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gene exp eng mm00468252 m1  (Thermo Fisher)
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Thermo Fisher gene exp eng mm00468252 m1
Gene Exp Eng Mm00468252 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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vasculife engs endothelial medium complete kit  (Lifeline Cell Technology)
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Lifeline Cell Technology vasculife engs endothelial medium complete kit
Vasculife Engs Endothelial Medium Complete Kit, supplied by Lifeline Cell Technology, 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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anti endoglin  (OriGene)
90
OriGene anti endoglin
(A) , Wild-type (WT) and KI mice HTRZ for either PS1 FAD mutant M146V (WT/M146V) or I213T (WT/I213T) were infused with vehicle (0.2% BSA in PBS) or VEGF-A (a total of 3.5μg in 100μl of vehicle) through the carotid artery for 15 days using a mini osmotic pump as in Methods. Left: Brain coronal sections (40μm thick) were prepared and immunostained with anti-Col IV antibodies to visualize brain vessels. Enhanced visualization surfaces were generated using Imaris software from representative confocal images of ipsilateral hemispheres. Scale bar: 50μm. Right: Graph shows total vessel length density in WT and PS1 FAD brains quantified using Imaris 9.9 software as in Methods. (B) , WT and HTRZ for PS1 FAD mutants M146V or I213T mice were injected through the carotid artery for 20 minutes with either vehicle or 100ng of VEGF-A in vehicle prepared as in 1A using a catheter as described in Methods. Brain microvessels (MV) were isolated as in Methods, lysed in Triton X-100 buffer, and subjected to immunoprecipitation (IP) with anti-VEGFR2 antibody or control IgG. Left: IPs were analyzed on Western blots (WBs) <t>using</t> <t>anti-endoglin</t> or anti-VEGFR2 antibodies (upper panel). Input samples are shown in lower panel. β-actin: loading control. Right: Graph shows quantification of endoglin co-IPed with VEGFR2, normalized to IPed VEGFR2. (C) , WT mice were infused for 15 days through the carotid artery with vehicle or VEGF-A in vehicle as in 1A using a mini osmotic pump (as in 1A). For RO injection, mice were treated with vehicle (2% DMSO, 30% PEG 300, 5% Tween-80 in ddH2O) or RO in vehicle (5mg/kg body weight) via five injections in tail vein one injection every three days, with first injection administered 1 hour before osmotic pump implantation. Brain coronal sections (40μm) were prepared and immunostained with anti-Col IV antibodies as in 1A. Left: Representative confocal images of ipsilateral hemispheres are shown prepared as in 1A. Scale bar: 50μm. Right: Graph shows total vessel length density quantified using Imaris software as in 1A. (D) , WT adult mice were treated with either 50μl vehicle as in 1C or 1mg/kg RO in vehicle via carotid artery as in Methods. 15-16 hrs later, 50 μl vehicle prepared as in 1A or 100ng VEGF-A in vehicle was administered via carotid artery for 10-20 minutes using a catheter as in 1B. Brain MVs were isolated and extracted as in 1B. Left: p-VEGFR2 (Tyr1054/Tyr1059), VEGFR2, p-ERK1/2 and ERK1/2 are detected on WBs of extracts with specific antibodies in MV extracts. Vinculin: loading control. Right: Graphs show fold change of phosphorylated to total protein ratio. (E) , WT mice and mice HTRZ for PS1 FAD mutant M146V (WT/M146V) or I213T (WT/I213T) were treated with vehicle or VEGF-A via carotid artery for 10-20 minutes using a catheter as in 1D. Brain MVs were isolated and extracted as in 1B. Left: p-VEGFR2 (Tyr1054/Tyr1059), VEGFR2, p-ERK1/2 and ERK1/2 are detected on WBs of extracts with specific antibodies in MV extracts. β-actin: loading control. Right: Graphs show fold change of phosphorylated to total protein ratio. (F) , WT pCECs were prepared and treated as in Methods with vehicle (DMSO) or RO (200nM in DMSO) and then stimulated with either vehicle (PBS) or VEGF-A (20ng in PBS) for 15min. Upper: Cells were co-immunostained with either anti-VEGFR2 antibodies (green) or early endosome marker Rab5 (red) and cell nuclei were stained with Hoechst (blue) as in Methods. Yellow fluorescence in merged images indicates co-localization of VEGFR2 with Rab5. Scale bar 0.5μm. Lower: Graph shows percent of VEGFR2 co-localized with Rab5 in RO-treated WT cells compared to vehicle-treated cells measured with Imaris software. (G) , pCECs from either WT or mice HTRZ for PS1 FAD mutant M146V (WT/M146V) or I213T (WT/I213T), were stimulated with vehicle or VEGF-A in vehicle as in 1F. Upper: Cells were co-stained with anti-VEGFR2 antibodies and early endosome marker Rab5 as in 1F. Cell nuclei were stained with Hoechst (blue) as in 1F. Yellow fluorescence in merged images indicates co-localization of VEGFR2 with Rab5. Scale bar 0.5μm. Lower: Graph shows percent of VEGFR2 co-localized with Rab5 in PS1 FAD WT/M146V or WT/I213T HTRZ mice compared to WT measured with Imaris software. For Figs A-G, data are shown as Mean ± S.E. from at least three independent experiments or as indicated in the dot plots. Statistical analysis was performed using two-way ANOVA followed by Tukey post-hoc test. ns = not significant, *p<0.05, **p<0.01, ***p<0.001.
Anti Endoglin, supplied by OriGene, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anti endoglin - by Bioz Stars, 2026-08
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j biomed photonics eng  (Photonics Inc)
86
Photonics Inc j biomed photonics eng
(A) , Wild-type (WT) and KI mice HTRZ for either PS1 FAD mutant M146V (WT/M146V) or I213T (WT/I213T) were infused with vehicle (0.2% BSA in PBS) or VEGF-A (a total of 3.5μg in 100μl of vehicle) through the carotid artery for 15 days using a mini osmotic pump as in Methods. Left: Brain coronal sections (40μm thick) were prepared and immunostained with anti-Col IV antibodies to visualize brain vessels. Enhanced visualization surfaces were generated using Imaris software from representative confocal images of ipsilateral hemispheres. Scale bar: 50μm. Right: Graph shows total vessel length density in WT and PS1 FAD brains quantified using Imaris 9.9 software as in Methods. (B) , WT and HTRZ for PS1 FAD mutants M146V or I213T mice were injected through the carotid artery for 20 minutes with either vehicle or 100ng of VEGF-A in vehicle prepared as in 1A using a catheter as described in Methods. Brain microvessels (MV) were isolated as in Methods, lysed in Triton X-100 buffer, and subjected to immunoprecipitation (IP) with anti-VEGFR2 antibody or control IgG. Left: IPs were analyzed on Western blots (WBs) <t>using</t> <t>anti-endoglin</t> or anti-VEGFR2 antibodies (upper panel). Input samples are shown in lower panel. β-actin: loading control. Right: Graph shows quantification of endoglin co-IPed with VEGFR2, normalized to IPed VEGFR2. (C) , WT mice were infused for 15 days through the carotid artery with vehicle or VEGF-A in vehicle as in 1A using a mini osmotic pump (as in 1A). For RO injection, mice were treated with vehicle (2% DMSO, 30% PEG 300, 5% Tween-80 in ddH2O) or RO in vehicle (5mg/kg body weight) via five injections in tail vein one injection every three days, with first injection administered 1 hour before osmotic pump implantation. Brain coronal sections (40μm) were prepared and immunostained with anti-Col IV antibodies as in 1A. Left: Representative confocal images of ipsilateral hemispheres are shown prepared as in 1A. Scale bar: 50μm. Right: Graph shows total vessel length density quantified using Imaris software as in 1A. (D) , WT adult mice were treated with either 50μl vehicle as in 1C or 1mg/kg RO in vehicle via carotid artery as in Methods. 15-16 hrs later, 50 μl vehicle prepared as in 1A or 100ng VEGF-A in vehicle was administered via carotid artery for 10-20 minutes using a catheter as in 1B. Brain MVs were isolated and extracted as in 1B. Left: p-VEGFR2 (Tyr1054/Tyr1059), VEGFR2, p-ERK1/2 and ERK1/2 are detected on WBs of extracts with specific antibodies in MV extracts. Vinculin: loading control. Right: Graphs show fold change of phosphorylated to total protein ratio. (E) , WT mice and mice HTRZ for PS1 FAD mutant M146V (WT/M146V) or I213T (WT/I213T) were treated with vehicle or VEGF-A via carotid artery for 10-20 minutes using a catheter as in 1D. Brain MVs were isolated and extracted as in 1B. Left: p-VEGFR2 (Tyr1054/Tyr1059), VEGFR2, p-ERK1/2 and ERK1/2 are detected on WBs of extracts with specific antibodies in MV extracts. β-actin: loading control. Right: Graphs show fold change of phosphorylated to total protein ratio. (F) , WT pCECs were prepared and treated as in Methods with vehicle (DMSO) or RO (200nM in DMSO) and then stimulated with either vehicle (PBS) or VEGF-A (20ng in PBS) for 15min. Upper: Cells were co-immunostained with either anti-VEGFR2 antibodies (green) or early endosome marker Rab5 (red) and cell nuclei were stained with Hoechst (blue) as in Methods. Yellow fluorescence in merged images indicates co-localization of VEGFR2 with Rab5. Scale bar 0.5μm. Lower: Graph shows percent of VEGFR2 co-localized with Rab5 in RO-treated WT cells compared to vehicle-treated cells measured with Imaris software. (G) , pCECs from either WT or mice HTRZ for PS1 FAD mutant M146V (WT/M146V) or I213T (WT/I213T), were stimulated with vehicle or VEGF-A in vehicle as in 1F. Upper: Cells were co-stained with anti-VEGFR2 antibodies and early endosome marker Rab5 as in 1F. Cell nuclei were stained with Hoechst (blue) as in 1F. Yellow fluorescence in merged images indicates co-localization of VEGFR2 with Rab5. Scale bar 0.5μm. Lower: Graph shows percent of VEGFR2 co-localized with Rab5 in PS1 FAD WT/M146V or WT/I213T HTRZ mice compared to WT measured with Imaris software. For Figs A-G, data are shown as Mean ± S.E. from at least three independent experiments or as indicated in the dot plots. Statistical analysis was performed using two-way ANOVA followed by Tukey post-hoc test. ns = not significant, *p<0.05, **p<0.01, ***p<0.001.
J Biomed Photonics Eng, supplied by Photonics Inc, 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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j biomed photonics eng - by Bioz Stars, 2026-08
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j geotech geoenviron eng  (Geotech Inc)
86
Geotech Inc j geotech geoenviron eng
(A) , Wild-type (WT) and KI mice HTRZ for either PS1 FAD mutant M146V (WT/M146V) or I213T (WT/I213T) were infused with vehicle (0.2% BSA in PBS) or VEGF-A (a total of 3.5μg in 100μl of vehicle) through the carotid artery for 15 days using a mini osmotic pump as in Methods. Left: Brain coronal sections (40μm thick) were prepared and immunostained with anti-Col IV antibodies to visualize brain vessels. Enhanced visualization surfaces were generated using Imaris software from representative confocal images of ipsilateral hemispheres. Scale bar: 50μm. Right: Graph shows total vessel length density in WT and PS1 FAD brains quantified using Imaris 9.9 software as in Methods. (B) , WT and HTRZ for PS1 FAD mutants M146V or I213T mice were injected through the carotid artery for 20 minutes with either vehicle or 100ng of VEGF-A in vehicle prepared as in 1A using a catheter as described in Methods. Brain microvessels (MV) were isolated as in Methods, lysed in Triton X-100 buffer, and subjected to immunoprecipitation (IP) with anti-VEGFR2 antibody or control IgG. Left: IPs were analyzed on Western blots (WBs) <t>using</t> <t>anti-endoglin</t> or anti-VEGFR2 antibodies (upper panel). Input samples are shown in lower panel. β-actin: loading control. Right: Graph shows quantification of endoglin co-IPed with VEGFR2, normalized to IPed VEGFR2. (C) , WT mice were infused for 15 days through the carotid artery with vehicle or VEGF-A in vehicle as in 1A using a mini osmotic pump (as in 1A). For RO injection, mice were treated with vehicle (2% DMSO, 30% PEG 300, 5% Tween-80 in ddH2O) or RO in vehicle (5mg/kg body weight) via five injections in tail vein one injection every three days, with first injection administered 1 hour before osmotic pump implantation. Brain coronal sections (40μm) were prepared and immunostained with anti-Col IV antibodies as in 1A. Left: Representative confocal images of ipsilateral hemispheres are shown prepared as in 1A. Scale bar: 50μm. Right: Graph shows total vessel length density quantified using Imaris software as in 1A. (D) , WT adult mice were treated with either 50μl vehicle as in 1C or 1mg/kg RO in vehicle via carotid artery as in Methods. 15-16 hrs later, 50 μl vehicle prepared as in 1A or 100ng VEGF-A in vehicle was administered via carotid artery for 10-20 minutes using a catheter as in 1B. Brain MVs were isolated and extracted as in 1B. Left: p-VEGFR2 (Tyr1054/Tyr1059), VEGFR2, p-ERK1/2 and ERK1/2 are detected on WBs of extracts with specific antibodies in MV extracts. Vinculin: loading control. Right: Graphs show fold change of phosphorylated to total protein ratio. (E) , WT mice and mice HTRZ for PS1 FAD mutant M146V (WT/M146V) or I213T (WT/I213T) were treated with vehicle or VEGF-A via carotid artery for 10-20 minutes using a catheter as in 1D. Brain MVs were isolated and extracted as in 1B. Left: p-VEGFR2 (Tyr1054/Tyr1059), VEGFR2, p-ERK1/2 and ERK1/2 are detected on WBs of extracts with specific antibodies in MV extracts. β-actin: loading control. Right: Graphs show fold change of phosphorylated to total protein ratio. (F) , WT pCECs were prepared and treated as in Methods with vehicle (DMSO) or RO (200nM in DMSO) and then stimulated with either vehicle (PBS) or VEGF-A (20ng in PBS) for 15min. Upper: Cells were co-immunostained with either anti-VEGFR2 antibodies (green) or early endosome marker Rab5 (red) and cell nuclei were stained with Hoechst (blue) as in Methods. Yellow fluorescence in merged images indicates co-localization of VEGFR2 with Rab5. Scale bar 0.5μm. Lower: Graph shows percent of VEGFR2 co-localized with Rab5 in RO-treated WT cells compared to vehicle-treated cells measured with Imaris software. (G) , pCECs from either WT or mice HTRZ for PS1 FAD mutant M146V (WT/M146V) or I213T (WT/I213T), were stimulated with vehicle or VEGF-A in vehicle as in 1F. Upper: Cells were co-stained with anti-VEGFR2 antibodies and early endosome marker Rab5 as in 1F. Cell nuclei were stained with Hoechst (blue) as in 1F. Yellow fluorescence in merged images indicates co-localization of VEGFR2 with Rab5. Scale bar 0.5μm. Lower: Graph shows percent of VEGFR2 co-localized with Rab5 in PS1 FAD WT/M146V or WT/I213T HTRZ mice compared to WT measured with Imaris software. For Figs A-G, data are shown as Mean ± S.E. from at least three independent experiments or as indicated in the dot plots. Statistical analysis was performed using two-way ANOVA followed by Tukey post-hoc test. ns = not significant, *p<0.05, **p<0.01, ***p<0.001.
J Geotech Geoenviron Eng, supplied by Geotech Inc, 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/eng/10__1007_slash_s44288___026___00503___8-397-0-1?v=Geotech+Inc
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j geotech geoenviron eng - by Bioz Stars, 2026-08
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int j innov technol explor eng  (Innov X Systems)
86
Innov X Systems int j innov technol explor eng
(A) , Wild-type (WT) and KI mice HTRZ for either PS1 FAD mutant M146V (WT/M146V) or I213T (WT/I213T) were infused with vehicle (0.2% BSA in PBS) or VEGF-A (a total of 3.5μg in 100μl of vehicle) through the carotid artery for 15 days using a mini osmotic pump as in Methods. Left: Brain coronal sections (40μm thick) were prepared and immunostained with anti-Col IV antibodies to visualize brain vessels. Enhanced visualization surfaces were generated using Imaris software from representative confocal images of ipsilateral hemispheres. Scale bar: 50μm. Right: Graph shows total vessel length density in WT and PS1 FAD brains quantified using Imaris 9.9 software as in Methods. (B) , WT and HTRZ for PS1 FAD mutants M146V or I213T mice were injected through the carotid artery for 20 minutes with either vehicle or 100ng of VEGF-A in vehicle prepared as in 1A using a catheter as described in Methods. Brain microvessels (MV) were isolated as in Methods, lysed in Triton X-100 buffer, and subjected to immunoprecipitation (IP) with anti-VEGFR2 antibody or control IgG. Left: IPs were analyzed on Western blots (WBs) <t>using</t> <t>anti-endoglin</t> or anti-VEGFR2 antibodies (upper panel). Input samples are shown in lower panel. β-actin: loading control. Right: Graph shows quantification of endoglin co-IPed with VEGFR2, normalized to IPed VEGFR2. (C) , WT mice were infused for 15 days through the carotid artery with vehicle or VEGF-A in vehicle as in 1A using a mini osmotic pump (as in 1A). For RO injection, mice were treated with vehicle (2% DMSO, 30% PEG 300, 5% Tween-80 in ddH2O) or RO in vehicle (5mg/kg body weight) via five injections in tail vein one injection every three days, with first injection administered 1 hour before osmotic pump implantation. Brain coronal sections (40μm) were prepared and immunostained with anti-Col IV antibodies as in 1A. Left: Representative confocal images of ipsilateral hemispheres are shown prepared as in 1A. Scale bar: 50μm. Right: Graph shows total vessel length density quantified using Imaris software as in 1A. (D) , WT adult mice were treated with either 50μl vehicle as in 1C or 1mg/kg RO in vehicle via carotid artery as in Methods. 15-16 hrs later, 50 μl vehicle prepared as in 1A or 100ng VEGF-A in vehicle was administered via carotid artery for 10-20 minutes using a catheter as in 1B. Brain MVs were isolated and extracted as in 1B. Left: p-VEGFR2 (Tyr1054/Tyr1059), VEGFR2, p-ERK1/2 and ERK1/2 are detected on WBs of extracts with specific antibodies in MV extracts. Vinculin: loading control. Right: Graphs show fold change of phosphorylated to total protein ratio. (E) , WT mice and mice HTRZ for PS1 FAD mutant M146V (WT/M146V) or I213T (WT/I213T) were treated with vehicle or VEGF-A via carotid artery for 10-20 minutes using a catheter as in 1D. Brain MVs were isolated and extracted as in 1B. Left: p-VEGFR2 (Tyr1054/Tyr1059), VEGFR2, p-ERK1/2 and ERK1/2 are detected on WBs of extracts with specific antibodies in MV extracts. β-actin: loading control. Right: Graphs show fold change of phosphorylated to total protein ratio. (F) , WT pCECs were prepared and treated as in Methods with vehicle (DMSO) or RO (200nM in DMSO) and then stimulated with either vehicle (PBS) or VEGF-A (20ng in PBS) for 15min. Upper: Cells were co-immunostained with either anti-VEGFR2 antibodies (green) or early endosome marker Rab5 (red) and cell nuclei were stained with Hoechst (blue) as in Methods. Yellow fluorescence in merged images indicates co-localization of VEGFR2 with Rab5. Scale bar 0.5μm. Lower: Graph shows percent of VEGFR2 co-localized with Rab5 in RO-treated WT cells compared to vehicle-treated cells measured with Imaris software. (G) , pCECs from either WT or mice HTRZ for PS1 FAD mutant M146V (WT/M146V) or I213T (WT/I213T), were stimulated with vehicle or VEGF-A in vehicle as in 1F. Upper: Cells were co-stained with anti-VEGFR2 antibodies and early endosome marker Rab5 as in 1F. Cell nuclei were stained with Hoechst (blue) as in 1F. Yellow fluorescence in merged images indicates co-localization of VEGFR2 with Rab5. Scale bar 0.5μm. Lower: Graph shows percent of VEGFR2 co-localized with Rab5 in PS1 FAD WT/M146V or WT/I213T HTRZ mice compared to WT measured with Imaris software. For Figs A-G, data are shown as Mean ± S.E. from at least three independent experiments or as indicated in the dot plots. Statistical analysis was performed using two-way ANOVA followed by Tukey post-hoc test. ns = not significant, *p<0.05, **p<0.01, ***p<0.001.
Int J Innov Technol Explor Eng, supplied by Innov X Systems, 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/eng/10__1007_slash_s44245___026___00241___8-596-0-2?v=Innov+X+Systems
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int j innov technol explor eng - by Bioz Stars, 2026-08
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electron j geotech eng  (Geotech Inc)
86
Geotech Inc electron j geotech eng
(A) , Wild-type (WT) and KI mice HTRZ for either PS1 FAD mutant M146V (WT/M146V) or I213T (WT/I213T) were infused with vehicle (0.2% BSA in PBS) or VEGF-A (a total of 3.5μg in 100μl of vehicle) through the carotid artery for 15 days using a mini osmotic pump as in Methods. Left: Brain coronal sections (40μm thick) were prepared and immunostained with anti-Col IV antibodies to visualize brain vessels. Enhanced visualization surfaces were generated using Imaris software from representative confocal images of ipsilateral hemispheres. Scale bar: 50μm. Right: Graph shows total vessel length density in WT and PS1 FAD brains quantified using Imaris 9.9 software as in Methods. (B) , WT and HTRZ for PS1 FAD mutants M146V or I213T mice were injected through the carotid artery for 20 minutes with either vehicle or 100ng of VEGF-A in vehicle prepared as in 1A using a catheter as described in Methods. Brain microvessels (MV) were isolated as in Methods, lysed in Triton X-100 buffer, and subjected to immunoprecipitation (IP) with anti-VEGFR2 antibody or control IgG. Left: IPs were analyzed on Western blots (WBs) <t>using</t> <t>anti-endoglin</t> or anti-VEGFR2 antibodies (upper panel). Input samples are shown in lower panel. β-actin: loading control. Right: Graph shows quantification of endoglin co-IPed with VEGFR2, normalized to IPed VEGFR2. (C) , WT mice were infused for 15 days through the carotid artery with vehicle or VEGF-A in vehicle as in 1A using a mini osmotic pump (as in 1A). For RO injection, mice were treated with vehicle (2% DMSO, 30% PEG 300, 5% Tween-80 in ddH2O) or RO in vehicle (5mg/kg body weight) via five injections in tail vein one injection every three days, with first injection administered 1 hour before osmotic pump implantation. Brain coronal sections (40μm) were prepared and immunostained with anti-Col IV antibodies as in 1A. Left: Representative confocal images of ipsilateral hemispheres are shown prepared as in 1A. Scale bar: 50μm. Right: Graph shows total vessel length density quantified using Imaris software as in 1A. (D) , WT adult mice were treated with either 50μl vehicle as in 1C or 1mg/kg RO in vehicle via carotid artery as in Methods. 15-16 hrs later, 50 μl vehicle prepared as in 1A or 100ng VEGF-A in vehicle was administered via carotid artery for 10-20 minutes using a catheter as in 1B. Brain MVs were isolated and extracted as in 1B. Left: p-VEGFR2 (Tyr1054/Tyr1059), VEGFR2, p-ERK1/2 and ERK1/2 are detected on WBs of extracts with specific antibodies in MV extracts. Vinculin: loading control. Right: Graphs show fold change of phosphorylated to total protein ratio. (E) , WT mice and mice HTRZ for PS1 FAD mutant M146V (WT/M146V) or I213T (WT/I213T) were treated with vehicle or VEGF-A via carotid artery for 10-20 minutes using a catheter as in 1D. Brain MVs were isolated and extracted as in 1B. Left: p-VEGFR2 (Tyr1054/Tyr1059), VEGFR2, p-ERK1/2 and ERK1/2 are detected on WBs of extracts with specific antibodies in MV extracts. β-actin: loading control. Right: Graphs show fold change of phosphorylated to total protein ratio. (F) , WT pCECs were prepared and treated as in Methods with vehicle (DMSO) or RO (200nM in DMSO) and then stimulated with either vehicle (PBS) or VEGF-A (20ng in PBS) for 15min. Upper: Cells were co-immunostained with either anti-VEGFR2 antibodies (green) or early endosome marker Rab5 (red) and cell nuclei were stained with Hoechst (blue) as in Methods. Yellow fluorescence in merged images indicates co-localization of VEGFR2 with Rab5. Scale bar 0.5μm. Lower: Graph shows percent of VEGFR2 co-localized with Rab5 in RO-treated WT cells compared to vehicle-treated cells measured with Imaris software. (G) , pCECs from either WT or mice HTRZ for PS1 FAD mutant M146V (WT/M146V) or I213T (WT/I213T), were stimulated with vehicle or VEGF-A in vehicle as in 1F. Upper: Cells were co-stained with anti-VEGFR2 antibodies and early endosome marker Rab5 as in 1F. Cell nuclei were stained with Hoechst (blue) as in 1F. Yellow fluorescence in merged images indicates co-localization of VEGFR2 with Rab5. Scale bar 0.5μm. Lower: Graph shows percent of VEGFR2 co-localized with Rab5 in PS1 FAD WT/M146V or WT/I213T HTRZ mice compared to WT measured with Imaris software. For Figs A-G, data are shown as Mean ± S.E. from at least three independent experiments or as indicated in the dot plots. Statistical analysis was performed using two-way ANOVA followed by Tukey post-hoc test. ns = not significant, *p<0.05, **p<0.01, ***p<0.001.
Electron J Geotech Eng, supplied by Geotech Inc, 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/eng/10__1007_slash_s41062___026___02657___3-388-0-2?v=Geotech+Inc
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electron j geotech eng - by Bioz Stars, 2026-08
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j rock mech geotech eng  (Geotech Inc)
86
Geotech Inc j rock mech geotech eng
(A) , Wild-type (WT) and KI mice HTRZ for either PS1 FAD mutant M146V (WT/M146V) or I213T (WT/I213T) were infused with vehicle (0.2% BSA in PBS) or VEGF-A (a total of 3.5μg in 100μl of vehicle) through the carotid artery for 15 days using a mini osmotic pump as in Methods. Left: Brain coronal sections (40μm thick) were prepared and immunostained with anti-Col IV antibodies to visualize brain vessels. Enhanced visualization surfaces were generated using Imaris software from representative confocal images of ipsilateral hemispheres. Scale bar: 50μm. Right: Graph shows total vessel length density in WT and PS1 FAD brains quantified using Imaris 9.9 software as in Methods. (B) , WT and HTRZ for PS1 FAD mutants M146V or I213T mice were injected through the carotid artery for 20 minutes with either vehicle or 100ng of VEGF-A in vehicle prepared as in 1A using a catheter as described in Methods. Brain microvessels (MV) were isolated as in Methods, lysed in Triton X-100 buffer, and subjected to immunoprecipitation (IP) with anti-VEGFR2 antibody or control IgG. Left: IPs were analyzed on Western blots (WBs) <t>using</t> <t>anti-endoglin</t> or anti-VEGFR2 antibodies (upper panel). Input samples are shown in lower panel. β-actin: loading control. Right: Graph shows quantification of endoglin co-IPed with VEGFR2, normalized to IPed VEGFR2. (C) , WT mice were infused for 15 days through the carotid artery with vehicle or VEGF-A in vehicle as in 1A using a mini osmotic pump (as in 1A). For RO injection, mice were treated with vehicle (2% DMSO, 30% PEG 300, 5% Tween-80 in ddH2O) or RO in vehicle (5mg/kg body weight) via five injections in tail vein one injection every three days, with first injection administered 1 hour before osmotic pump implantation. Brain coronal sections (40μm) were prepared and immunostained with anti-Col IV antibodies as in 1A. Left: Representative confocal images of ipsilateral hemispheres are shown prepared as in 1A. Scale bar: 50μm. Right: Graph shows total vessel length density quantified using Imaris software as in 1A. (D) , WT adult mice were treated with either 50μl vehicle as in 1C or 1mg/kg RO in vehicle via carotid artery as in Methods. 15-16 hrs later, 50 μl vehicle prepared as in 1A or 100ng VEGF-A in vehicle was administered via carotid artery for 10-20 minutes using a catheter as in 1B. Brain MVs were isolated and extracted as in 1B. Left: p-VEGFR2 (Tyr1054/Tyr1059), VEGFR2, p-ERK1/2 and ERK1/2 are detected on WBs of extracts with specific antibodies in MV extracts. Vinculin: loading control. Right: Graphs show fold change of phosphorylated to total protein ratio. (E) , WT mice and mice HTRZ for PS1 FAD mutant M146V (WT/M146V) or I213T (WT/I213T) were treated with vehicle or VEGF-A via carotid artery for 10-20 minutes using a catheter as in 1D. Brain MVs were isolated and extracted as in 1B. Left: p-VEGFR2 (Tyr1054/Tyr1059), VEGFR2, p-ERK1/2 and ERK1/2 are detected on WBs of extracts with specific antibodies in MV extracts. β-actin: loading control. Right: Graphs show fold change of phosphorylated to total protein ratio. (F) , WT pCECs were prepared and treated as in Methods with vehicle (DMSO) or RO (200nM in DMSO) and then stimulated with either vehicle (PBS) or VEGF-A (20ng in PBS) for 15min. Upper: Cells were co-immunostained with either anti-VEGFR2 antibodies (green) or early endosome marker Rab5 (red) and cell nuclei were stained with Hoechst (blue) as in Methods. Yellow fluorescence in merged images indicates co-localization of VEGFR2 with Rab5. Scale bar 0.5μm. Lower: Graph shows percent of VEGFR2 co-localized with Rab5 in RO-treated WT cells compared to vehicle-treated cells measured with Imaris software. (G) , pCECs from either WT or mice HTRZ for PS1 FAD mutant M146V (WT/M146V) or I213T (WT/I213T), were stimulated with vehicle or VEGF-A in vehicle as in 1F. Upper: Cells were co-stained with anti-VEGFR2 antibodies and early endosome marker Rab5 as in 1F. Cell nuclei were stained with Hoechst (blue) as in 1F. Yellow fluorescence in merged images indicates co-localization of VEGFR2 with Rab5. Scale bar 0.5μm. Lower: Graph shows percent of VEGFR2 co-localized with Rab5 in PS1 FAD WT/M146V or WT/I213T HTRZ mice compared to WT measured with Imaris software. For Figs A-G, data are shown as Mean ± S.E. from at least three independent experiments or as indicated in the dot plots. Statistical analysis was performed using two-way ANOVA followed by Tukey post-hoc test. ns = not significant, *p<0.05, **p<0.01, ***p<0.001.
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(A) , Wild-type (WT) and KI mice HTRZ for either PS1 FAD mutant M146V (WT/M146V) or I213T (WT/I213T) were infused with vehicle (0.2% BSA in PBS) or VEGF-A (a total of 3.5μg in 100μl of vehicle) through the carotid artery for 15 days using a mini osmotic pump as in Methods. Left: Brain coronal sections (40μm thick) were prepared and immunostained with anti-Col IV antibodies to visualize brain vessels. Enhanced visualization surfaces were generated using Imaris software from representative confocal images of ipsilateral hemispheres. Scale bar: 50μm. Right: Graph shows total vessel length density in WT and PS1 FAD brains quantified using Imaris 9.9 software as in Methods. (B) , WT and HTRZ for PS1 FAD mutants M146V or I213T mice were injected through the carotid artery for 20 minutes with either vehicle or 100ng of VEGF-A in vehicle prepared as in 1A using a catheter as described in Methods. Brain microvessels (MV) were isolated as in Methods, lysed in Triton X-100 buffer, and subjected to immunoprecipitation (IP) with anti-VEGFR2 antibody or control IgG. Left: IPs were analyzed on Western blots (WBs) using anti-endoglin or anti-VEGFR2 antibodies (upper panel). Input samples are shown in lower panel. β-actin: loading control. Right: Graph shows quantification of endoglin co-IPed with VEGFR2, normalized to IPed VEGFR2. (C) , WT mice were infused for 15 days through the carotid artery with vehicle or VEGF-A in vehicle as in 1A using a mini osmotic pump (as in 1A). For RO injection, mice were treated with vehicle (2% DMSO, 30% PEG 300, 5% Tween-80 in ddH2O) or RO in vehicle (5mg/kg body weight) via five injections in tail vein one injection every three days, with first injection administered 1 hour before osmotic pump implantation. Brain coronal sections (40μm) were prepared and immunostained with anti-Col IV antibodies as in 1A. Left: Representative confocal images of ipsilateral hemispheres are shown prepared as in 1A. Scale bar: 50μm. Right: Graph shows total vessel length density quantified using Imaris software as in 1A. (D) , WT adult mice were treated with either 50μl vehicle as in 1C or 1mg/kg RO in vehicle via carotid artery as in Methods. 15-16 hrs later, 50 μl vehicle prepared as in 1A or 100ng VEGF-A in vehicle was administered via carotid artery for 10-20 minutes using a catheter as in 1B. Brain MVs were isolated and extracted as in 1B. Left: p-VEGFR2 (Tyr1054/Tyr1059), VEGFR2, p-ERK1/2 and ERK1/2 are detected on WBs of extracts with specific antibodies in MV extracts. Vinculin: loading control. Right: Graphs show fold change of phosphorylated to total protein ratio. (E) , WT mice and mice HTRZ for PS1 FAD mutant M146V (WT/M146V) or I213T (WT/I213T) were treated with vehicle or VEGF-A via carotid artery for 10-20 minutes using a catheter as in 1D. Brain MVs were isolated and extracted as in 1B. Left: p-VEGFR2 (Tyr1054/Tyr1059), VEGFR2, p-ERK1/2 and ERK1/2 are detected on WBs of extracts with specific antibodies in MV extracts. β-actin: loading control. Right: Graphs show fold change of phosphorylated to total protein ratio. (F) , WT pCECs were prepared and treated as in Methods with vehicle (DMSO) or RO (200nM in DMSO) and then stimulated with either vehicle (PBS) or VEGF-A (20ng in PBS) for 15min. Upper: Cells were co-immunostained with either anti-VEGFR2 antibodies (green) or early endosome marker Rab5 (red) and cell nuclei were stained with Hoechst (blue) as in Methods. Yellow fluorescence in merged images indicates co-localization of VEGFR2 with Rab5. Scale bar 0.5μm. Lower: Graph shows percent of VEGFR2 co-localized with Rab5 in RO-treated WT cells compared to vehicle-treated cells measured with Imaris software. (G) , pCECs from either WT or mice HTRZ for PS1 FAD mutant M146V (WT/M146V) or I213T (WT/I213T), were stimulated with vehicle or VEGF-A in vehicle as in 1F. Upper: Cells were co-stained with anti-VEGFR2 antibodies and early endosome marker Rab5 as in 1F. Cell nuclei were stained with Hoechst (blue) as in 1F. Yellow fluorescence in merged images indicates co-localization of VEGFR2 with Rab5. Scale bar 0.5μm. Lower: Graph shows percent of VEGFR2 co-localized with Rab5 in PS1 FAD WT/M146V or WT/I213T HTRZ mice compared to WT measured with Imaris software. For Figs A-G, data are shown as Mean ± S.E. from at least three independent experiments or as indicated in the dot plots. Statistical analysis was performed using two-way ANOVA followed by Tukey post-hoc test. ns = not significant, *p<0.05, **p<0.01, ***p<0.001.

Journal: bioRxiv

Article Title: PS FAD mutants and γ-secretase inhibition accumulate VEGFR2-derived peptide VCTF1 suppressing brain VEGFR2 dimerization, angiogenesis and neuroprotection

doi: 10.64898/2026.05.12.724648

Figure Lengend Snippet: (A) , Wild-type (WT) and KI mice HTRZ for either PS1 FAD mutant M146V (WT/M146V) or I213T (WT/I213T) were infused with vehicle (0.2% BSA in PBS) or VEGF-A (a total of 3.5μg in 100μl of vehicle) through the carotid artery for 15 days using a mini osmotic pump as in Methods. Left: Brain coronal sections (40μm thick) were prepared and immunostained with anti-Col IV antibodies to visualize brain vessels. Enhanced visualization surfaces were generated using Imaris software from representative confocal images of ipsilateral hemispheres. Scale bar: 50μm. Right: Graph shows total vessel length density in WT and PS1 FAD brains quantified using Imaris 9.9 software as in Methods. (B) , WT and HTRZ for PS1 FAD mutants M146V or I213T mice were injected through the carotid artery for 20 minutes with either vehicle or 100ng of VEGF-A in vehicle prepared as in 1A using a catheter as described in Methods. Brain microvessels (MV) were isolated as in Methods, lysed in Triton X-100 buffer, and subjected to immunoprecipitation (IP) with anti-VEGFR2 antibody or control IgG. Left: IPs were analyzed on Western blots (WBs) using anti-endoglin or anti-VEGFR2 antibodies (upper panel). Input samples are shown in lower panel. β-actin: loading control. Right: Graph shows quantification of endoglin co-IPed with VEGFR2, normalized to IPed VEGFR2. (C) , WT mice were infused for 15 days through the carotid artery with vehicle or VEGF-A in vehicle as in 1A using a mini osmotic pump (as in 1A). For RO injection, mice were treated with vehicle (2% DMSO, 30% PEG 300, 5% Tween-80 in ddH2O) or RO in vehicle (5mg/kg body weight) via five injections in tail vein one injection every three days, with first injection administered 1 hour before osmotic pump implantation. Brain coronal sections (40μm) were prepared and immunostained with anti-Col IV antibodies as in 1A. Left: Representative confocal images of ipsilateral hemispheres are shown prepared as in 1A. Scale bar: 50μm. Right: Graph shows total vessel length density quantified using Imaris software as in 1A. (D) , WT adult mice were treated with either 50μl vehicle as in 1C or 1mg/kg RO in vehicle via carotid artery as in Methods. 15-16 hrs later, 50 μl vehicle prepared as in 1A or 100ng VEGF-A in vehicle was administered via carotid artery for 10-20 minutes using a catheter as in 1B. Brain MVs were isolated and extracted as in 1B. Left: p-VEGFR2 (Tyr1054/Tyr1059), VEGFR2, p-ERK1/2 and ERK1/2 are detected on WBs of extracts with specific antibodies in MV extracts. Vinculin: loading control. Right: Graphs show fold change of phosphorylated to total protein ratio. (E) , WT mice and mice HTRZ for PS1 FAD mutant M146V (WT/M146V) or I213T (WT/I213T) were treated with vehicle or VEGF-A via carotid artery for 10-20 minutes using a catheter as in 1D. Brain MVs were isolated and extracted as in 1B. Left: p-VEGFR2 (Tyr1054/Tyr1059), VEGFR2, p-ERK1/2 and ERK1/2 are detected on WBs of extracts with specific antibodies in MV extracts. β-actin: loading control. Right: Graphs show fold change of phosphorylated to total protein ratio. (F) , WT pCECs were prepared and treated as in Methods with vehicle (DMSO) or RO (200nM in DMSO) and then stimulated with either vehicle (PBS) or VEGF-A (20ng in PBS) for 15min. Upper: Cells were co-immunostained with either anti-VEGFR2 antibodies (green) or early endosome marker Rab5 (red) and cell nuclei were stained with Hoechst (blue) as in Methods. Yellow fluorescence in merged images indicates co-localization of VEGFR2 with Rab5. Scale bar 0.5μm. Lower: Graph shows percent of VEGFR2 co-localized with Rab5 in RO-treated WT cells compared to vehicle-treated cells measured with Imaris software. (G) , pCECs from either WT or mice HTRZ for PS1 FAD mutant M146V (WT/M146V) or I213T (WT/I213T), were stimulated with vehicle or VEGF-A in vehicle as in 1F. Upper: Cells were co-stained with anti-VEGFR2 antibodies and early endosome marker Rab5 as in 1F. Cell nuclei were stained with Hoechst (blue) as in 1F. Yellow fluorescence in merged images indicates co-localization of VEGFR2 with Rab5. Scale bar 0.5μm. Lower: Graph shows percent of VEGFR2 co-localized with Rab5 in PS1 FAD WT/M146V or WT/I213T HTRZ mice compared to WT measured with Imaris software. For Figs A-G, data are shown as Mean ± S.E. from at least three independent experiments or as indicated in the dot plots. Statistical analysis was performed using two-way ANOVA followed by Tukey post-hoc test. ns = not significant, *p<0.05, **p<0.01, ***p<0.001.

Article Snippet: Mouse monoclonal anti-Flag tag (M2; F1804) was from Millipore Sigma, anti-GAPDH (2118S) from Cell Signaling Technologies (Beverly, MA), anti-VEGFR2 (OTI12C1) from Origene, anti-endoglin (CD-105; NBP2-22122) and anti-LAMP2 (NBP2-22217) from Novus Biologicals, Inc, anti-Rab5 (D-11) and anti-Rab7 (B-3) from Santa Cruz Biotechnology, Inc. Chicken polyclonal anti-GFAP (ab4674) was from Abcam.

Techniques: Mutagenesis, Generated, Software, Injection, Isolation, Immunoprecipitation, Control, Western Blot, Marker, Staining, Fluorescence

(A), Brain tissue extracts were prepared as in Methods from twelve PS1 FAD patients each carrying a different PS1 mutation, and twelve non-demented controls described in Methods. Left: VEGFR2 dimers and monomers were detected in brain extracts on WBs using anti-VEGFR2 antibody D5B1. Representative gels with control (C1-4) or FAD samples (FAD1-4) expressing mutants P264L, A260V, N135S and P242H respectively are shown. Vinculin: loading control. Right: Graph shows the fold change in VEGFR2 dimer to monomer ratio of FAD and control samples. (B), Brain tissue extract from control and PS1 FAD patient brains described in 7A were prepared and IPed with anti-endoglin antibody (ab252345) or IgG as in Methods. Upper panel: VEGFR2 co-IPed with endoglin was detected on WBs using an anti-VEGFR2 antibody as in 7A. Lower panel: Input samples are shown. Representative gel with control samples (C1, C2) and FAD samples (FAD1, FAD2) expressing mutants A260V and P264L respectively is shown. β-actin: loading control. Right: Graph shows relative levels of VEGFR2 co-precipitated with endoglin. (C), Brain sections from control and PS1 FAD patients were prepared as in Methods and stained for Col IV as in 1A. Upper: Representative images show brain vessels in either PS1 FAD or control (CT) brain sections. Scale bar: 80μm. Lower: Graph shows total vessel length density in PS1 FAD and CT brains quantified with Imaris software as in 1A. A-C , bars represent Mean ± S.E. For statistical analysis, unpaired t-test was performed. *p < 0.05, **p<0.01 and ***p<0.001.

Journal: bioRxiv

Article Title: PS FAD mutants and γ-secretase inhibition accumulate VEGFR2-derived peptide VCTF1 suppressing brain VEGFR2 dimerization, angiogenesis and neuroprotection

doi: 10.64898/2026.05.12.724648

Figure Lengend Snippet: (A), Brain tissue extracts were prepared as in Methods from twelve PS1 FAD patients each carrying a different PS1 mutation, and twelve non-demented controls described in Methods. Left: VEGFR2 dimers and monomers were detected in brain extracts on WBs using anti-VEGFR2 antibody D5B1. Representative gels with control (C1-4) or FAD samples (FAD1-4) expressing mutants P264L, A260V, N135S and P242H respectively are shown. Vinculin: loading control. Right: Graph shows the fold change in VEGFR2 dimer to monomer ratio of FAD and control samples. (B), Brain tissue extract from control and PS1 FAD patient brains described in 7A were prepared and IPed with anti-endoglin antibody (ab252345) or IgG as in Methods. Upper panel: VEGFR2 co-IPed with endoglin was detected on WBs using an anti-VEGFR2 antibody as in 7A. Lower panel: Input samples are shown. Representative gel with control samples (C1, C2) and FAD samples (FAD1, FAD2) expressing mutants A260V and P264L respectively is shown. β-actin: loading control. Right: Graph shows relative levels of VEGFR2 co-precipitated with endoglin. (C), Brain sections from control and PS1 FAD patients were prepared as in Methods and stained for Col IV as in 1A. Upper: Representative images show brain vessels in either PS1 FAD or control (CT) brain sections. Scale bar: 80μm. Lower: Graph shows total vessel length density in PS1 FAD and CT brains quantified with Imaris software as in 1A. A-C , bars represent Mean ± S.E. For statistical analysis, unpaired t-test was performed. *p < 0.05, **p<0.01 and ***p<0.001.

Article Snippet: Mouse monoclonal anti-Flag tag (M2; F1804) was from Millipore Sigma, anti-GAPDH (2118S) from Cell Signaling Technologies (Beverly, MA), anti-VEGFR2 (OTI12C1) from Origene, anti-endoglin (CD-105; NBP2-22122) and anti-LAMP2 (NBP2-22217) from Novus Biologicals, Inc, anti-Rab5 (D-11) and anti-Rab7 (B-3) from Santa Cruz Biotechnology, Inc. Chicken polyclonal anti-GFAP (ab4674) was from Abcam.

Techniques: Mutagenesis, Control, Expressing, Staining, Software