anti vegfr1 ab (R&D Systems)
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anti vegfr1 ab
Anti Vegfr1 Ab, supplied by R&D Systems, 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/1663/VEGFR1%2FR2%2FR3+Antibody+(FLT1%2F1663)/pm22653973-34-13-18
Average 90 stars, based on 1 article reviews
Anti Vegfr1 Ab, supplied by R&D Systems, 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/1663/VEGFR1%2FR2%2FR3+Antibody+(FLT1%2F1663)/pm22653973-34-13-18
Average 90 stars, based on 1 article reviews
anti vegfr1 ab - by Bioz Stars,
2026-10
90/100 stars
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1) Product Images from "VEGFR1 stimulates a CXCR4-dependent translocation of megakaryocytes to the vascular niche, enhancing platelet production in mice."
Article Title: VEGFR1 stimulates a CXCR4-dependent translocation of megakaryocytes to the vascular niche, enhancing platelet production in mice.
Journal: Blood
doi: 10.1182/blood-2011-09-378174
Figure Legend Snippet: Figure 1. VEGFR1 stimulation, but not VEGFR2 stimu- lation, is responsible VEGF-A165–induced thrombocy- tosis. (A-B) Mice were administered either VEGF-A165 (100 g/kg intraperitoneally), PlGF-2, VEGF-E (100 g/kg intraperitoneally), or vehicle (PBS) each day for 4 con- secutive days. (A) Some groups of mice receiving the 4-day VEGF-A165 regimen were also administered block- ing Abs to either VEGFR1, VEGFR2, VEGFR1&2, or control IgG 20 minutes before VEGF-A165 administration on days 1 and 3. Enumeration of circulating platelets was then conducted 24 hours after last growth factor adminis- tration. Bone marrow or spleens were also harvested, and MKs were identified by flow cytometry via forward and side scatter and CD41 expression. (C) Percentage of MKs expressing VEGFR1 and VEGFR2 in vehicle con- trol–treated mice. (D) The number of MKs per million cells from bone marrow or spleen; n 5-6 animals per group. Data are expressed as mean SEM; *P .05; ***P .001 compared with control or as indicated.
Techniques Used: Blocking Assay, Control, Cytometry, Expressing
Figure Legend Snippet: Figure 2. Effect of VEGFR1 and VEGFR2 stimulation on MK maturation. Mice were administered either VEGF-A165 (100 g/kg intraperitoneally), PlGF-2, VEGF-E (100 g/kg intraperitoneally), or vehicle (PBS) each day for 4 consecutive days. (A-B) Representative histograms of CD41 MKs stained with TOPRO-3 revealing respective peaks of increasing DNA ploidy number. (A) CD41 MKs with 2n, and (B) 2n peak subtracted to reveal 4n to 128n. (C) Percentage of bone marrow and splenic MKs with a ploidy number of 16n or greater in mice administered either VEGF-A165, PlGF-2, or VEGF-E. (D) Histogram revealing spread of bone marrow MK ploidy above 16n in mice administered either VEGF-A165, PlGF-2, or VEGF-E; n 5-6 animals per group. Data are expressed as mean SEM; *P .05 com- pared with control.
Techniques Used: Staining, Control
Figure Legend Snippet: Figure 5. VEGFR1 increases MK migration to vascu- lar niche via a CXCR4-dependent process. Mice were administered either VEGF-A165, PlGF-2, VEGF-E (100 g/kg intraperitoneally), or vehicle (PBS) each day for 4 consecutive days before bone marrow and spleens were harvested 24 hours later. (A) Percentage of CD41
Techniques Used: Migration
Figure Legend Snippet: Figure 4. VEGFR1 stimulation redistributes MKs to the vascular niche. Mice were administered either VEGF-A165, PlGF-2, VEGF-E (100 g/kg intraperitoneally), or vehicle (PBS) each day for 4 consecutive days before femurs were excised for bone marrow histology. (A) Quantification of MKs per field of view, and (B) quantification of the number of MKs adjacent to sinusoidal vessels; n 5-6 animals per group. Data are expressed as mean SEM; ***P .001 compared with control.
Techniques Used: Control
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![SUP physically interacts with TPL through its EAR motif (DLELRL). ( A ) Yeast two-hybrid assays testing interaction between TPL [fused to the <t>GAL4</t> DNA-binding domain (DBD)] and wild-type SUP (DLELRL), mSUP (DLE A R A ) or mSUP (DLE G R G ) [each fused to the <t>GAL4</t> <t>activation</t> <t>domain</t> (AD)]. Growth on selection (right panel) detects a physical interaction between TPL and wild-type SUP (DLELRL) only. ( B ) In vitro pull-down assays using GST-tagged N-TPL show a strong interaction with SBP-tagged wild-type SUP (DLELRL) that is weakened by mutation of the EAR motif in SUP (DLE A R A ). Ponceau S staining shows efficient GST protein expression. Full-length blots and quantification of Western blot signal intensities are presented in Supplementary Fig. S3](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_5690/pmc12595690/pmc12595690__12870_2025_7553_Fig2_HTML.jpg)
![CRISPR-generated EAR mutations disrupt physical interaction between SUP and TPL. ( A ) Yeast two-hybrid assays testing interaction between TPL [fused to the GAL4 DNA-binding domain (DBD)] and wild-type SUP (DLELRL), mSUP (DLELL) or mSUP (∆EAR) [each fused to the GAL4 activation domain (AD)]. Growth on selection (right panel) indicates physical interaction between TPL and wild-type SUP (DLELRL) only. ( B ) In vitro pull-down assays using GST-tagged N-TPL show a strong interaction with SBP-tagged wild-type SUP (DLELRL) which is weakened by mutation of the EAR motif in CRISPR allele mSUP (DLELL). Ponceau S staining shows efficient GST protein expression. Full-length blots and quantification of Western blot signal intensities are presented in Supplementary Fig. S7](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_5690/pmc12595690/pmc12595690__12870_2025_7553_Fig5_HTML.jpg)