhibition of VEGFR-3 (hF4-3C5), VEGFR-2 (IMC-1121b) or VEGFR-1 (IMC-18F1) on LEC Akt (S473) phosphorylation in response to VEGF-C (100 ng/ml). E , Effect of inhibition of PI3K (AS252424, LY294002) or Raf/MEK (PD98059) on Akt (S473) phosphorylation in LECs in response to VEGF-C (100 ng/ml). Serum-free vehicle treated LEC lysate is indicated by ‘0′ in all blots. n = 3. Densitometry analysis is shown for each blot either italicized or graphed; where integrated intensity of phosphorylated molecules was firstly compared to that of the total target protein for each sample, and then expressed as fold increase in integrated density compared to VEGF-C treated control samples. P value calculated using one-way ANOVA. For panels A-B data is compared to time-point zero; panels D-E data is compared to VEGF-C treated control, except where indicated for serum free/VEGF-C treatment comparison. Columns: mean; bars: s.e.m.; P<0.05 (*), P<0.01 (**); P<0.001 (***).

    Article Snippet: The other antibodies used were: anti-phospho PI3K p85 (Tyr458/p55 Tyr199; Cat. no. 4228; Millipore, MA) and total PI3K p85 (Cat. no. 06–19; Millipore); mouse anti-human CD31 (Clone: JC70A, Cat. no. M0823; DAKO, Denmark); mouse anti-human podoplanin (Clone: D2-40, Cat. no. 730-23; Signet Laboratories, MA); mouse anti-human VEGFR-2 (Cat. no. AF357; R&D Systems, MN), goat anti-human VEGFR-3 (Cat. no. AF349; R&D Systems); mouse anti-human pan-actin (Clone: Ab-5, NeoMarkers, CA); Alexa Fluor 488- and 568-conjugated secondary antibodies (Invitrogen, CA), and IRDye700DX conjugated anti-mouse IgG and IRDye800CW conjugated anti-rabbit IgG (Rockland Immunochemicals, PA).

    Techniques: Western Blot, Concentration Assay, Inhibition

    Western blotting analysis of phosphorylated P70S6K ( A, top left ) and eNOS (S1177) ( B, top left ) in prostatic LECs following 15 minute stimulation with ligand: VEGF-C (100 ng/ml), VEGF-A (100 ng/ml), VEGF-C156S (250 ng/ml), VEGF-D (250 ng/ml) and VEGF-E (100 ng/ml). Time- and concentration-dependent phosphorylation of P70S6K ( A, top right ), eNOS (S1177) ( B, top right ), and PLCγ1 (Tyr783) ( C, top left ) in LECs in response to VEGF-C. The effect of inhibition of VEGFR-3 (hF4-3C5), VEGFR-2 (IMC-1121b) or VEGFR-1 (IMC-18F1) on phosphorylation of P70S6K ( A, bottom left ), eNOS (S1177) ( B, bottom left ); and VEGFR-3 (hF4-3C5) on PLCγ1 (Tyr783) ( C, bottom right ) on LEC response to VEGF-C (100 ng/ml). The effect of AS252424, LY294002, PD98059, and U-73122 on phosphorylation of P70S6K ( A, top right ), eNOS (S1177) ( B, bottom right ), and PLCγ1 (Tyr783) ( C, bottom right ) on LECs in response to VEGF-C. The effect of VEGF-C on phosphorylation of PLCγ2 (Tyr759, Tyr1217) in LECs ( C, bottom left ). Control serum-free vehicle treated LEC lysate is indicated by ‘0′ in all blots. n = 3. Densitometry analysis is shown under each blot in italics; where integrated intensity of phosphorylated molecules was firstly compared to that of the total target protein for each sample, and then expressed as fold change in integrated density compared to either serum-free (A, top left and right panels ; B, top left and right panels ; C, top and bottom left panels ) or VEGF-C treated control samples (A, bottom left and right panels ; B, bottom left and right panels ; C, bottom and bottom left panels ).

    Journal: PLoS ONE

    Article Title: Vascular Endothelial Growth Factor Receptor-3 Directly Interacts with Phosphatidylinositol 3-Kinase to Regulate Lymphangiogenesis

    doi: 10.1371/journal.pone.0039558

    Figure Lengend Snippet: Western blotting analysis of phosphorylated P70S6K ( A, top left ) and eNOS (S1177) ( B, top left ) in prostatic LECs following 15 minute stimulation with ligand: VEGF-C (100 ng/ml), VEGF-A (100 ng/ml), VEGF-C156S (250 ng/ml), VEGF-D (250 ng/ml) and VEGF-E (100 ng/ml). Time- and concentration-dependent phosphorylation of P70S6K ( A, top right ), eNOS (S1177) ( B, top right ), and PLCγ1 (Tyr783) ( C, top left ) in LECs in response to VEGF-C. The effect of inhibition of VEGFR-3 (hF4-3C5), VEGFR-2 (IMC-1121b) or VEGFR-1 (IMC-18F1) on phosphorylation of P70S6K ( A, bottom left ), eNOS (S1177) ( B, bottom left ); and VEGFR-3 (hF4-3C5) on PLCγ1 (Tyr783) ( C, bottom right ) on LEC response to VEGF-C (100 ng/ml). The effect of AS252424, LY294002, PD98059, and U-73122 on phosphorylation of P70S6K ( A, top right ), eNOS (S1177) ( B, bottom right ), and PLCγ1 (Tyr783) ( C, bottom right ) on LECs in response to VEGF-C. The effect of VEGF-C on phosphorylation of PLCγ2 (Tyr759, Tyr1217) in LECs ( C, bottom left ). Control serum-free vehicle treated LEC lysate is indicated by ‘0′ in all blots. n = 3. Densitometry analysis is shown under each blot in italics; where integrated intensity of phosphorylated molecules was firstly compared to that of the total target protein for each sample, and then expressed as fold change in integrated density compared to either serum-free (A, top left and right panels ; B, top left and right panels ; C, top and bottom left panels ) or VEGF-C treated control samples (A, bottom left and right panels ; B, bottom left and right panels ; C, bottom and bottom left panels ).

    Article Snippet: The other antibodies used were: anti-phospho PI3K p85 (Tyr458/p55 Tyr199; Cat. no. 4228; Millipore, MA) and total PI3K p85 (Cat. no. 06–19; Millipore); mouse anti-human CD31 (Clone: JC70A, Cat. no. M0823; DAKO, Denmark); mouse anti-human podoplanin (Clone: D2-40, Cat. no. 730-23; Signet Laboratories, MA); mouse anti-human VEGFR-2 (Cat. no. AF357; R&D Systems, MN), goat anti-human VEGFR-3 (Cat. no. AF349; R&D Systems); mouse anti-human pan-actin (Clone: Ab-5, NeoMarkers, CA); Alexa Fluor 488- and 568-conjugated secondary antibodies (Invitrogen, CA), and IRDye700DX conjugated anti-mouse IgG and IRDye800CW conjugated anti-rabbit IgG (Rockland Immunochemicals, PA).

    Techniques: Western Blot, Concentration Assay, Inhibition

    A : Western blot analysis of VEGFR-1 and VEGFR-2 from gestational age-matched normal pregnant women (NP, 1–5) and preeclamptic women (PE, 6–10). B : Maternal plasma concentration of VEGFR1, VEGFR2 and Eng (mean±SE, pg/ml) at inclusion (Incl), delivery (day 0, D 0) and during post partum (day 1 to day 5, D 1 to D 5). PE: severe preeclampsia (plain line), NP: normal pregnancies (dashed line).

    Journal: PLoS ONE

    Article Title: Differential Expression of Vegfr-2 and Its Soluble Form in Preeclampsia

    doi: 10.1371/journal.pone.0033475

    Figure Lengend Snippet: A : Western blot analysis of VEGFR-1 and VEGFR-2 from gestational age-matched normal pregnant women (NP, 1–5) and preeclamptic women (PE, 6–10). B : Maternal plasma concentration of VEGFR1, VEGFR2 and Eng (mean±SE, pg/ml) at inclusion (Incl), delivery (day 0, D 0) and during post partum (day 1 to day 5, D 1 to D 5). PE: severe preeclampsia (plain line), NP: normal pregnancies (dashed line).

    Article Snippet: After being washed, the membranes were incubated overnight at 4°C with either the VEGFR-2 antibody (AF357, diluted 1∶500, R&D Systems) or the VEGFR-1 antibody (AF321, diluted 1∶500, R&D Systems) in TBS-T containing 1% BSA.

    Techniques: Western Blot, Concentration Assay

    A : Schematic representation of pre-mRNA exon-intron structure of VEGFR-2 (central shadowed box not at scale) with primers used to discriminate membrane bound VEGFR-2 mRNA (upper box, exon 13-exon 16; 634 bp) and soluble VEGFR-2 mRNA (lower box, exon 13-intron 13; 278 bp). B : Relative mRNA levels are expressed as arbitrary units (A.U.). NP: normal pregnancies, PE: severe preeclampsia. ** P <0.001 compared to NP group; ns: non-significant compared to NP group.

    Journal: PLoS ONE

    Article Title: Differential Expression of Vegfr-2 and Its Soluble Form in Preeclampsia

    doi: 10.1371/journal.pone.0033475

    Figure Lengend Snippet: A : Schematic representation of pre-mRNA exon-intron structure of VEGFR-2 (central shadowed box not at scale) with primers used to discriminate membrane bound VEGFR-2 mRNA (upper box, exon 13-exon 16; 634 bp) and soluble VEGFR-2 mRNA (lower box, exon 13-intron 13; 278 bp). B : Relative mRNA levels are expressed as arbitrary units (A.U.). NP: normal pregnancies, PE: severe preeclampsia. ** P <0.001 compared to NP group; ns: non-significant compared to NP group.

    Article Snippet: After being washed, the membranes were incubated overnight at 4°C with either the VEGFR-2 antibody (AF357, diluted 1∶500, R&D Systems) or the VEGFR-1 antibody (AF321, diluted 1∶500, R&D Systems) in TBS-T containing 1% BSA.

    Techniques:

    Placental villi from a normal pregnant women (A, C, E and F) and from a preeclamptic women (B–D): VEGFR-1 is expressed in the cytotrophoblasts, syncytiotrophoblasts (arrow) and also in some endothelial cells (white arrow head). VEGFR-2 is mainly localized in vascular endothelial cells (arrows) in placentas of both groups as identified by serial section immunostaining with CD31.

    Journal: PLoS ONE

    Article Title: Differential Expression of Vegfr-2 and Its Soluble Form in Preeclampsia

    doi: 10.1371/journal.pone.0033475

    Figure Lengend Snippet: Placental villi from a normal pregnant women (A, C, E and F) and from a preeclamptic women (B–D): VEGFR-1 is expressed in the cytotrophoblasts, syncytiotrophoblasts (arrow) and also in some endothelial cells (white arrow head). VEGFR-2 is mainly localized in vascular endothelial cells (arrows) in placentas of both groups as identified by serial section immunostaining with CD31.

    Article Snippet: After being washed, the membranes were incubated overnight at 4°C with either the VEGFR-2 antibody (AF357, diluted 1∶500, R&D Systems) or the VEGFR-1 antibody (AF321, diluted 1∶500, R&D Systems) in TBS-T containing 1% BSA.

    Techniques: Immunostaining

    The level of soluble VEGFR-2 was evaluated in serum of SCID mice that were sacrificed on day 21 after injection of the OSC-19 cells. Rapamycin treatment significantly increased the level of soluble VEGFR-2 in serum of SCID mice (p = 0.0001; t-test). Serum samples from 9 control mice and 10 rapamycin-treated mice were evaluated.

    Journal: BMC Cancer

    Article Title: Anti-lymphangiogenic properties of mTOR inhibitors in head and neck squamous cell carcinoma experimental models

    doi: 10.1186/1471-2407-13-320

    Figure Lengend Snippet: The level of soluble VEGFR-2 was evaluated in serum of SCID mice that were sacrificed on day 21 after injection of the OSC-19 cells. Rapamycin treatment significantly increased the level of soluble VEGFR-2 in serum of SCID mice (p = 0.0001; t-test). Serum samples from 9 control mice and 10 rapamycin-treated mice were evaluated.

    Article Snippet: The effects of rapamycin treatment on serum levels of soluble VEGFR-2 in mouse serum samples were determined using a mouse VEGFR-2 ELISA kit (R&D Systems, Minneapolis, MN) according to manufacturer's instructions.

    Techniques: Injection

    The information of ten studies detecting  VEGF  level in serum.

    Journal: Journal of Cancer

    Article Title: Evaluation of Detection Methods and Values of Circulating Vascular Endothelial Growth Factor in Lung Cancer

    doi: 10.7150/jca.22020

    Figure Lengend Snippet: The information of ten studies detecting VEGF level in serum.

    Article Snippet: Tony Mok , Asia Caucasian , 303 , Protective Multicenter Randomized , ELISA(R&D Systems Minneapolis, MN) , Microplate reader (Bio-Tek Elx 800) , VEGF,VEGFR-1,VEGFR-2,bFGF,ICAM,PlGF, E-selection , 0, every 6week , IIIB-IV /NSCLC , Chemotherapy.

    Techniques: Enzyme-linked Immunosorbent Assay

    The information of sixteen studies detecting  VEGF  level in plasma.

    Journal: Journal of Cancer

    Article Title: Evaluation of Detection Methods and Values of Circulating Vascular Endothelial Growth Factor in Lung Cancer

    doi: 10.7150/jca.22020

    Figure Lengend Snippet: The information of sixteen studies detecting VEGF level in plasma.

    Article Snippet: Tony Mok , Asia Caucasian , 303 , Protective Multicenter Randomized , ELISA(R&D Systems Minneapolis, MN) , Microplate reader (Bio-Tek Elx 800) , VEGF,VEGFR-1,VEGFR-2,bFGF,ICAM,PlGF, E-selection , 0, every 6week , IIIB-IV /NSCLC , Chemotherapy.

    Techniques: Enzyme-linked Immunosorbent Assay

    The information of studies detecting  VEGF  level in sputum, MPE, and EBC.

    Journal: Journal of Cancer

    Article Title: Evaluation of Detection Methods and Values of Circulating Vascular Endothelial Growth Factor in Lung Cancer

    doi: 10.7150/jca.22020

    Figure Lengend Snippet: The information of studies detecting VEGF level in sputum, MPE, and EBC.

    Article Snippet: Tony Mok , Asia Caucasian , 303 , Protective Multicenter Randomized , ELISA(R&D Systems Minneapolis, MN) , Microplate reader (Bio-Tek Elx 800) , VEGF,VEGFR-1,VEGFR-2,bFGF,ICAM,PlGF, E-selection , 0, every 6week , IIIB-IV /NSCLC , Chemotherapy.

    Techniques: