- MA5-14957 - Invitrogen Antibodies NOS3 antibody

Submitted references Protective effects of endothelial progenitor cell microvesicles carrying miR‑98‑5p on angiotensin II‑induced rat kidney cell injury.

Mai H, Huang Z, Zhang X, Zhang Y, Chen J, Chen M, Zhang Y, Song Y, Wang B, Lin Y, Gu S
Experimental and therapeutic medicine 2022 Nov;24(5):702

Peroxidasin promotes diabetic vascular endothelial dysfunction induced by advanced glycation end products via NOX2/HOCl/Akt/eNOS pathway.

Jing Cao, Zhang G, Liu Z, Xu Q, Li C, Cheng G, Shi R
Redox biology 2021 Sep;45:102031

Fibroblast growth factor 21 Ameliorates diabetes-induced endothelial dysfunction in mouse aorta via activation of the CaMKK2/AMPKα signaling pathway.

Ying L, Li N, He Z, Zeng X, Nan Y, Chen J, Miao P, Ying Y, Lin W, Zhao X, Lu L, Chen M, Cen W, Guo T, Li X, Huang Z, Wang Y
Cell death & disease 2019 Sep 11;10(9):665

Telomerase reverse transcriptase protects against angiotensin II-induced microvascular endothelial dysfunction.

Ait-Aissa K, Kadlec AO, Hockenberry J, Gutterman DD, Beyer AM
American journal of physiology. Heart and circulatory physiology 2018 May 1;314(5):H1053-H1060

IGF-1 receptor cleavage in hypertension.

Cirrik S, Schmid-Schönbein GW
Hypertension research : official journal of the Japanese Society of Hypertension 2018 Jun;41(6):406-413

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Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Western blot was performed using Anti-Phospho-eNOS (Ser1177) Monoclonal Antibody (H.83.2) (Product # MA5-14957) and a 160 kDa band corresponding to Phospho-eNOS (Ser1177) was observed to be upregulated upon treatment with VEGF (10 ng/mL for 60 min) and H2O2 (300 µM for 30 min). Whole cell extracts (30 µg lysate) of HAEC (Lane 1), HAEC treated with VEGF (10 ng/mL for 60 min) (Lane 2), HUVEC (Lane 3), HUVEC treated with VEGF (10 ng/mL for 60 min) (Lane 4), HAEC (Lane 5) and HAEC treated with H2O2 (300 µM for 30 min) (Lane 6) were electrophoresed using NuPAGE™ 4-12% Bis-Tris Protein Gel (Product # NP0322BOX). Resolved proteins were then transferred onto a nitrocellulose membrane (Product # IB23001) by iBlot® 2 Dry Blotting System (Product # IB21001). The blot was probed with the primary antibody (1:1000 dilution) and detected by chemiluminescence with Goat anti-Rabbit IgG (H+L) Superclonal™ Recombinant Secondary Antibody, HRP (Product # A27036,1:20000 dilution) using the iBright™ FL1500 Imaging System (Product # A44115). Chemiluminescent detection was performed using SuperSignal™ West Atto Ultimate Sensitivity Substrate (Product # A38556).

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Western blot analysis of Phospho-eNOS pSer1177 in extracts from BAEC cells, phosphatase or VEGF-treated using Phospho-eNOS pSer1177 monoclonal antibody (Product # MA5-14957) (upper) or an ENOS polyclonal antibody (lower).

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Fig. 5 p-AKT and peNOS levels in WKY and SHR aorta rings incubated in HEPES buffer at 37 degC for 20 min in the presence (IGF-1) or absence (NS) of 100 nM IGF-1. Representative images are shown a, c . An antibody against p-AKT recognized a band in the range of 60 kDa a , an antibody against peNOS recognized a band in the range of 140 kDa c , and the anti-beta-actin antibody recognized a band at 45 kDa a , c . The p-AKT and peNOS band densities were normalized to the respective beta-actin signal. Bar graphs show the means +- SD of the band densities for p-AKT b and peNOS d ( n = 4)

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Fig. 1 Long-term treatment of HFD-STZ-Induced T2D mice with rFGF21 improves hyperglycemia, insulin resistance and endothelium-dependent relaxation of aorta. a-e HFD-STZ-induced T2D mice were treated for 33 days with rFGF21 (0.5 mg/kg body weight) or buffer control. a Random fed blood glucose ( n = 10). b IPGTT over the course of 120 mins ( n = 7-9). c Integrated AUC for changes in blood glucose levels ( n = 7-9). d Dose-dependent relaxation of aorta to ACh ( n = 5-7). e Phosphorylation level of eNOS in aortas as determined by western blot analysis (upper panel) and quantitation using ImageJ software (lower panel) ( n = 3). All data are presented as mean +- SEM. * p < 0.05 vs Control; # p < 0.05 vs T2D

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Fig. 2 Long-term treatment of db/db mice with rFGF21 improves hyperglycemia, insulin resistance and endothelium-dependent relaxation of aorta. a-e db/db mice were treated for 33 days with rFGF21 (0.5 mg/kg body weight) or buffer control; littermate db/m mice served as controls. a Random fed blood glucose ( n = 5-6). b IPGTT over the course of 120 mins ( n = 5-6). c Integrated AUC for changes in blood glucose levels ( n = 5-6). d Dose-dependent relaxation of aorta to ACh ( n = 5-6). e Phosphorylation level of eNOS in aortas as determined by western blot analysis (upper panel) and quantitation using ImageJ software (lower panel) ( n = 3). All data are presented as mean +- SEM. * p < 0.05 vs Control; # p < 0.05 vs db/db

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Fig. 3 Long-term treatment of T1D mice with rFGF21 improves endothelium-dependent relaxation of aorta. a-c STZ-induced T1D mice were treated for 30 days with rFGF21 (0.5 mg/kg body weight) or buffer control; littermate db/m mice served as controls. a Random fed blood glucose ( n = 8-9). b Dose-dependent relaxation of aorta to ACh ( n = 7-8). c Phosphorylation level of eNOS in aortas as determined by western blot analysis (upper panel) and quantitation using ImageJ software (lower panel) ( n = 3). All data are presented as mean +- SEM. * p < 0.05 vs Control; # p < 0.05 vs T1D

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Fig. 5 RFGF21 improves endothelium-dependent relaxation, alleviates oxidative stress and enhances AMPK signaling in aortas challenged with HG. a-e Aortas isolated form C57BL/6 J mice in Kreb's buffer were pretreated with FIIN-4 (10 muM) or Compound C (10 muM) for 30 mins and exposed to either HG (30 mM) alone or HG plus rFGF21 (0.01 mg/mL) for an additional 2 h. a Dose-dependent relaxation to ACh ( n = 8-18). b NO 2 and NO 3 levels stimulated by ACh (6 x 10 -8 M) for 3 mins ( n = 5). c Phosphorylation level of eNOS stimulated by ACh (6 x 10 -8 M) for 3 mins as determined by western blot analysis (upper panel) and quantitation using ImageJ software (lower panel) ( n = 4). d Immunofluorescent DHE staining ( n = 6). The upper panel shows DHE staining and the lower panel shows quantitation using ImageJ software. Scale bars, 100 mum. e Phosphorylation level of AMPKalpha as determined by western blot analysis (upper panel) and quantitation using ImageJ software (lower panel) ( n = 4). f mRNA levels of CAT, HO-1 and Nrf-2 as determined by real-time PCR analysis ( n = 6). All data are presented as mean +- SEM. * p < 0.05 vs Control; # p < 0.05 vs HG; + p < 0.05 vs HG + FGF21

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Fig. 6 RFGF21 activates CaMKK2 to upregulate AMPKalpha activity, improve endothelium-dependent relaxation and alleviate oxidative stress in aortas challenged with HG. a Aortas isolated form C57BL/6J mice were pretreated with FIIN-4 (10 muM) for 30 mins and exposed to either HG (30 mM) alone or HG plus rFGF21 (0.01 mg/mL) for an additional 2 h. Phosphorylation level of CaMKK2 as determined by western blot analysis (upper panel) and quantitation using ImageJ software (lower panel) ( n = 4). b-g Aortas isolated form C57BL/6J mice were pretreated with STO-609 (5 mug/mL) for 30 mins and exposed to either HG (30 mM) alone or HG plus rFGF21 (0.01 mg/mL) for an additional 2 h. b Dose-dependent relaxation to ACh ( n = 5). c NO 2 and NO 3 levels stimulated by ACh (6 x 10 -8 M) for 3 mins ( n = 5). d Phosphorylation level of eNOS stimulated by ACh (6 x 10 -8 M) for 3 mins as determined by western blot analysis (upper panel) and quantitation using ImageJ software (lower panel) ( n = 4). e Immunofluorescent DHE staining ( n = 6). The upper panel shows DHE staining and the lower panel shows quantitation using ImageJ software. Scale bars, 100 mum. (f, g) Phosphorylation level of AMPKalpha ( f ) and ACC ( g ) as determined by western blot analysis (upper panel) and quantitation using ImageJ software (lower panel) ( n = 4). All data are presented as mean +- SEM. * p < 0.05 vs Control; # p < 0.05 vs HG; + p < 0.05 vs HG + FGF21

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Fig. 7 RFGF21 induces relaxation of aorta via CaMKK2/ AMPKalpha mediated activation of eNOS. a Dose-dependent relaxation of aorta from C57BL/6J mice to rFGF21 pretreated with FIIN-4 (10 muM) or Compound C (10 muM) for 30 mins ( n = 7-12). b , c Phosphorylation level of eNOS ( b ) and AMPKalpha ( c ) in aortas from C57BL/6 J mice pretreated with FIIN-4 (10 muM) or Compound C (10 muM) for 30 mins and exposed to rFGF21 (0.01 mg/mL) for 3 mins as determined by western blot analysis (upper panel) and quantitation using ImageJ software (lower panel) ( n = 3). d Dose-dependent relaxation of aorta from C57BL/6J mice to rFGF21 pretreated with STO-609 (5 mug/mL) for 30 mins ( n = 9-10). e-g Phosphorylation level of eNOS ( e ), AMPKalpha ( f ) and ACC ( g ) in aortas from C57BL/6J mice pretreated with STO-609 (5 mug/mL) for 30 mins and exposed to rFGF21 (0.01 mg/mL) for 3 mins as determined by western blot analysis (upper panel) and quantitation using ImageJ software (lower panel) ( n = 4). All data are presented as mean +- SEM. * p < 0.05 vs Control; # p < 0.05 vs FGF21

MA5-14957

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